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Publisher: Medknow Publishers   (Total: 429 journals)

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Showing 1 - 200 of 429 Journals sorted alphabetically
Acta Medica Intl.     Open Access   (SJR: 0.101, CiteScore: 0)
Advanced Arab Academy of Audio-Vestibulogy J.     Open Access  
Advanced Biomedical Research     Open Access  
Advances in Human Biology     Open Access   (Followers: 3)
Advances in Skeletal Muscle Function Assessment     Open Access  
African J. for Infertility and Assisted Conception     Open Access  
African J. of Medical and Health Sciences     Open Access   (Followers: 2)
African J. of Paediatric Surgery     Open Access   (Followers: 7, SJR: 0.25, CiteScore: 1)
African J. of Trauma     Open Access   (Followers: 1)
Ain-Shams J. of Anaesthesiology     Open Access   (Followers: 3)
Al-Azhar Assiut Medical J.     Open Access  
Al-Basar Intl. J. of Ophthalmology     Open Access   (Followers: 1)
Alexandria J. of Pediatrics     Open Access  
Ancient Science of Life     Open Access   (Followers: 5)
Anesthesia : Essays and Researches     Open Access   (Followers: 10)
Annals of African Medicine     Open Access   (Followers: 1, SJR: 0.258, CiteScore: 1)
Annals of Bioanthropology     Open Access   (Followers: 4)
Annals of Cardiac Anaesthesia     Open Access   (Followers: 14, SJR: 0.308, CiteScore: 1)
Annals of Indian Academy of Neurology     Open Access   (Followers: 3, SJR: 0.434, CiteScore: 1)
Annals of Indian Academy of Otorhinolaryngology Head and Neck Surgery     Open Access  
Annals of Indian Psychiatry     Open Access  
Annals of Maxillofacial Surgery     Open Access   (Followers: 6)
Annals of Medical and Health Sciences Research     Open Access   (Followers: 7)
Annals of Nigerian Medicine     Open Access   (Followers: 1)
Annals of Pediatric Cardiology     Open Access   (Followers: 8, SJR: 0.352, CiteScore: 1)
Annals of Saudi Medicine     Open Access   (SJR: 0.238, CiteScore: 1)
Annals of Thoracic Medicine     Open Access   (Followers: 6, SJR: 0.524, CiteScore: 1)
Annals of Tropical Medicine and Public Health     Open Access   (Followers: 13, SJR: 0.152, CiteScore: 0)
Annals of Tropical Pathology     Open Access  
Apollo Medicine     Open Access  
APOS Trends in Orthodontics     Open Access  
Arab J. of Interventional Radiology     Open Access  
Archives of Cardiovascular Imaging     Open Access   (Followers: 1, SJR: 0.187, CiteScore: 0)
Archives of Intl. Surgery     Open Access   (Followers: 10, SJR: 0.302, CiteScore: 1)
Archives of Medicine and Health Sciences     Open Access   (Followers: 3)
Archives of Medicine and Surgery     Open Access  
Archives of Pharmacy Practice     Open Access   (Followers: 6, SJR: 0.102, CiteScore: 0)
Archives of Trauma Research     Open Access   (Followers: 3, SJR: 0.37, CiteScore: 2)
Asia Pacific J. of Clinical Trials : Nervous System Diseases     Open Access  
Asia-Pacific J. of Oncology Nursing     Open Access   (Followers: 4)
Asian J. of Andrology     Open Access   (Followers: 1, SJR: 0.856, CiteScore: 2)
Asian J. of Neurosurgery     Open Access   (Followers: 2)
Asian J. of Oncology     Open Access   (Followers: 1)
Asian J. of Transfusion Science     Open Access   (Followers: 1, SJR: 0.35, CiteScore: 1)
Asian Pacific J. of Reproduction     Open Access   (SJR: 0.227, CiteScore: 1)
Asian Pacific J. of Tropical Biomedicine     Open Access   (Followers: 2, SJR: 0.491, CiteScore: 2)
Asian Pacific J. of Tropical Medicine     Open Access   (Followers: 1, SJR: 0.561, CiteScore: 2)
Astrocyte     Open Access  
Avicenna J. of Medicine     Open Access   (Followers: 1)
AYU : An international quarterly journal of research in Ayurveda     Open Access   (Followers: 6)
Benha Medical J.     Open Access  
Biomedical and Biotechnology Research J.     Open Access  
BLDE University J. of Health Sciences     Open Access  
Brain Circulation     Open Access  
Bulletin of Faculty of Physical Therapy     Open Access   (Followers: 1)
Canadian J. of Rural Medicine     Full-text available via subscription   (SJR: 0.202, CiteScore: 0)
Cancer Translational Medicine     Open Access   (Followers: 2)
Cardiology Plus     Open Access  
Chinese Medical J.     Open Access   (Followers: 10, SJR: 0.52, CiteScore: 1)
CHRISMED J. of Health and Research     Open Access  
Clinical Cancer Investigation J.     Open Access  
Clinical Dermatology Review     Open Access   (Followers: 2)
Clinical Trials in Degenerative Diseases     Open Access  
Clinical Trials in Orthopedic Disorders     Open Access  
Community Acquired Infection     Open Access  
Conservation and Society     Open Access   (Followers: 10, SJR: 0.811, CiteScore: 2)
Contemporary Clinical Dentistry     Open Access   (Followers: 4, SJR: 0.353, CiteScore: 1)
Current Medical Issues     Open Access   (Followers: 1)
CytoJ.     Open Access   (Followers: 2, SJR: 0.543, CiteScore: 1)
Delta J. of Ophthalmology     Open Access  
Dental Hypotheses     Open Access   (Followers: 3, SJR: 0.152, CiteScore: 0)
Dental Research J.     Open Access   (Followers: 11, SJR: 0.416, CiteScore: 1)
Dentistry and Medical Research     Open Access  
Digital Medicine     Open Access  
Drug Development and Therapeutics     Open Access  
Education for Health     Open Access   (Followers: 6, SJR: 0.242, CiteScore: 0)
Egyptian J. of Bronchology     Open Access  
Egyptian J. of Cardiothoracic Anesthesia     Open Access  
Egyptian J. of Cataract and Refractive Surgery     Open Access   (Followers: 1, SJR: 1.799, CiteScore: 2)
Egyptian J. of Chest Diseases and Tuberculosis     Open Access   (Followers: 3, SJR: 0.155, CiteScore: 0)
Egyptian J. of Dermatology and Venerology     Open Access   (Followers: 1)
Egyptian J. of Haematology     Open Access   (Followers: 1)
Egyptian J. of Internal Medicine     Open Access   (Followers: 1)
Egyptian J. of Neurology, Psychiatry and Neurosurgery     Open Access   (Followers: 1, SJR: 0.127, CiteScore: 0)
Egyptian J. of Obesity, Diabetes and Endocrinology     Open Access   (Followers: 1)
Egyptian J. of Otolaryngology     Open Access   (Followers: 2)
Egyptian J. of Psychiatry     Open Access   (Followers: 2)
Egyptian J. of Surgery     Open Access   (Followers: 1)
Egyptian Nursing J.     Open Access  
Egyptian Orthopaedic J.     Open Access   (Followers: 2)
Egyptian Pharmaceutical J.     Open Access  
Egyptian Retina J.     Open Access  
Egyptian Rheumatology and Rehabilitation     Open Access  
Endodontology     Open Access  
Endoscopic Ultrasound     Open Access   (SJR: 0.822, CiteScore: 2)
Environmental Disease     Open Access   (Followers: 3)
Eurasian J. of Pulmonology     Open Access  
European J. of Dentistry     Open Access   (Followers: 2, SJR: 0.749, CiteScore: 2)
European J. of General Dentistry     Open Access   (Followers: 1, SJR: 0.12, CiteScore: 0)
European J. of Prosthodontics     Open Access   (Followers: 3)
European J. of Psychology and Educational Studies     Open Access   (Followers: 11, SJR: 0.113, CiteScore: 0)
Fertility Science and Research     Open Access  
Formosan J. of Surgery     Open Access   (SJR: 0.112, CiteScore: 0)
Genome Integrity     Open Access   (Followers: 3, SJR: 0.153, CiteScore: 0)
Glioma     Open Access  
Global J. of Transfusion Medicine     Open Access   (Followers: 1)
Gynecology and Minimally Invasive Therapy     Open Access   (SJR: 0.311, CiteScore: 1)
Hamdan Medical J.     Open Access  
Heart and Mind     Open Access  
Heart India     Open Access   (Followers: 1)
Heart Views     Open Access   (Followers: 2)
Hepatitis B Annual     Open Access   (Followers: 3)
Ibnosina J. of Medicine and Biomedical Sciences     Open Access  
IJS Short Reports     Open Access  
Imam J. of Applied Sciences     Open Access  
Indian Anaesthetists Forum     Open Access  
Indian Dermatology Online J.     Open Access   (Followers: 3)
Indian J. of Allergy, Asthma and Immunology     Open Access   (Followers: 1)
Indian J. of Anaesthesia     Open Access   (Followers: 7, SJR: 0.478, CiteScore: 1)
Indian J. of Burns     Open Access   (Followers: 1)
Indian J. of Cancer     Open Access   (Followers: 1, SJR: 0.361, CiteScore: 1)
Indian J. of Cerebral Palsy     Open Access   (Followers: 1)
Indian J. of Community Medicine     Open Access   (Followers: 2, SJR: 0.37, CiteScore: 1)
Indian J. of Critical Care Medicine     Open Access   (Followers: 3, SJR: 0.604, CiteScore: 1)
Indian J. of Dental Research     Open Access   (Followers: 4, SJR: 0.266, CiteScore: 1)
Indian J. of Dental Sciences     Open Access  
Indian J. of Dentistry     Open Access   (Followers: 1)
Indian J. of Dermatology     Open Access   (Followers: 2, SJR: 0.468, CiteScore: 1)
Indian J. of Dermatology, Venereology and Leprology     Open Access   (Followers: 5, SJR: 0.445, CiteScore: 1)
Indian J. of Dermatopathology and Diagnostic Dermatology     Open Access  
Indian J. of Drugs in Dermatology     Open Access   (Followers: 1, SJR: 0.791, CiteScore: 1)
Indian J. of Endocrinology and Metabolism     Open Access   (Followers: 4, SJR: 0.568, CiteScore: 1)
Indian J. of Health Sciences     Open Access   (Followers: 2)
Indian J. of Medical and Paediatric Oncology     Open Access   (SJR: 0.425, CiteScore: 1)
Indian J. of Medical Microbiology     Open Access   (Followers: 1, SJR: 0.503, CiteScore: 1)
Indian J. of Medical Research     Open Access   (Followers: 4, SJR: 0.656, CiteScore: 1)
Indian J. of Medical Sciences     Open Access   (Followers: 2, SJR: 0.102, CiteScore: 0)
Indian J. of Multidisciplinary Dentistry     Open Access   (Followers: 1)
Indian J. of Nephrology     Open Access   (Followers: 2, SJR: 0.347, CiteScore: 1)
Indian J. of Nuclear Medicine     Open Access   (Followers: 2, SJR: 0.23, CiteScore: 0)
Indian J. of Occupational and Environmental Medicine     Open Access   (Followers: 3, SJR: 0.225, CiteScore: 1)
Indian J. of Ophthalmology     Open Access   (Followers: 4, SJR: 0.498, CiteScore: 1)
Indian J. of Oral Health and Research     Open Access  
Indian J. of Oral Sciences     Open Access   (Followers: 1)
Indian J. of Orthopaedics     Open Access   (Followers: 8, SJR: 0.392, CiteScore: 1)
Indian J. of Otology     Open Access   (Followers: 1, SJR: 0.199, CiteScore: 0)
Indian J. of Paediatric Dermatology     Open Access   (Followers: 2)
Indian J. of Pain     Open Access   (Followers: 1)
Indian J. of Palliative Care     Open Access   (Followers: 5, SJR: 0.454, CiteScore: 1)
Indian J. of Pathology and Microbiology     Open Access   (Followers: 2, SJR: 0.276, CiteScore: 1)
Indian J. of Pharmacology     Open Access   (SJR: 0.412, CiteScore: 1)
Indian J. of Plastic Surgery     Open Access   (Followers: 12, SJR: 0.311, CiteScore: 0)
Indian J. of Psychiatry     Open Access   (Followers: 3, SJR: 0.408, CiteScore: 1)
Indian J. of Psychological Medicine     Open Access   (SJR: 0.368, CiteScore: 1)
Indian J. of Public Health     Open Access   (Followers: 1)
Indian J. of Radiology and Imaging     Open Access   (Followers: 4)
Indian J. of Research in Homoeopathy     Open Access  
Indian J. of Respiratory Care     Open Access  
Indian J. of Rheumatology     Open Access   (SJR: 0.119, CiteScore: 0)
Indian J. of Sexually Transmitted Diseases and AIDS     Open Access   (Followers: 2, SJR: 0.34, CiteScore: 0)
Indian J. of Social Psychiatry     Open Access   (Followers: 2)
Indian J. of Transplantation     Open Access  
Indian J. of Urology     Open Access   (Followers: 3, SJR: 0.434, CiteScore: 1)
Indian J. of Vascular and Endovascular Surgery     Open Access   (Followers: 2)
Indian Spine J.     Open Access  
Industrial Psychiatry J.     Open Access   (Followers: 2)
Intervention     Open Access   (Followers: 1)
Intl. Archives of Health Sciences     Open Access  
Intl. J. of Abdominal Wall and Hernia Surgery     Open Access   (Followers: 1)
Intl. J. of Academic Medicine     Open Access  
Intl. J. of Advanced Medical and Health Research     Open Access  
Intl. J. of Applied and Basic Medical Research     Open Access  
Intl. J. of Clinical and Experimental Physiology     Open Access   (Followers: 1)
Intl. J. of Clinicopathological Correlation     Open Access  
Intl. J. of Community Dentistry     Open Access  
Intl. J. of Critical Illness and Injury Science     Open Access   (Followers: 1, SJR: 0.192, CiteScore: 0)
Intl. J. of Educational and Psychological Researches     Open Access   (Followers: 4)
Intl. J. of Environmental Health Engineering     Open Access   (Followers: 1)
Intl. J. of Forensic Odontology     Open Access   (Followers: 1)
Intl. J. of Green Pharmacy     Open Access   (Followers: 3, SJR: 0.142, CiteScore: 0)
Intl. J. of Growth Factors and Stem Cells in Dentistry     Open Access  
Intl. J. of Health & Allied Sciences     Open Access   (Followers: 3)
Intl. J. of Health System and Disaster Management     Open Access   (Followers: 3)
Intl. J. of Heart Rhythm     Open Access  
Intl. J. of Medicine and Public Health     Open Access   (Followers: 6)
Intl. J. of Mycobacteriology     Open Access   (SJR: 0.535, CiteScore: 1)
Intl. J. of Noncommunicable Diseases     Open Access  
Intl. J. of Nutrition, Pharmacology, Neurological Diseases     Open Access   (Followers: 4, SJR: 0.17, CiteScore: 0)
Intl. J. of Oral Health Sciences     Open Access   (Followers: 2)
Intl. J. of Orofacial Biology     Open Access   (Followers: 1)
Intl. J. of Orofacial Research     Open Access   (Followers: 1)
Intl. J. of Orthodontic Rehabilitation     Open Access  
Intl. J. of Pedodontic Rehabilitation     Open Access  
Intl. J. of Pharmaceutical Investigation     Open Access   (Followers: 1)
Intl. J. of Preventive Medicine     Open Access   (Followers: 1, SJR: 0.623, CiteScore: 1)
Intl. J. of Shoulder Surgery     Open Access   (Followers: 5, SJR: 0.653, CiteScore: 1)
Intl. J. of the Cardiovascular Academy     Open Access   (SJR: 0.105, CiteScore: 0)
Intl. J. of Trichology     Open Access   (SJR: 0.4, CiteScore: 1)
Intl. J. of Yoga     Open Access   (Followers: 14)
Intl. J. of Yoga : Philosophy, Psychology and Parapsychology     Open Access   (Followers: 5)

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Journal Cover
Journal of Carcinogenesis
Journal Prestige (SJR): 0.662
Citation Impact (citeScore): 2
Number of Followers: 1  

  This is an Open Access Journal Open Access journal
ISSN (Print) 1477-3163 - ISSN (Online) 1477-3163
Published by Medknow Publishers Homepage  [429 journals]
  • Evidence-based approaches to reduce cancer health disparities: Discover,
           develop, deliver, and disseminate

    • Authors: Priyanka P Desai, Jana B Lampe, Sulaimon A Bakre, Riyaz M Basha, Harlan P Jones, Jamboor K Vishwanatha
      Pages: 1 - 1
      Abstract: Priyanka P Desai, Jana B Lampe, Sulaimon A Bakre, Riyaz M Basha, Harlan P Jones, Jamboor K Vishwanatha
      Journal of Carcinogenesis 2018 17(1):1-1
      The Texas Center for Health Disparities (TCHD) at the University of North Texas Health Science Center is a National Institute on Minority Health and Health Disparities-funded, specialized center of excellence for health disparities. TCHD organized its 12th annual conference focusing on “Evidence-Based Approaches to Reduce Cancer Health Disparities: Discover, Develop, Deliver, and Disseminate.” At this conference, experts in health care, biomedical sciences, and public health gathered to discuss the current status and strategies for reducing cancer health disparities. The meeting was conducted in three sessions on breast cancer, prostate cancer, and colorectal cancer disparities, in addition to roundtable discussions and a poster session. Each session highlighted differences in the effects of cancer, based on factors such as race/ethnicity, gender, socioeconomic status, and geographical location. In each session, expert speakers presented their findings, and this was followed by a discussion panel made up of experts in that field and cancer survivors, who responded to questions from the audience. This article summarizes the approaches to fundamental, translational, clinical, and public health issues in cancer health disparities discussed at the conference.
      Citation: Journal of Carcinogenesis 2018 17(1):1-1
      PubDate: Wed,28 Feb 2018
      DOI: 10.4103/jcar.JCar_13_17
      Issue No: Vol. 17, No. 1 (2018)
       
  • Oncogenic and tumor suppressive roles of special AT-rich sequence-binding
           protein

    • Authors: Qiao Yi Chen, Max Costa
      Pages: 2 - 2
      Abstract: Qiao Yi Chen, Max Costa
      Journal of Carcinogenesis 2018 17(1):2-2
      In recent years, research efforts have been centered on the functional roles of special AT-rich sequence-binding protein (SATB2) in cancer development. Existing studies differ in the types of tumor tissues and cell lines used, resulting in mixed results, which hinder the clear understanding of whether SATB2 acts as a tumor suppressor or promoter. Literature search for this review consisted of a basic search on PubMed using keywords "SATB2" and "special AT-rich sequence-binding protein 2." Each article was then selected for further examination based on relevance of the title. In consideration to possible missing data from a primary PubMed search, after coding for relevant information, articles listed in the references section were filtered for further review. The current literature suggests that SATB2 can act both as a tumor suppressor and as a promoter since it can be regulated by multiple factors and is able to target different downstream genes in various types of cancer cell lines as well as tissues. Future studies should focus on its contradictory roles in different types of tumors. This paper provides a comprehensive review of currently available research on the role of SATB2 in different cancer cells and tissues and may provide some insight into the contradictory roles of SATB2 in cancer development.
      Citation: Journal of Carcinogenesis 2018 17(1):2-2
      PubDate: Thu,5 Apr 2018
      DOI: 10.4103/jcar.JCar_8_17
      Issue No: Vol. 17, No. 1 (2018)
       
  • Review of hepatocellular carcinoma: Epidemiology, etiology, and
           carcinogenesis

    • Authors: Yezaz Ahmed Ghouri, Idrees Mian, Julie H Rowe
      Pages: 1 - 1
      Abstract: Yezaz Ahmed Ghouri, Idrees Mian, Julie H Rowe
      Journal of Carcinogenesis 2017 16(1):1-1
      Since the 1970s, the epidemic of hepatocellular carcinoma (HCC) has spread beyond the Eastern Asian predominance and has been increasing in Northern hemisphere, especially in the United States (US) and Western Europe. It occurs more commonly in males in the fourth and fifth decades of life. Among all cancers, HCC is one of the fastest growing causes of death in the US and poses a significant economic burden on healthcare. Chronic liver disease due to hepatitis B virus or hepatitis C virus and alcohol accounts for the majority of HCC cases. Incidence of nonalcoholic fatty liver disease has been on the risem and it has also been associated with the development of HCC. Its pathogenesis varies based on the underlying etiological factor although majority of cases develop in the setting of background cirrhosis. Carcinogenesis of HCC includes angiogenesis, chronic inflammation, and tumor macroenvironment and microenvironment. There is a significant role of both intrinsic genetic risk factors and extrinsic influences such as alcohol or viral infections that lead to the development of HCC. Understanding its etiopathogenesis helps select appropriate diagnostic tests and treatments.
      Citation: Journal of Carcinogenesis 2017 16(1):1-1
      PubDate: Mon,29 May 2017
      DOI: 10.4103/jcar.JCar_9_16
      Issue No: Vol. 16, No. 1 (2017)
       
  • Role of matrix metalloproteinase 13 gene expression in the evaluation of
           radiation response in oral squamous cell carcinoma

    • Authors: Shankar Sharan Singh, Madan Lal Brahma Bhatt, Vandana Singh Kushwaha, Anshuman Singh, Rajendra Kumar, Rajeev Gupta, Devendra Parmar
      Pages: 2 - 2
      Abstract: Shankar Sharan Singh, Madan Lal Brahma Bhatt, Vandana Singh Kushwaha, Anshuman Singh, Rajendra Kumar, Rajeev Gupta, Devendra Parmar
      Journal of Carcinogenesis 2017 16(1):2-2
      BACKGROUND: Matrix Metalloproteinase 13 (MMP13) is a member of collagenase family and it is involved in the degradation of extracellular matrix and basement membrane protein. It is thought to be associated with tumor invasion and metastasis. Elevated MMP13 expression has been found in carcinoma of the breast, urinary bladder, head and neck and others. It is observed that MMP13 gene is also correlated with radiation response in OSCC (Oral squamous cell carcinoma) cell line based study. The present study correlates the MMP13 expressions with clinicopathological parameters and radiation response in OSCC patients. MATERIALS AND METHODS: The MMP13 mRNA levels were determined by employing qRT-PCR (real-time quantitative reverse transcriptase-polymerase chain reaction). RESULTS: We observed high expression of MMP13 mRNA in OSCC patients when compared with matched controls. Statistically significant up regulation of MMP13 mRNA expression was found in tobacco chewers, advanced T-stage (p < 0.001) and lymph node metastasis (p < 0.01). MMP13 mRNA levels were also elevated in non responders as compared to responders to radiation treatment. CONCLUSIONS: To the best of our knowledge, this is the first report that indicates role of MMP13 in radiation response in OSCC patients and could be used as potential bio-marker for radiotherapy treatment in OSCC patients.
      Citation: Journal of Carcinogenesis 2017 16(1):2-2
      PubDate: Mon,19 Jun 2017
      DOI: 10.4103/jcar.JCar_5_16
      Issue No: Vol. 16, No. 1 (2017)
       
  • The impact of gender, race, socioeconomic status, and treatment on
           outcomes in esophageal cancer: A population-based analysis

    • Authors: Phu N Tran, Thomas H Taylor, Samuel J Klempner, Jason A Zell
      Pages: 3 - 3
      Abstract: Phu N Tran, Thomas H Taylor, Samuel J Klempner, Jason A Zell
      Journal of Carcinogenesis 2017 16(1):3-3
      Background: African Americans and Hispanics are reported to have higher mortality from esophageal cancer (EC) than Caucasians. In this study, we analyzed the independent effects of race, gender, treatment, and socioeconomic status (SES) on overall survival (OS). Methods: Data for all EC cases between 2004 and 2010 with follow-up through 2012 were obtained from the California Cancer Registry. We conducted descriptive analyses of clinical variables and survival analyses by Kaplan–Meier and Cox proportional hazards methods. Results: African Americans and Hispanics were more likely to be in the lower SES strata and less likely to receive surgery than Caucasians in this cohort. The proportion of patients receiving chemotherapy and radiotherapy was similar across different racial/ethnic groups. After adjustment for stage, grade, histology, treatments, and SES in multivariate analyses, the mortality risk in African Americans (hazard ratio [HR] 0.96, 95% confidence interval [CI] 0.85–1.07) and Hispanics (HR 0.96, 95% CI 0.89–1.07) did not differ from Caucasians (HR = 1.00, referent), with histology, SES, and surgery largely accounting for unadjusted OS differences. We also observed that African American men had higher adjusted risk of death relative to Caucasian men (HR 1.24, 95% CI 1.07–1.42), but this effect was not observed for African American women compared to Caucasian women (HR 1.12, 95% CI 0.94–1.35). Conclusions: Race is not an independent risk factor for OS in our population-based analysis of EC cases. Rather, observed differences in OS by race/ethnicity result from differences in cancer histology, SES, surgery, and gender. Our findings support further health disparities research for this disease.
      Citation: Journal of Carcinogenesis 2017 16(1):3-3
      PubDate: Mon,18 Sep 2017
      DOI: 10.4103/jcar.JCar_4_17
      Issue No: Vol. 16, No. 1 (2017)
       
  • Nicotine and lung cancer

    • Authors: Graham W Warren, Anurag K Singh
      Pages: 1 - 1
      Abstract: Graham W Warren, Anurag K Singh
      Journal of Carcinogenesis 2013 12(1):1-1
      Tobacco use in cancer patients is associated with increased cancer treatment failure and decreased survival. Nicotine is one of over 7,000 compounds in tobacco smoke and nicotine is the principal chemical associated with addiction. The purpose of this article is to review the tumor promoting activities of nicotine. Nicotine and its metabolites can promote tumor growth through increased proliferation, angiogenesis, migration, invasion, epithelial to mesenchymal transition, and stimulation of autocrine loops associated with tumor growth. Furthermore, nicotine can decrease the biologic effectiveness of conventional cancer treatments such as chemotherapy and radiotherapy. Common mechanisms appear to involve activation of nicotinic acetylcholine receptors and beta-adrenergic receptors leading to downstream activation of parallel signal transduction pathways that facilitate tumor progression and resistance to treatment. Data suggest that nicotine may be an important mechanism by which tobacco promotes tumor development, progression, and resistance to cancer treatment.
      Citation: Journal of Carcinogenesis 2013 12(1):1-1
      PubDate: Thu,31 Jan 2013
      DOI: 10.4103/1477-3163.106680
      Issue No: Vol. 12, No. 1 (2013)
       
  • Lung cancer screening update

    • Authors: Samjot Singh Dhillon, Gregory Loewen, Vijayvel Jayaprakash, Mary E Reid
      Pages: 2 - 2
      Abstract: Samjot Singh Dhillon, Gregory Loewen, Vijayvel Jayaprakash, Mary E Reid
      Journal of Carcinogenesis 2013 12(1):2-2
      Lung cancer is the leading cause of cancer-related mortality globally and the American cancer society estimates approximately 226,160 new cases and 160,340 deaths from lung cancer in the USA in the year 2012. The majority of lung cancers are diagnosed in the later stages which impacts the overall survival. The 5-year survival rate for pathological st age IA lung cancer is 73% but drops to only 13% for stage IV. Thus, early detection through screening and prevention are the keys to reduce the global burden of lung cancer. This article discusses the current state of lung cancer screening, including the results of the National Lung Cancer Screening Trial, the consideration of implementing computed tomography screening, and a brief overview of the role of bronchoscopy in early detection and potential biomarkers that may aid in the early diagnosis of lung cancer.
      Citation: Journal of Carcinogenesis 2013 12(1):2-2
      PubDate: Thu,31 Jan 2013
      DOI: 10.4103/1477-3163.106681
      Issue No: Vol. 12, No. 1 (2013)
       
  • Lung cancer biomarkers: State of the art

    • Authors: Sangeetha Subramaniam, Ram Krishna Thakur, Vinod Kumar Yadav, Ranjan Nanda, Shantanu Chowdhury, Anurag Agrawal
      Pages: 3 - 3
      Abstract: Sangeetha Subramaniam, Ram Krishna Thakur, Vinod Kumar Yadav, Ranjan Nanda, Shantanu Chowdhury, Anurag Agrawal
      Journal of Carcinogenesis 2013 12(1):3-3
      Lung cancer is one of the deadliest cancers worldwide, with the highest incidence and mortality amongst all cancers. While the prognosis of lung cancer is generally grim, with 5-year survival rates of only 15%, there is hope, and evidence, that early detection of lung cancer can reduce mortality. Today, only computed tomography screening has shown to lead to early detection and reduction in mortality, but is limited by being anatomic in nature, unable to differentiate between inflammatory and neoplastic pathways, and therefore, susceptible to false positives. There is increasing interest in biomarkers for lung cancer, especially those that predict metastatic risk. Some biomarkers like DNA mutations and epigenetic changes potentially require tissue from the at-risk site; some like serum proteins and miRNAs are minimally invasive, but may not be specific to the lung. In comparison, emerging biomarkers from exhaled breath, like volatile organic compounds (VOC), and exhaled breath condensate, e.g., small molecules and nucleic acids, have the potential to combine the best of both. This mini review is intended to provide an overview of the field, briefly discussing the potential of what is known and highlighting the exciting recent developments, particularly with miRNAs and VOCs.
      Citation: Journal of Carcinogenesis 2013 12(1):3-3
      PubDate: Thu,28 Feb 2013
      DOI: 10.4103/1477-3163.107958
      Issue No: Vol. 12, No. 1 (2013)
       
  • Missense allele of a single nucleotide polymorphism rs2294008 attenuated
           antitumor effects of prostate stem cell antigen in gallbladder cancer
           cells

    • Authors: Hiroe Ono, Dai Chihara, Fumiko Chiwaki, Kazuyoshi Yanagihara, Hiroki Sasaki, Hiromi Sakamoto, Hideo Tanaka, Teruhiko Yoshida, Norihisa Saeki, Keitaro Matsuo
      Pages: 4 - 4
      Abstract: Hiroe Ono, Dai Chihara, Fumiko Chiwaki, Kazuyoshi Yanagihara, Hiroki Sasaki, Hiromi Sakamoto, Hideo Tanaka, Teruhiko Yoshida, Norihisa Saeki, Keitaro Matsuo
      Journal of Carcinogenesis 2013 12(1):4-4
      Background: Prostate stem cell antigen (PSCA), an organ-dependent tumor suppressor, is down regulated in gallbladder cancer (GBC). It is anticipated that the missense allele C of the single nucleotide polymorphism (SNP) rs2294008 (T/C) in the translation initiation codon of the gene affects the gene's biological function and has some influence on GBC susceptibility. We examined the biological effect of the C allele on the function of the gene and the relation between the C allele and GBC susceptibility. Materials and Methods: Functional analysis of the SNP was conducted by introducing PSCA cDNA harboring the allele to a GBC cell line TGBC- 1TKB and performing colony formation assays in vitro and tumor formation assays in mice. The effect on transcriptional regulation was assessed by reporter assays. The association study was conducted on 44 Japanese GBC cases and 173 controls. Results: The PSCA cDNA harboring the C allele showed lower cell growth inhibition activity (20% reduction) than that with the T allele. Concordantly, when injected into subcutaneous tissues of mice, the GBC cell line stably expressing the cDNA with the C allele formed tumors of almost the same size as that of the control cells, but the cell line expressing the cDNA with the T allele showed slower growth. The upstream DNA fragment harboring the C allele had more transcriptional activity than that with the T allele. The C allele showed positive correlation to GBC but no statistical significant odds ratio (OR = 1.77, 95% confidence interval 0.85-3.70, P value = 0.127 in dominant model). Conclusions: The missense allele was shown to have a biological effect, attenuating antitumor activities of PSCA, and consequently it may be a potential risk for GBC development. An association study in a larger sample size may reveal a significant association between the allele and GBC.
      Citation: Journal of Carcinogenesis 2013 12(1):4-4
      PubDate: Sat,16 Mar 2013
      DOI: 10.4103/1477-3163.109030
      Issue No: Vol. 12, No. 1 (2013)
       
  • Human endogenous retroviral K element encodes fusogenic activity in
           melanoma cells

    • Authors: Gengming Huang, Zhongwu Li, Xiaohua Wan, Yue Wang, Jianli Dong
      Pages: 5 - 5
      Abstract: Gengming Huang, Zhongwu Li, Xiaohua Wan, Yue Wang, Jianli Dong
      Journal of Carcinogenesis 2013 12(1):5-5
      Introduction and Hypothesis: Nuclear atypia with features of multi nuclei have been detected in human melanoma specimens. We found that the K type human endogenous retroviral element (HERV K) is expressed in such cells. Since cellular syncytia can form when cells are infected with retroviruses, we hypothesized that HERV K expressed in melanoma cells may contribute to the formation of multinuclear atypia cells in melanoma. Experiments and Results: We specifically inhibited HERV K expression using RNA interference (RNAi) and monoclonal antibodies and observed dramatic reduction of intercellular fusion of cultured melanoma cells. Importantly, we identified loss of heterozygosity (LOH)of D19S433 in a cell clone that survived and proliferated after cell fusion. Conclusion: Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages.
      Citation: Journal of Carcinogenesis 2013 12(1):5-5
      PubDate: Sat,16 Mar 2013
      DOI: 10.4103/1477-3163.109032
      Issue No: Vol. 12, No. 1 (2013)
       
  • Cell of origin of lung cancer

    • Authors: Jennifer M Hanna, Mark W Onaitis
      Pages: 6 - 6
      Abstract: Jennifer M Hanna, Mark W Onaitis
      Journal of Carcinogenesis 2013 12(1):6-6
      Lung cancer is the leading cause of cancer deaths worldwide, and current therapies are disappointing. Elucidation of the cell(s) of origin of lung cancer may lead to new therapeutics. In addition, the discovery of putative cancer-initiating cells with stem cell properties in solid tumors has emerged as an important area of cancer research that may explain the resistance of these tumors to currently available therapeutics. Progress in our understanding of normal tissue stem cells, tumor cell of origin, and cancer stem cells has been hampered by the heterogeneity of the disease, the lack of good in vivo transplantation models to assess stem cell behavior, and an overall incomplete understanding of the epithelial stem cell hierarchy. As such, a systematic computerized literature search of the MEDLINE database was used to identify articles discussing current knowledge about normal lung and lung cancer stem cells or progenitor cells. In this review, we discuss what is currently known about the role of cancer-initiating cells and normal stem cells in the development of lung tumors.
      Citation: Journal of Carcinogenesis 2013 12(1):6-6
      PubDate: Sat,16 Mar 2013
      DOI: 10.4103/1477-3163.109033
      Issue No: Vol. 12, No. 1 (2013)
       
  • Targeted agents in non-small cell lung cancer therapy: What is there on
           the horizon?

    • Authors: Victoria M Villaflor, Ravi Salgia
      Pages: 7 - 7
      Abstract: Victoria M Villaflor, Ravi Salgia
      Journal of Carcinogenesis 2013 12(1):7-7
      Lung cancer is a heterogeneous group of diseases. There has been much research in lung cancer over the past decade which has advanced our ability to treat these patients with a more personalized approach. The scope of this paper is to review the literature and give a broad understanding of the current molecular targets for which we currently have therapies as well as other targets for which we may soon have therapies. Additionally, we will cover some of the issues of resistance with these targeted therapies. The molecular targets we intend to discuss are epidermal growth factor receptor (EGFR), Vascular endothelial growth factor (VEGF), anaplastic large-cell lymphoma kinase (ALK), KRAS, C-MET/RON, PIK3CA. ROS-1, RET Fibroblast growth factor receptor (FGFR). Ephrins and their receptors, BRAF, and immunotherapies/vaccines. This manuscript only summarizes the work which has been done to date and in no way is meant to be comprehensive.
      Citation: Journal of Carcinogenesis 2013 12(1):7-7
      PubDate: Tue,19 Mar 2013
      DOI: 10.4103/1477-3163.109253
      Issue No: Vol. 12, No. 1 (2013)
       
  • Digitoxin induces apoptosis in cancer cells by inhibiting nuclear factor
           of activated T-cells-driven c-MYC expression

    • Authors: Qing Feng Yang, Clifton L Dalgard, Ofer Eidelman, Catherine Jozwik, Bette S Pollard, Meera Srivastava, Harvey B Pollard
      Pages: 8 - 8
      Abstract: Qing Feng Yang, Clifton L Dalgard, Ofer Eidelman, Catherine Jozwik, Bette S Pollard, Meera Srivastava, Harvey B Pollard
      Journal of Carcinogenesis 2013 12(1):8-8
      Background : Cardiac glycosides such as digitoxin have been shown to directly cause apoptotic death of cancer cells both in vitro, and in vivo. However, the mechanism connecting cardiac glycoside action to apoptosis is not known. It has been reported that compounds resembling digitoxin are able to reduce c-MYC expression. Furthermore, it has been previously shown that the transcription of c-MYC depends on nuclear factor of activated T-cells (NFAT) binding sites in the c-MYC promoter. We have therefore hypothesized that NFAT might mediate digitoxin effects on c-MYC mRNA message. Materials and Methods : We have chosen to study this process in HeLa cells where structurally intact c-MYC genes in 8q24 co-localize with human papilloma virus 18 at all integration sites. Results : Here we show that within the 1 st h following treatment with digitoxin, a significant reduction in c-MYC mRNA occurs. This is followed by a precipitous loss of c-MYC protein, activation of caspase 3, and subsequent apoptotic cell death. To test the NFAT-dependence mechanism, we analyzed the effects of digitoxin on NFAT isoform-dependent auto-activation of a NFAT-luciferase expression system. Drug dependent effects on expression varied according to each of the four canonical NFAT isoforms (1, 2, 3 or 4). The most digitoxin-sensitive NFAT isoform was NFAT1. Using c-MYC chromatin immune precipitation, we find that digitoxin inhibits interaction of NFAT1 with the proximal c-MYC promoter. Conclusions : These results suggest that the carcinotoxic activity of digitoxin includes suppression of NFAT-driven c-MYC expression.
      Citation: Journal of Carcinogenesis 2013 12(1):8-8
      PubDate: Mon,20 May 2013
      DOI: 10.4103/1477-3163.112268
      Issue No: Vol. 12, No. 1 (2013)
       
  • Applications of metabolomics in cancer research

    • Authors: Kathleen A Vermeersch, Mark P Styczynski
      Pages: 9 - 9
      Abstract: Kathleen A Vermeersch, Mark P Styczynski
      Journal of Carcinogenesis 2013 12(1):9-9
      The first discovery of metabolic changes in cancer occurred almost a century ago. While the genetic underpinnings of cancer have dominated its study since then, altered metabolism has recently been acknowledged as a key hallmark of cancer and metabolism-focused research has received renewed attention. The emerging field of metabolomics - which attempts to profile all metabolites within a cell or biological system - is now being used to analyze cancer metabolism on a system-wide scale, painting a broad picture of the altered pathways and their interactions with each other. While a large fraction of cancer metabolomics research is focused on finding diagnostic biomarkers, metabolomics is also being used to obtain more fundamental mechanistic insight into cancer and carcinogenesis. Applications of metabolomics are also emerging in areas such as tumor staging and assessment of treatment efficacy. This review summarizes contributions that metabolomics has made in cancer research and presents the current challenges and potential future directions within the field.
      Citation: Journal of Carcinogenesis 2013 12(1):9-9
      PubDate: Tue,18 Jun 2013
      DOI: 10.4103/1477-3163.113622
      Issue No: Vol. 12, No. 1 (2013)
       
  • Stage-specific analysis of plasma protein profiles in ovarian cancer:
           Difference in-gel electrophoresis analysis of pooled clinical samples

    • Authors: Mark J Bailey, Kristy L Shield-Artin, Karen Oliva, Mustafa Ayhan, Simone Reisman, Gregory E Rice
      Pages: 10 - 10
      Abstract: Mark J Bailey, Kristy L Shield-Artin, Karen Oliva, Mustafa Ayhan, Simone Reisman, Gregory E Rice
      Journal of Carcinogenesis 2013 12(1):10-10
      Introduction: Ovarian cancer is the leading cause of death from gynecological cancer. Non-specific symptoms early in disease and the lack of specific biomarkers hinder early diagnosis. Multi-marker blood screening tests have shown promise for improving identification of early stage disease; however, available tests lack sensitivity, and specificity. Materials and Methods: In this study, pooled deeply-depleted plasma from women with Stage 1, 2 or 3 ovarian cancer and healthy controls were used to compare the 2-dimensional gel electrophoresis (2-DE) protein profiles and identify potential novel markers of ovarian cancer progression. Results/Discussion: Stage-specific variation in biomarker expression was observed. For example, apolipoprotein A1 expression is relatively low in control and Stage 1, but shows a substantial increase in Stage 2 and 3, thus, potential of utility for disease confirmation rather than early detection. A better marker for early stage disease was tropomyosin 4 (TPM4). The expression of TPM4 increased by 2-fold in Stage 2 before returning to "normal" levels in Stage 3 disease. Multiple isoforms were also identified for some proteins and in some cases, displayed stage-specific expression. An interesting example was fibrinogen alpha, for which 8 isoforms were identified. Four displayed a moderate increase at Stage 1 and a substantial increase for Stages 2 and 3 while the other 4 showed only moderate increases. Conclusion: Herein is provided an improved summary of blood protein profiles for women with ovarian cancer stratified by stage.
      Citation: Journal of Carcinogenesis 2013 12(1):10-10
      PubDate: Sat,29 Jun 2013
      DOI: 10.4103/1477-3163.114216
      Issue No: Vol. 12, No. 1 (2013)
       
  • Effects of maternal dietary exposure to cadmium during pregnancy on
           mammary cancer risk among female offspring

    • Authors: Jennifer Davis, Galam Khan, Mary Beth Martin, Leena Hilakivi-Clarke
      Pages: 11 - 11
      Abstract: Jennifer Davis, Galam Khan, Mary Beth Martin, Leena Hilakivi-Clarke
      Journal of Carcinogenesis 2013 12(1):11-11
      Background: Since heavy metal cadmium is an endocrine disrupting chemical, we investigated whether maternal exposure to cadmium during the pregnancy alters mammary tumorigenesis among female offspring. Methods: From gestation day 10 to day 19, pregnant rat dams were fed modified American Institute of Nutrition (AIN93G) diet containing 39% energy from fat (baseline diet), or the baseline diet containing moderate (75 μg/kg of feed) or high (150 μg/kg) cadmium levels. Some dams were injected with 10 μg 17β-estradiol (E2) daily between gestation days 10 and 19. Results: Rats exposed to a moderate cadmium dose in utero were heavier and exhibited accelerated puberty onset. Both moderate and high cadmium dose led to increased circulating testosterone levels and reduced the expression of androgen receptor in the mammary gland. The moderate cadmium dose mimicked the effects of in utero E2 exposure on mammary gland morphology and increased both the number of terminal end buds and pre-malignant hyperplastic alveolar nodules (HANs), but in contrast to the E2, it did not increase 7, 12-dimethylbenz (a) anthracene-induced mammary tumorigenesis. Conclusions: The effects of in utero cadmium exposure were dependent on the dose given to pregnant dams: Moderate, but not high, cadmium dose mimicked some of the effects seen in the in utero E2 exposed rats, such as increased HANs in the mammary gland.
      Citation: Journal of Carcinogenesis 2013 12(1):11-11
      PubDate: Sat,29 Jun 2013
      DOI: 10.4103/1477-3163.114219
      Issue No: Vol. 12, No. 1 (2013)
       
  • Epidermal growth factor receptor mutation in lung adenocarcinoma in India:
           A single center study

    • Authors: Dinesh Chandra Doval, Saud Azam, Ullas Batra, Kumardeep Dutta Choudhury, Vineet Talwar, Sunil Kumar Gupta, Anurag Mehta
      Pages: 12 - 12
      Abstract: Dinesh Chandra Doval, Saud Azam, Ullas Batra, Kumardeep Dutta Choudhury, Vineet Talwar, Sunil Kumar Gupta, Anurag Mehta
      Journal of Carcinogenesis 2013 12(1):12-12
      Background: Adenocarcinoma, a subgroup of non-small cell lung cancer, is the most frequent form occurring in the non-smokers. Mutation in tyrosine kinase domain of epidermal growth factor receptor (EGFR) has been a common feature observed in lung adenocarcinoma. The study was carried out to detect the prevalence of EGFR mutation in lung adenocarcinoma. Materials and Methods: EGFR mutation status in 166 lung adenocarcinoma patients was obtained retrospectively. Mutation tests were performed on paraffin embedded tissue blocks as a routine diagnostic procedure by polymerase chain reaction followed by direct nucleotide sequencing. Patient's demographics and other clinical details were obtained from the medical records. Results: EGFR mutation was detected in 43/166 (25.9%) patients. Gender wise mutation was observed as 18/55 (32.7%) in females and 25/111 (22.5%) in males. Overall, EGFR mutation was correlated with never smokers and distant metastasis ( P < 0.05), but not associated with the gender, disease stage and pleural effusion. Exon 19 deletions were significantly correlated with females, never smokers, pleural effusion and distant metastasis ( P < 0.05). However, point mutation on exon 21 did not show any statistical association with the above variables. Median overall survival was 22 months (95% confidence interval, 15.4-28.6). Female sex, EGFR mutation and absence of metastasis are associated with good prognosis. Conclusion: EGFR mutation in lung adenocarcinoma was higher in never smokers, females and patients with distant metastasis. However, it was not linked with tobacco smoking. The prevalence of EGFR mutation observed is in range with the previously published reports from the Asian countries.
      Citation: Journal of Carcinogenesis 2013 12(1):12-12
      PubDate: Fri,12 Jul 2013
      DOI: 10.4103/1477-3163.114970
      Issue No: Vol. 12, No. 1 (2013)
       
  • Mapping cancer cell metabolism with 13 C flux analysis: Recent progress
           and future challenges

    • Authors: Casey Scott Duckwall, Taylor Athanasaw Murphy, Jamey Dale Young
      Pages: 13 - 13
      Abstract: Casey Scott Duckwall, Taylor Athanasaw Murphy, Jamey Dale Young
      Journal of Carcinogenesis 2013 12(1):13-13
      The reprogramming of energy metabolism is emerging as an important molecular hallmark of cancer cells. Recent discoveries linking specific metabolic alterations to cancer development have strengthened the idea that altered metabolism is more than a side effect of malignant transformation, but may in fact be a functional driver of tumor growth and progression in some cancers. As a result, dysregulated metabolic pathways have become attractive targets for cancer therapeutics. This review highlights the application of 13 C metabolic flux analysis (MFA) to map the flow of carbon through intracellular biochemical pathways of cancer cells. We summarize several recent applications of MFA that have identified novel biosynthetic pathways involved in cancer cell proliferation and shed light on the role of specific oncogenes in regulating these pathways. Through such studies, it has become apparent that the metabolic phenotypes of cancer cells are not as homogeneous as once thought, but instead depend strongly on the molecular alterations and environmental factors at play in each case.
      Citation: Journal of Carcinogenesis 2013 12(1):13-13
      PubDate: Wed,24 Jul 2013
      DOI: 10.4103/1477-3163.115422
      Issue No: Vol. 12, No. 1 (2013)
       
  • Cancer metabolism meets systems biology: Pyruvate kinase isoform PKM2 is a
           metabolic master regulator

    • Authors: Fabian V Filipp
      Pages: 14 - 14
      Abstract: Fabian V Filipp
      Journal of Carcinogenesis 2013 12(1):14-14
      Pyruvate kinase activity is controlled by a tightly woven regulatory network. The oncofetal isoform of pyruvate kinase (PKM2) is a master regulator of cancer metabolism. PKM2 engages in parallel, feed-forward, positive and negative feedback control contributing to cancer progression. Besides its metabolic role, non-metabolic functions of PKM2 as protein kinase and transcriptional coactivator for c-MYC and hypoxia-inducible factor 1-alpha are essential for epidermal growth factor receptor activation-induced tumorigenesis. These biochemical activities are controlled by a shift in the oligomeric state of PKM2 that includes acetylation, oxidation, phosphorylation, prolyl hydroxylation and sumoylation. Metabolically active PKM2 tetramer is allosterically regulated and responds to nutritional and stress signals. Metabolically inactive PKM2 dimer is imported into the nucleus and can function as protein kinase stimulating transcription. A systems biology approach to PKM2 at the genome, transcriptome, proteome, metabolome and fluxome level reveals how differences in biomolecular structure translate into a global rewiring of cancer metabolism. Cancer systems biology takes us beyond the Warburg effect, opening unprecedented therapeutic opportunities.
      Citation: Journal of Carcinogenesis 2013 12(1):14-14
      PubDate: Wed,24 Jul 2013
      DOI: 10.4103/1477-3163.115423
      Issue No: Vol. 12, No. 1 (2013)
       
  • Restoration of the methylation status of hypermethylated gene promoters by
           microRNA-29b in human breast cancer: A novel epigenetic therapeutic
           approach

    • Authors: Athena Starlard-Davenport, Kristi Kutanzi, Volodymyr Tryndyak, Beverly Word, Beverly Lyn-Cook
      Pages: 15 - 15
      Abstract: Athena Starlard-Davenport, Kristi Kutanzi, Volodymyr Tryndyak, Beverly Word, Beverly Lyn-Cook
      Journal of Carcinogenesis 2013 12(1):15-15
      It is well established that transcriptional silencing of critical tumor-suppressor genes by DNA methylation is a fundamental component in the initiation of breast cancer. However, the involvement of microRNAs (miRNAs) in restoring abnormal DNA methylation patterns in breast cancer is not well understood. Therefore, we investigated whether miRNA-29b, due to its complimentarity to the 3'- untranslated region of DNA methyltransferase 3A (DNMT3A) and DNMT3B, could restore normal DNA methylation patterns in human breast cancers and breast cancer cell lines. We demonstrated that transfection of pre-miRNA-29b into less aggressive MCF-7 cells, but not MDA-MB-231 mesenchymal cells, inhibited cell proliferation, decreased DNMT3A and DNMT3B messenger RNA (mRNA), and decreased promoter methylation status of ADAM23 , CCNA1, CCND2, CDH1, CDKN1C, CDKN2A, HIC1, RASSF1, SLIT2, TNFRSF10D, and TP73 tumor-suppressor genes. Using methylation polymerase chain reaction (PCR) arrays and real-time PCR, we also demonstrated that the methylation status of several critical tumor-suppressor genes increased as stage of breast disease increased, while miRNA-29b mRNA levels were significantly decreased in breast cancers versus normal breast. This increase in methylation status was accompanied by an increase in DNMT1 and DNMT3B mRNA in advanced stage of human breast cancers and in MCF-7, MDA-MB-361, HCC70, Hs-578T, and MDA-MB-231 breast cancer cells as compared to normal breast specimens and MCF-10-2A, a non-tumorigenic breast cell line, respectively. Our findings highlight the potential for a new epigenetic approach in improving breast cancer therapy by targeting DNMT3A and DNMT3B through miRNA-29b in non-invasive epithelial breast cancer cells.
      Citation: Journal of Carcinogenesis 2013 12(1):15-15
      PubDate: Fri,26 Jul 2013
      DOI: 10.4103/1477-3163.115720
      Issue No: Vol. 12, No. 1 (2013)
       
  • Unravelling the connection between metabolism and tumorigenesis through
           studies of the liver kinase B1 tumour suppressor

    • Authors: David B Shackelford
      Pages: 16 - 16
      Abstract: David B Shackelford
      Journal of Carcinogenesis 2013 12(1):16-16
      The liver kinase B1 (LKB1) tumour suppressor functions as a master regulator of growth, metabolism and survival in cells, which is frequently mutated in sporadic human non-small cell lung and cervical cancers. LKB1 functions as a key upstream activator of the AMP-activated protein kinase (AMPK), a central metabolic switch found in all eukaryotes that govern glucose and lipid metabolism and autophagy in response to alterations in nutrients and intracellular energy levels. The LKB1/AMPK signalling pathway suppresses mammalian target of rapamycin complex 1 (mTORC1), an essential regulator of cell growth in all eukaryotes that is deregulated in a majority of human cancers. LKB1 inactivation in cancer leads to both tumorigenesis and metabolic deregulation through the AMPK and mTORC1-signalling axis and there remain critical challenges to elucidate the direct role LKB1 inactivation plays in driving aberrant metabolism and tumour growth. This review addresses past and current efforts to delineate the molecular mechanisms fueling metabolic deregulation and tumorigenesis following LKB1 inactivation as well as translational promise of therapeutic strategies aimed at targeting LKB1-deficient tumors.
      Citation: Journal of Carcinogenesis 2013 12(1):16-16
      PubDate: Thu,8 Aug 2013
      DOI: 10.4103/1477-3163.116323
      Issue No: Vol. 12, No. 1 (2013)
       
  • Dealing with hunger: Metabolic stress responses in tumors

    • Authors: Michael A Reid, Mei Kong
      Pages: 17 - 17
      Abstract: Michael A Reid, Mei Kong
      Journal of Carcinogenesis 2013 12(1):17-17
      Increased nutrient uptake and usage is a hallmark of many human malignancies. During the course of tumorigenesis, cancer cells often outstrip their local nutrient supply leading to periods of nutrient deprivation. Interestingly, cancer cells often develop strategies to adapt and survive these challenging conditions. Accordingly, understanding these processes is critical for developing therapies that target cancer metabolism. Exciting new progress has been made in elucidating the mechanisms used by cancer cells under nutrient restricted conditions. In this review, we highlight recent studies that have brought insight into how cancer cells deal with low nutrient environments.
      Citation: Journal of Carcinogenesis 2013 12(1):17-17
      PubDate: Mon,30 Sep 2013
      DOI: 10.4103/1477-3163.119111
      Issue No: Vol. 12, No. 1 (2013)
       
  • Intersection of Smoking, Human immunodeficiency virus/acquired
           immunodeficiency syndrome and Cancer: Proceedings of the 8 th Annual Texas
           Conference on Health Disparities

    • Authors: Smrithi Rajendiran, Meghana V Kashyap, Jamboor K Vishwanatha
      Pages: 18 - 18
      Abstract: Smrithi Rajendiran, Meghana V Kashyap, Jamboor K Vishwanatha
      Journal of Carcinogenesis 2013 12(1):18-18
      The Texas Center for Health Disparities, a National Institute on Minority Health and Health Disparities Center of Excellence, presents an annual conference to discuss prevention, awareness education and ongoing research about health disparities both in Texas and among the national population. The 2013 Texas Conference on Health Disparities brought together experts, in research, patient care and community outreach, on the "Intersection of Smoking, Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and Cancer". Smoking, HIV/AIDS and cancer are three individual areas of public health concern, each with its own set of disparities and risk factors based on race, ethnicity, gender, geography and socio-economic status. Disparities among patient populations, in which these issues are found to be comorbid, provide valuable information on goals for patient care. The conference consisted of three sessions addressing "Comorbidities and Treatment", "Public Health Perspectives", and "Best Practices". This article summarizes the basic science, clinical correlates and public health data presented by the speakers.
      Citation: Journal of Carcinogenesis 2013 12(1):18-18
      PubDate: Sat,5 Oct 2013
      DOI: 10.4103/1477-3163.119388
      Issue No: Vol. 12, No. 1 (2013)
       
  • Obesity, metabolism and the microenvironment: Links to cancer

    • Authors: Sneha Sundaram, Amy R Johnson, Liza Makowski
      Pages: 19 - 19
      Abstract: Sneha Sundaram, Amy R Johnson, Liza Makowski
      Journal of Carcinogenesis 2013 12(1):19-19
      Historically, cancer research has focused on identifying mutations or amplification of genes within the tumor, which informed the development of targeted therapies against affected pathways. This work often considers tumor cells in isolation; however, it is becoming increasingly apparent that the microenvironment surrounding tumor cells strongly influences tumor onset and progression. This is the so-called "seed and soil" hypothesis wherein the seed (cancer cell) is fed and molded by the metabolites, growth factors, modifications of the extracellular matrix or angiogenic factors provided by the soil (or stroma). Currently, 65% of the US population is obese or overweight; similarly staggering figures are reported in US children and globally. Obesity mediates and can exacerbate, both normal and tumor microenvironment dysfunction. Many obesity-associated endocrine, metabolic and inflammatory mediators are suspected to play a role in oncogenesis by modifying systemic nutrient metabolism and the nutrient substrates available locally in the stroma. It is vitally important to understand the biological processes linking obesity and cancer to develop better intervention strategies aimed at curbing the carcinogenic events associated with obesity. In this review, obesity-driven changes in both the normal and tumor microenvironment, alterations in metabolism, and release of signaling molecules such as endocrine, growth, and inflammatory mediators will be highlighted. In addition, we will discuss the effects of the timing of obesity onset or particular "windows of susceptibility," with a focus on breast cancer etiology.
      Citation: Journal of Carcinogenesis 2013 12(1):19-19
      PubDate: Wed,9 Oct 2013
      DOI: 10.4103/1477-3163.119606
      Issue No: Vol. 12, No. 1 (2013)
       
  • O-6-methylguanine-deoxyribonucleic acid methyltransferase methylation
           enhances response to temozolomide treatment in esophageal cancer

    • Authors: Rifat Hasina, Mosmi Surati, Ichiro Kawada, Qudsia Arif, George B Carey, Rajani Kanteti, Aliya N Husain, Mark K Ferguson, Everett E Vokes, Victoria M Villaflor, Ravi Salgia
      Pages: 20 - 20
      Abstract: Rifat Hasina, Mosmi Surati, Ichiro Kawada, Qudsia Arif, George B Carey, Rajani Kanteti, Aliya N Husain, Mark K Ferguson, Everett E Vokes, Victoria M Villaflor, Ravi Salgia
      Journal of Carcinogenesis 2013 12(1):20-20
      Background: World-wide, esophageal cancer is a growing epidemic and patients frequently present with advanced disease that is surgically inoperable. Hence, chemotherapy is the predominate treatment. Cytotoxic platinum compounds are mostly used, but their efficacy is only moderate. Newer alkylating agents have shown promise in other tumor types, but little is known about their utility in esophageal cancer. Methods: We utilized archived human esophageal cancer samples and esophageal cancer cell lines to evaluate O-6-methylguanine-deoxyribonucleic acid methyltransferase (MGMT) hypermethylation status and determined sensitivity to the alkylating drug temozolomide (TMZ). Immunoblot analysis was performed to determine MGMT protein expression in cell lines. To assess and confirm the effect of TMZ treatment in a methylated esophageal cancer cell line in vivo, a mouse flank xenograft tumor model was utilized. Results: Nearly 71% (12/17) of adenocarcinoma and 38% (3/8) of squamous cell carcinoma (SCC) patient samples were MGMT hypermethylated. Out of four adenocarcinoma and nine SCC cell lines tested, one of each histology was hypermethylated. Immunoblot analyses confirmed that hypermethylated cell lines did not express the MGMT protein. In vitro cell viability assays showed the methylated Kyse-140 and FLO cells to be sensitive to TMZ at an IC 50 of 52-420 μM, whereas unmethylated cells Kyse-410 and SKGT-4 did not respond. In an in vivo xenograft tumor model with Kyse-140 cells, which are MGMT hypermethylated, TMZ treatment abrogated tumor growth by more than 60%. Conclusion: MGMT methylation may be an important biomarker in subsets of esophageal cancers and targeting by TMZ may be utilized to successfully treat these patients.
      Citation: Journal of Carcinogenesis 2013 12(1):20-20
      PubDate: Mon,28 Oct 2013
      DOI: 10.4103/1477-3163.120632
      Issue No: Vol. 12, No. 1 (2013)
       
  • p53 and regulation of tumor metabolism

    • Authors: Peng Jiang, Wenjing Du, Xiaolu Yang
      Pages: 21 - 21
      Abstract: Peng Jiang, Wenjing Du, Xiaolu Yang
      Journal of Carcinogenesis 2013 12(1):21-21
      The tumor suppressor p53 plays a pre-eminent role in protecting against cancer, through its ability to sense various stresses and in turn invoke anti-proliferative and repair responses. Emerging evidence suggest that p53 is both a central sentinel for metabolic stresses and a master regulator of metabolic fluxes. This newly identified function of p53, along with the ability of p53 to induce senescence, appears to be crucial for the prevention of oncogenic transformation. A better understanding of the reciprocal regulation of p53 and metabolism, as well as p53-mediated connection between metabolism and senescence, may lead to the identification of valuable targets for tumor therapy.
      Citation: Journal of Carcinogenesis 2013 12(1):21-21
      PubDate: Fri,6 Dec 2013
      DOI: 10.4103/1477-3163.122760
      Issue No: Vol. 12, No. 1 (2013)
       
  • Targeted therapies in development for non-small cell lung cancer

    • Authors: Thanyanan Reungwetwattana, Grace Kho Dy
      Pages: 22 - 22
      Abstract: Thanyanan Reungwetwattana, Grace Kho Dy
      Journal of Carcinogenesis 2013 12(1):22-22
      The iterative discovery in various malignancies during the past decades that a number of aberrant tumorigenic processes and signal transduction pathways are mediated by "druggable" protein kinases has led to a revolutionary change in drug development. In non-small cell lung cancer (NSCLC), the ErbB family of receptors (e.g., EGFR [epidermal growth factor receptor], HER2 [human epidermal growth factor receptor 2]), RAS (rat sarcoma gene), BRAF (v-raf murine sarcoma viral oncogene homolog B1), MAPK (mitogen-activated protein kinase) c-MET (c-mesenchymal-epithelial transition), FGFR (fibroblast growth factor receptor), DDR2 (discoidin domain receptor 2), PIK3CA (phosphatidylinositol-4,5-bisphosphate3-kinase, catalytic subunit alpha)), PTEN (phosphatase and tensin homolog), AKT (protein kinase B), ALK (anaplastic lym phoma kinase), RET (rearranged during transfection), ROS1 (reactive oxygen species 1) and EPH (erythropoietin-producing hepatoma) are key targets of various agents currently in clinical development. These oncogenic targets exert their selective growth advantage through various intercommunicating pathways, such as through RAS/RAF/MEK, phosphoinositide 3-kinase/AKT/mammalian target of rapamycin and SRC-signal transduction and transcription signaling. The recent clinical studies, EGFR tyrosine kinase inhibitors and crizotinib were considered as strongly effective targeted therapies in metastatic NSCLC. Currently, five molecular targeted agents were approved for treatment of advanced NSCLC: Gefitinib, erlotinib and afatinib for positive EGFR mutation, crizotinib for positive echinoderm microtubule-associated protein-like 4 (EML4)-ALK translocation and bevacizumab. Moreover, oncogenic mutant proteins are subject to regulation by protein trafficking pathways, specifically through the heat shock protein 90 system. Drug combinations affecting various nodes in these signaling and intracellular processes are predicted and demonstrated to be synergistic and advantageous in overcoming treatment resistance compared with monotherapy approaches. Understanding the role of the tumor microenvironment in the development and maintenance of the malignant phenotype provided additional therapeutic approaches as well. More recently, improved knowledge on tumor immunology has set the stage for promising immunotherapies in NSCLC. This review will focus on the rationale for the development of targeted therapies in NSCLC and the various strategies employed in preventing or overcoming the inevitable occurrence of treatment resistance.
      Citation: Journal of Carcinogenesis 2013 12(1):22-22
      PubDate: Tue,31 Dec 2013
      DOI: 10.4103/1477-3163.123972
      Issue No: Vol. 12, No. 1 (2013)
       
  • Comparative metabolism of benzo[a]pyrene by human keratinocytes infected
           with high-risk human papillomavirus types 16 and 18 as episomal or
           integrated genomes

    • Authors: Neil Trushin, Samina Alam, Karam El-Bayoumy, Jacek Krzeminski, Shantu G Amin, Jenny Gullett, Craig Meyers, Bogdan Prokopczyk
      Pages: 1 - 1
      Abstract: Neil Trushin, Samina Alam, Karam El-Bayoumy, Jacek Krzeminski, Shantu G Amin, Jenny Gullett, Craig Meyers, Bogdan Prokopczyk
      Journal of Carcinogenesis 2012 11(1):1-1
      Background: Infection with human papillomavirus (HPV) is a critical factor in the development of cervical cancer. Smoking is an additional risk factor. Tobacco smoke carcinogens, such as benzo[a]pyrene (B[a]P), and their cytochrome P450-related metabolites are present in significantly higher levels in the cervical mucus of women smokers than in nonsmokers. We determined the metabolism and P450 expression of B[a]P-treated human keratinocytes infected with HPV-16 or -18. Materials and Methods: Monolayer cultures of uninfected primary human foreskin keratinocytes, human vaginal and cervical keratinocytes carrying episomal genomes of HPV-16 and -18, respectively, and invasive cervical carcinoma cell lines carrying either HPV-16 or -18 genomes integrated into the host DNA, were incubated with 0.1 μM [3H]B[a]P. The resulting oxidative metabolites were analyzed and quantified by radioflow high-performance liquid chromatography. Additionally, all cell lines were incubated with unlabeled 0.1 μM B[a]P for Western blot analysis of cytochrome P450 1A1 and 1B1. Results: Significant enhancement in levels of both detoxification and activation metabolites was found in incubations with all types of HPV-infected cells compared with control incubations (P < 0.05). The highest capacity to metabolize B[a]P was observed with cells containing integrated HPV-18 genomes. Induction of cytochrome 1B1 was observed in HPV-16 and -18 integrated, and in HPV-16 episomal cell types. Conclusions: Both viral genotype and genomic status in the host cell affect B[a]P metabolism and cytochrome P450 1B1 expression. An increase of DNA-damaging metabolites might result from exposure of HPV-infected women to cigarette smoke carcinogens.
      Citation: Journal of Carcinogenesis 2012 11(1):1-1
      PubDate: Fri,27 Jan 2012
      DOI: 10.4103/1477-3163.92309
      Issue No: Vol. 11, No. 1 (2012)
       
  • "The Lower Threshold" phenomenon in tumor cells toward endogenous
           digitalis-like compounds: Responsible for tumorigenesis?

    • Authors: Heidrun Weidemann
      Pages: 2 - 2
      Abstract: Heidrun Weidemann
      Journal of Carcinogenesis 2012 11(1):2-2
      Since their first discovery as potential anti-cancer drugs decades ago, there is increasing evidence that digitalis-like compounds (DLC) have anti-tumor effects. Less is known about endogenous DLC (EDLC) metabolism and regulation. As stress hormones synthesized in and secreted from the adrenal gland, they likely take part in the hypothalamo-pituitary-adrenal (HPA) axis. In a previous study, we revealed reduced EDLC concentrations in plasma and organs from immune-compromised animals and proposed that a similar situation of a deregulated HPA axis with "adrenal EDLF exhaustion" may contribute to tumorigenesis in chronic stress situations. Here, we put forward the hypothesis that a lowered EDLC response threshold of tumor cells as compared with normal cells increases the risk of tumorigenesis, especially in those individuals with reduced EDLC plasma concentrations after chronic stress exposure. We will evaluate this hypothesis by (a) summarizing the effects of different DLC concentrations on tumor as compared with normal cells and (b) reviewing some essential differences in the Na/K-ATPase of tumor as compared with normal cells (isoform pattern, pump activity, mutations of other signalosome receptors). We will conclude that (1) tumor cells, indeed, seem to have their individual "physiologic" EDLC response range that already starts at pmolar levels and (2) that individuals with markedly reduced (pmolar) EDLC plasma levels are predisposed to cancer because these EDLC concentrations will predominantly stimulate the proliferation of tumor cells. Finally, we will summarize preliminary results from our department supporting this hypothesis.
      Citation: Journal of Carcinogenesis 2012 11(1):2-2
      PubDate: Fri,17 Feb 2012
      Issue No: Vol. 11, No. 1 (2012)
       
  • The cellular functions of RASSF1A and its inactivation in prostate cancer

    • Authors: Karishma S Amin, Partha P Banerjee
      Pages: 3 - 3
      Abstract: Karishma S Amin, Partha P Banerjee
      Journal of Carcinogenesis 2012 11(1):3-3
      Epigenetic events significantly impact the transcriptome of cells and often contribute to the onset and progression of human cancers. RASSF1A (Ras-association domain family 1 isoform A), a well-known tumor suppressor gene, is frequently silenced by epigenetic mechanisms such as promoter hypermethylation in a wide range of cancers. In the past decade a vast body of literature has emerged describing the silencing of RASSF1A expression in various cancers and demonstrating its ability to reverse the cancerous phenotype when re-expressed in cancer cells. However, the mechanisms by which RASSF1A exerts its tumor suppressive properties have not been entirely defined. RASSF1A appears to mediate three important cellular processes: microtubule stability, cell cycle progression, and the induction of apoptosis through specific molecular interactions with key factors involved in these processes. Loss of function of RASSF1A leads to accelerated cell cycle progression and resistance to apoptotic signals, resulting in increased cell proliferation. In this review, we attempt to summarize the current understanding of the biological functions of RASSF1A and provide insight that the development of targeted drugs to restore RASSF1A function holds promise for the treatment of prostate cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):3-3
      PubDate: Fri,17 Feb 2012
      DOI: 10.4103/1477-3163.93000
      Issue No: Vol. 11, No. 1 (2012)
       
  • Oncogenic activation in prostate cancer progression and metastasis:
           Molecular insights and future challenges

    • Authors: Subhamoy Dasgupta, Srinivasa Srinidhi, Jamboor K Vishwanatha
      Pages: 4 - 4
      Abstract: Subhamoy Dasgupta, Srinivasa Srinidhi, Jamboor K Vishwanatha
      Journal of Carcinogenesis 2012 11(1):4-4
      Prostate cancer is a leading cause of death among men in the United States, and currently early diagnosis and appropriate treatment remain key approaches for patient care. Molecularly prostate cancer cells carry multiple perturbations that generate malignant phenotype capable of uncontrolled growth, survival, and invasion-metastasis to other organs. These alterations are acquired both by genetic and epigenetic changes in tumor cells resulting in the activation of growth factor receptors, signaling proteins, kinases, transcription factors and coregulators, and multiple proteases required for the progression of the disease. Recent advances provide novel insights into the molecular functions of these oncogenic activators, implicating potential therapeutic targeting opportunities for the treatment of prostate cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):4-4
      PubDate: Fri,17 Feb 2012
      DOI: 10.4103/1477-3163.93001
      Issue No: Vol. 11, No. 1 (2012)
       
  • Plastics and carcinogenesis: The example of vinyl chloride

    • Authors: Paul Wesley Brandt-Rauf, Yongliang Li, Changmin Long, Regina Monaco, Gopala Kovvali, Marie-Jeanne Marion
      Pages: 5 - 5
      Abstract: Paul Wesley Brandt-Rauf, Yongliang Li, Changmin Long, Regina Monaco, Gopala Kovvali, Marie-Jeanne Marion
      Journal of Carcinogenesis 2012 11(1):5-5
      The manufacture, use and disposal of various plastics can pose numerous health risks, including the risk of cancer. A model example of carcinogenic risk from plastics is provided by polyvinyl chloride, since it is composed of the known human carcinogen vinyl chloride (VC). In recent years, much has been learned about the molecular biological pathways of VC carcinogenesis. This has led to molecular epidemiologic studies of VC carcinogenesis in exposed human populations which have identified useful biomarkers of exposure, effect and susceptibility for VC. These studies have in turn provided the basis for new molecular approaches for the prevention and treatment of VC cancers. This model could have much wider applicability for many other carcinogenic exposures and many other human cancers.
      Citation: Journal of Carcinogenesis 2012 11(1):5-5
      PubDate: Mon,12 Mar 2012
      DOI: 10.4103/1477-3163.93700
      Issue No: Vol. 11, No. 1 (2012)
       
  • Prostate cancer stem cells: The case for model systems

    • Authors: Paul G Hynes, Kathleen Kelly
      Pages: 6 - 6
      Abstract: Paul G Hynes, Kathleen Kelly
      Journal of Carcinogenesis 2012 11(1):6-6
      Advanced prostate cancers are treated with androgen deprivation therapy, which usually leads to a rapid and significant reduction in tumor burden but subsequent development of castration-resistant and metastatic disease almost always occurs. The source of tumor heterogeneity and the accompanying mechanisms leading to treatment resistance are major areas of prostate cancer research. Although our understanding of tumor heterogeneity is evolving, the functional isolation of tumor propagating populations, also known as cancer stem cells (CSCs), is fundamental to the identification and molecular characterization of castration-resistant prostate cancer cells. Of clinical importance, knowledge of prostate CSCs has implications for design of next generation-targeted therapies aimed at both eradicating primary tumor mass and preventing castration-resistant disease. The inability to routinely transplant fractionated primary human prostate tumors has prevented progress in analyzing the source of heterogeneous and treatment-resistant populations in prostate cancer. Here, we briefly overview the mechanisms of castration resistance, including the hypothesis for the existence of androgen-independent prostate CSCs. Finally, we discuss the interpretation of preclinical models and their utility for characterizing prostate CSCs in androgen-replete and androgen-deprived conditions.
      Citation: Journal of Carcinogenesis 2012 11(1):6-6
      PubDate: Mon,12 Mar 2012
      DOI: 10.4103/1477-3163.93701
      Issue No: Vol. 11, No. 1 (2012)
       
  • The burden of prostate cancer in Asian nations

    • Authors: Jennifer Cullen, Sally Elsamanoudi, Stephen A Brassell, Yongmei Chen, Monica Colombo, Amita Srivastava, David G McLeod
      Pages: 7 - 7
      Abstract: Jennifer Cullen, Sally Elsamanoudi, Stephen A Brassell, Yongmei Chen, Monica Colombo, Amita Srivastava, David G McLeod
      Journal of Carcinogenesis 2012 11(1):7-7
      Introduction: In this review, the International Agency for Research on Cancer's cancer epidemiology databases were used to examine prostate cancer (PCa) age-standardized incidence rates (ASIR) in selected Asian nations, including Cancer Incidence in Five Continents (CI5) and GLOBOCAN databases, in an effort to determine whether ASIRs are rising in regions of the world with historically low risk of PCa development. Materials and Methods: Asian nations with adequate data quality were considered for this review. PCa ASIR estimates from CI5 and GLOBOCAN 2008 public use databases were examined in the four eligible countries: China, Japan, Korea and Singapore. Time trends in PCa ASIRs were examined using CI5 Volumes I-IX. Results: While PCa ASIRs remain much lower in the Asian nations examined than in North America, there is a clear trend of increasing PCa ASIRs in the four countries examined. Conclusion: Efforts to systematically collect cancer incidence data in Asian nations must be expanded. Current CI5 data indicate a rise in PCa ASIR in several populous Asian countries. If these rates continue to rise, it is uncertain whether there will be sufficient resources in place, in terms of trained personnel and infrastructure for medical treatment and continuum of care, to handle the increase in PCa patient volume. The recommendation by some experts to initiate PSA screening in Asian nations could compound a resource shortfall. Obtaining accurate estimates of PCa incidence in these countries is critically important for preparing for a potential shift in the public health burden posed by this disease.
      Citation: Journal of Carcinogenesis 2012 11(1):7-7
      PubDate: Mon,19 Mar 2012
      DOI: 10.4103/1477-3163.94025
      Issue No: Vol. 11, No. 1 (2012)
       
  • Prolonged sulforaphane treatment does not enhance tumorigenesis in
           oncogenic K-ras and xenograft mouse models of lung cancer

    • Authors: Ponvijay Kombairaju, Jinfang Ma, Rajesh K Thimmulappa, G Shengbin Yan, Edward Gabrielson, Anju Singh, Shyam Biswal
      Pages: 8 - 8
      Abstract: Ponvijay Kombairaju, Jinfang Ma, Rajesh K Thimmulappa, G Shengbin Yan, Edward Gabrielson, Anju Singh, Shyam Biswal
      Journal of Carcinogenesis 2012 11(1):8-8
      Background: Sulforaphane (SFN), an activator of nuclear factor erythroid-2 related factor 2 (Nrf2), is a promising chemopreventive agent which is undergoing clinical trial for several diseases. Studies have indicated that there is gain of Nrf2 function in lung cancer and other solid tumors because of mutations in the inhibitor Kelch-like ECH-associated protein 1 (Keap1). More recently, several oncogenes have been shown to activate Nrf2 signaling as the main prosurvival pathway mediating ROS detoxification, senescence evasion, and neoplastic transformation. Thus, it is important to determine if there is any risk of enhanced lung tumorigenesis associated with prolonged administration of SFN using mouse models of cancer. Materials and Methods: We evaluated the effect of prolonged SFN treatment on oncogenic K-ras (K-ras LSL-G12D )-driven lung tumorigenesis. One week post mutant-K-ras expression, mice were treated with SFN (0.5 mg, 5 d/wk) for 3 months by means of a nebulizer. Fourteen weeks after mutant K-ras expression (K-ras LSL-G12D ), mice were sacrificed, and lung sections were screened for neoplastic foci. Expression of Nrf2-dependent genes was measured using real time RT-PCR. We also determined the effect of prolonged SFN treatment on the growth of preclinical xenograft models using human A549 (with mutant K-ras and Keap1 allele) and H1975 [with mutant epidermal growth factor receptor (EGFR) allele] nonsmall cell lung cancer cells. Results: Systemic SFN administration did not promote the growth of K-ras LSL-G12D -induced lung tumors and had no significant effect on the growth of A549 and H1975 established tumor xenografts in nude mice. Interestingly, localized delivery of SFN significantly attenuated the growth of A549 tumors in nude mice, suggesting an Nrf2-independent antitumorigenic activity of SFN. Conclusions: Our results demonstrate that prolonged SFN treatment does not promote lung tumorigenesis in various mouse models of lung cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):8-8
      PubDate: Fri,13 Jul 2012
      DOI: 10.4103/1477-3163.98459
      Issue No: Vol. 11, No. 1 (2012)
       
  • Constitutive over expression of IL-1β, IL-6, NF-κB, and Stat3 is
           a potential cause of lung tumorgenesis in urethane (ethyl carbamate)
           induced Balb/c mice

    • Authors: Chandradeo Narayan, Arvind Kumar
      Pages: 9 - 9
      Abstract: Chandradeo Narayan, Arvind Kumar
      Journal of Carcinogenesis 2012 11(1):9-9
      Background: Lung cancer is a leading cause of cancer death. There has been found a substantial gap in the understanding of lung cancer genesis at the molecular level. We developed urethane (ethyl carbamate) induced lung tumor mice model to understand the mechanism and molecules involved in the cancer genesis. There might be many molecules involved, but we subsequently emphasized here the study of alternation in the expression of NF- κB, Stat3, and inflammatory cytokines interleukin-1β and interleukin-6 to hypothesize that the microenvironment created by these molecules is promoting tumor formation. Materials and Methods: 7-8 week old Balb/c mice of either sex were given intraperitoneal (i.p.) injection of urethane (1g/kgbw) for eight consecutive weeks. Histopathological analysis was done to detect abnormality or invasions occurred in the lung tissues. Automated cell counter was used to count the number of inflammatory cells. The expression of NF-κB, Stat3, and IL-1β was observed at translational level by western blot, while the expression of IL-1β and IL-6 was observed at transcriptional level by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) method. Secretion of IL-1β and IL-6 in the blood was measured by enzyme-linked immunosorbent assay (ELISA) method at different time intervals. Results: Histopathological analysis showed various lung cancer stages hyperplasia, atypical adenomatous hyperplasia, and adenocarcinoma. Increased population of inflammatory cells, persistant expression of NF-κB, Stat3, pStat3, and IL-1β at translational level, while at transcriptional level constitutive enhanced expression of IL-1β and IL-6 followed by increased secretion of IL-1β and IL-6 in the blood were observed in urethane-injected mice in comparison to phosphate buffer saline (PBS) injected mice at 12, 24, and 36 weeks . Conclusions: Overexpression of key molecules such as NF-κB, Stat3, pStat3, IL-1β, and IL-6 might have caused chronic inflammation, leading to the progression of lung cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):9-9
      PubDate: Tue,24 Jul 2012
      DOI: 10.4103/1477-3163.98965
      Issue No: Vol. 11, No. 1 (2012)
       
  • Caloric restriction reduced 1, 2-dimethylhydrazine-induced aberrant crypt
           foci and induces the expression of Sirtuins in colonic mucosa of F344 rats
           

    • Authors: Mariko Tomita
      Pages: 10 - 10
      Abstract: Mariko Tomita
      Journal of Carcinogenesis 2012 11(1):10-10
      Background: Caloric restriction (CR), a lowering of caloric intake without malnutrition, is associated with longevity. CR also decreases incidences of age-related diseases including cancer. The sirtuins (SIRTs) have been implicated as a key mediator for the beneficial effects of CR on longevity. However, the underlying mechanisms by which CR decreases cancer risk have not yet been fully elucidated. Materials and Methods: The present study was conducted to determine whether CR would modify the growth of preneoplastic colonic aberrant crypt foci (ACF). We also analyzed the expression of SIRTs to elucidate the molecular mechanisms of cancer-preventive effects of CR. F344 rats were fed a CR diet (60% of ad libitum diet) or a basal diet ad libitum. Then, the animals were given subcutaneous injection of either 1, 2-dimethylhydrazine (DMH) that enhances cell proliferation of colonic mucosa or saline. All animals were sacrificed at 5 weeks after the beginning of the experiment. Results: The number of ACF in colonic mucosa was significantly decreased in DMH-treated rats with CR as compared to in those without CR. No ACF was found in DMH-untreated animals with or without CR. Also, we found that CR decreased the cell proliferation of colonic mucosa in DMH-treated rats. The expressions of anti-apoptotic gene, Survivin, and cell cycle progression-associated gene, Cyclin D1, were increased by DMH-treatment. Both of the genes expressions were declined by CR in those of DMH-treated rats. The expressions of all SIRT1-7 mRNAs were significantly increased by CR in DMH-treated rats. Conclusion: As previous studies demonstrated that SIRT1 down-regulates Survivin and Cyclin D1, our findings suggest that at least SIRT1 protect colonic mucosa from formation and development of ACF by increasing apoptosis and reducing excessive cell growth in colon epithelial cells.
      Citation: Journal of Carcinogenesis 2012 11(1):10-10
      PubDate: Sat,28 Jul 2012
      DOI: 10.4103/1477-3163.99176
      Issue No: Vol. 11, No. 1 (2012)
       
  • Acyclic retinoid in chemoprevention of hepatocellular carcinoma: Targeting
           phosphorylated retinoid X receptor-α for prevention of liver
           carcinogenesis

    • Authors: Masahito Shimizu, Yohei Shirakami, Kenji Imai, Koji Takai, Hisataka Moriwaki
      Pages: 11 - 11
      Abstract: Masahito Shimizu, Yohei Shirakami, Kenji Imai, Koji Takai, Hisataka Moriwaki
      Journal of Carcinogenesis 2012 11(1):11-11
      One of the key features of hepatocellular carcinoma (HCC) is the high rate of intrahepatic recurrence that correlates with poor prognosis. Therefore, in order to improve the clinical outcome for patients with HCC, development of a chemopreventive agent that can decrease or delay the incidence of recurrence is a critical issue for urgent investigation. Acyclic retinoid (ACR), a synthetic retinoid, successfully improves HCC patient survival by preventing recurrence and the formation of secondary tumors. A malfunction of the retinoid X receptor-α (RXRα) due to phosphorylation by the Ras-MAPK signaling pathway plays a critical role in liver carcinogenesis, and ACR exerts chemopreventive effects on HCC development by inhibiting RXRα phosphorylation. Here, we review the relationship between retinoid signaling abnormalities and liver disease, the mechanisms of how RXRα phosphorylation contributes to liver carcinogenesis, and the detailed effects of ACR on preventing HCC development, especially based on the results of our basic and clinical research. We also outline the concept of "clonal deletion and inhibition" therapy, which is defined as the removal and inhibition of latent malignant clones from the liver before they expand into clinically detectable HCC, because ACR prevents the development of HCC by implementing this concept. Looking toward the future, we discuss "combination chemoprevention" using ACR as a key drug since it can generate a synergistic effect, and may thus be an effective new strategy for the prevention of HCC.
      Citation: Journal of Carcinogenesis 2012 11(1):11-11
      PubDate: Thu,30 Aug 2012
      DOI: 10.4103/1477-3163.100398
      Issue No: Vol. 11, No. 1 (2012)
       
  • CyclinD1 protein plays different roles in modulating chemoresponses in
           MCF7 and MDA-MB231 cells

    • Authors: Yuan Sun, Dianzhong Luo, D Joshua Liao
      Pages: 12 - 12
      Abstract: Yuan Sun, Dianzhong Luo, D Joshua Liao
      Journal of Carcinogenesis 2012 11(1):12-12
      Background : CyclinD1 is an essential sensor and activator of cell cycle initiation and progression; overexpression of cyclinD1 is linked to various human cancers, including breast cancer. The elevated cyclinD1 in some types of cancers is believed to be associated with tumor progression and response to systemic treatments. Aims : In this study, we anticipate to address the questions in human breast cancer; the function of cyclinD1 in mediating chemoresponses; and the signaling pathway cooperating with cyclinD1 to interfere with the drug functions. Materials and Methods: Using the cell clones, concurrent ectopic expression of the wild-type or K112E-mutated human cyclinD1 protein in the MCF7 and MDA-MB231 (MB231) breast cancer cells to study the function of cyclinD1 in responses to the chemotherapeutic treatments. Three drugs, cisplatin (CDDP), 5-fluorouracil (5-FU), and Gemzar were used in this study; the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle and cell death analysis, clonogenic survival assay, acridine orange (AO)/ethidium bromide (EB) staining, and Western blot assay were conducted to evaluate the drugs' effects in the cell clones. Results: The cell clones expressing the D1 protein in MCF7 and MB231 cells result in distinct effects on the responses to chemotherapeutic treatments. Particularly with Gemzar, ectopic expression of cyclinD1 protein in MCF7 cells results in a potentiated effect, which is CDK4 kinase activity dependent, whereas in MB231 cells, an opposite effect was observed. Moreover, our results suggested that the distinct chemosensitivities among those cell clones were not resulted from accelerated cell cycle, cell proliferation driven by the cyclinD1CDK4/6-Rb-E2F signaling chain, rather, they were results of the cell cycle-independent functions led by cyclinD1 alone or in complex with CDK4. Conclusions: Our results suggest that the functions of cyclinD1 protein in modulating chemoresponses in the MCF7 and MB231 cells are independent to its function as cell cycle initiator through activation of CDK4/6. Furthermore, the signals modulated by cyclinD1 upon treatment are determined by the drug and the cellular network.
      Citation: Journal of Carcinogenesis 2012 11(1):12-12
      PubDate: Thu,30 Aug 2012
      DOI: 10.4103/1477-3163.100401
      Issue No: Vol. 11, No. 1 (2012)
       
  • Alterations in keratins and associated proteins during 4-
           Nitroquinoline-1-oxide induced rat oral carcinogenesis

    • Authors: Deepak Kanojia, Sharada S Sawant, Anita M Borges, Arvind D Ingle, Milind M Vaidya
      Pages: 14 - 14
      Abstract: Deepak Kanojia, Sharada S Sawant, Anita M Borges, Arvind D Ingle, Milind M Vaidya
      Journal of Carcinogenesis 2012 11(1):14-14
      Background: Oral squamous cell carcinoma (OSCC) is the sixth largest group of malignancies globally and the single largest group of malignancies in the Indian subcontinent. Despite the advances in treatment and therapeutic modalities the five year survival rate of OSCC has not changed in the last few decades, and remains less than 40%. Several studies have focused on defining molecular markers that can either detect cancer at an early stage or can predict patient's outcome. However, such markers are still undefined. Keratins (K) are epithelia predominant intermediate filament proteins which are expressed in a differentiation dependent and site specific manner. Keratins are being used as biomarkers in different epithelial disorders including cancer. They are associated with desmoplakin and α6β4 integrin which are components of desmosomes and hemidesmosomes respectively. Materials and Methods: 4-Nitroquinoline 1-Oxide (4NQO) was used as a carcinogen for the development of various stages of oral carcinogenesis in rat lingual mucosa. Two-Dimentional gel electrophoresis was performed for the separation of Keratins followed by western blotting for their specific identification. Western blotting and RT PCR was carried out for desmoplakin and α6β4 integrin respectively to understand their levels. Immunohistochemical analysis was carried out to further study the localization of desmoplakin and α6 integrin. Results: In this study we have analysed the alterations in Keratins and associated proteins during sequential stages of 4NQO induced rat oral carcinogenesis. Our results showed that the alterations primarily begin after the dysplastic changes in the lingual epithelium like the elevation of Keratins 5/6a, ectopic expression of Keratin 8, increase in suprabasal expression of α6 integrin and increase in desmoplakin levels. Most of these alterations persisted till the development of SCC except desmoplakin, the levels of which were downregulated in papillomatous lesions and SCC. Many of these alterations have also been documented in human oral carcinogensis. Conclusion: Thus, 4NQO model of rat lingual carcinogenesis reproduces majority of the changes that are seen in human oral carcinogenesis and it can be exploited for the development of biomarkers.
      Citation: Journal of Carcinogenesis 2012 11(1):14-14
      PubDate: Thu,13 Sep 2012
      DOI: 10.4103/1477-3163.100861
      Issue No: Vol. 11, No. 1 (2012)
       
  • Aberrant glycogen synthase kinase 3&#946; in the development of
           pancreatic cancer

    • Authors: Takeo Shimasaki, Ayako Kitano, Yoshiharu Motoo, Toshinari Minamoto
      Pages: 15 - 15
      Abstract: Takeo Shimasaki, Ayako Kitano, Yoshiharu Motoo, Toshinari Minamoto
      Journal of Carcinogenesis 2012 11(1):15-15
      Development and progression of pancreatic cancer involves general metabolic disorder, local chronic inflammation, and multistep activation of distinct oncogenic molecular pathways. These pathologic processes result in a highly invasive and metastatic tumor phenotype that is a major obstacle to curative surgical intervention, infusional gemcitabine-based chemotherapy, and radiation therapy. Many clinical trials with chemical compounds and therapeutic antibodies targeting growth factors, angiogenic factors, and matrix metalloproteinases have failed to demonstrate definitive therapeutic benefits to refractory pancreatic cancer patients. Glycogen synthase kinase 3β (GSK3β), a serine/threonine protein kinase, has emerged as a therapeutic target in common chronic and progressive diseases, including cancer. Here we review accumulating evidence for a pathologic role of GSK3β in promoting tumor cell survival, proliferation, invasion, and resistance to chemotherapy and radiation in pancreatic cancer. We also discuss the putative involvement of GSK3β in mediating metabolic disorder, local inflammation, and molecular alteration leading to pancreatic cancer development. Taken together, we highlight potential therapeutic as well as preventive effects of GSK3β inhibition in pancreatic cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):15-15
      PubDate: Thu,13 Sep 2012
      DOI: 10.4103/1477-3163.100866
      Issue No: Vol. 11, No. 1 (2012)
       
  • Breast cancer disparities: Frontline strategies, proceedings of the 7 th
           annual texas conference on health disparities

    • Authors: Marilyne Kpetemey, Meghana V Kashyap, Lee Gibbs, Jamboor K Vishwanatha
      Pages: 16 - 16
      Abstract: Marilyne Kpetemey, Meghana V Kashyap, Lee Gibbs, Jamboor K Vishwanatha
      Journal of Carcinogenesis 2012 11(1):16-16
      There are striking disparities in health status, access to health care, and risk factors among racial and ethnic minorities and the general population in Texas. The disparities are multifactorial comprising genetic, sociocultural, and environmental variables. The Texas Center for Health Disparities (TCHD), a NIMHD Center of Excellence (COE), aims to prevent, reduce, and eliminate health disparities in the communities through research, education, and community-based programs. As part of the center's outreach activities, an annual conference is organized to build awareness and knowledge on health disparities. The overall theme for the 2012 conference was "Battling Breast Cancer Disparities: Frontline Strategies". The scientific program consisted of three sessions: "Breakthroughs in Breast Cancer", "Triple Negative Breast Cancer," and "Hormone Resistant Breast Cancer" featuring different aspects of bench-research from molecular biology, proteomics, and genetics to the clinical aspects such as detection, diagnosis, and finally to community-based approaches. This article summarizes the proceedings of the meeting providing salient strategies and best practices presented by the speakers.
      Citation: Journal of Carcinogenesis 2012 11(1):16-16
      PubDate: Sat,27 Oct 2012
      DOI: 10.4103/1477-3163.102950
      Issue No: Vol. 11, No. 1 (2012)
       
  • Meat consumption, ornithine decarboxylase gene polymorphism, and outcomes
           after colorectal cancer diagnosis

    • Authors: Jason A Zell, Bruce S Lin, Argyrios Ziogas, Hoda Anton-Culver
      Pages: 17 - 17
      Abstract: Jason A Zell, Bruce S Lin, Argyrios Ziogas, Hoda Anton-Culver
      Journal of Carcinogenesis 2012 11(1):17-17
      Background: Dietary arginine and meat consumption are implicated in colorectal cancer (CRC) progression via polyamine-dependent processes. Polymorphism in the polyamine-regulatory gene, ornithine decarboxylase 1 (Odc1, rs2302615) is prognostic for CRC-specific mortality. Here, we examined joint effects of meat consumption and Odc1 polymorphism on CRC-specific mortality. Materials and Methods: The analytic cohort was comprised of 329 incident stage I-III CRC cases diagnosed 1994-1996 with follow- up through March 2008. Odc1 genotyping was conducted using primers that amplify a 172-bp fragment containing the polymorphic base at +316. Dietary questionnaires were administered at cohort entry. Multivariate Cox proportional hazards regression analysis for CRC-specific mortality was stratified by tumor, node, metastasis (TNM) stage, and adjusted for clinically relevant variables, plus meat consumption (as a continuous variable, i.e., the number of medium-sized servings/week), Odc1 genotype, and a term representing the meat consumption and Odc1 genotype interaction. The primary outcome was the interaction of Odc1 and meat intake on CRC-specific mortality, as assessed by departures from multiplicative joint effects. Results: Odc1 genotype distribution was 51% GG, 49% GA/AA. In the multivariate model, there was a significant interaction between meat consumption and Odc1 genotype, P-int = 0.01. Among Odc1 GA/AA CRC cases in meat consumption Quartiles 1-3, increased mortality risk was observed when compared to GG cases (adjusted hazards ratio (HR) = 7.06 [95% CI 2.34-21.28]) - a difference not found among cases in the highest dietary meat consumption Quartile 4. Conclusions: Effects of meat consumption on CRC-specific mortality risk differ based on genetic polymorphism at Odc1. These results provide further evidence that polyamine metabolism and its modulation by dietary factors such as meat may have relevance to CRC outcomes.
      Citation: Journal of Carcinogenesis 2012 11(1):17-17
      PubDate: Wed,28 Nov 2012
      DOI: 10.4103/1477-3163.104004
      Issue No: Vol. 11, No. 1 (2012)
       
  • Subsite-based alterations in miR-21, miR-125b, and miR-203 in squamous
           cell carcinoma of the oral cavity and correlation to important target
           proteins

    • Authors: Linda Boldrup, Philip J Coates, Magnus Wahlgren, Göran Laurell, Karin Nylander
      Pages: 18 - 18
      Abstract: Linda Boldrup, Philip J Coates, Magnus Wahlgren, Göran Laurell, Karin Nylander
      Journal of Carcinogenesis 2012 11(1):18-18
      Background: MicroRNAs (miRNAs) are small noncoding RNA molecules with an essential role in regulation of gene expression. miRNA expression profiles differ between tumor and normal control tissue in many types of cancers and miRNA profiling is seen as a promising field for finding new diagnostic and prognostic tools. Materials and Methods: In this study, we have analyzed expression of three miRNAs, miR-21, miR-125b, and miR-203, and their potential target proteins p53 and p63, known to be deregulated in squamous cell carcinoma of the head and neck (SCCHN), in two distinct and one mixed subsite in squamous cell carcinoma in the oral cavity. Results: We demonstrate that levels of miRNA differ between tumors of different subsites with tongue tumors showing significant deregulation of all three miRNAs, whereas gingival tumors only showed significant downregulation of miR-125b and the mixed group of tumors in tongue/floor of the mouth showed significant deregulation of miR-21 and miR-125b. In the whole group of oral squamous cell carcinoma (SCC), a significant negative correlation was seen between miR-125b and p53 as well as a significant correlation between TP53 mutation status and miR-125b. Conclusion: The present data once again emphasize the need to take subsite into consideration when analyzing oral SCC and clearly show that data from in vitro studies cannot be transferred directly to the in vivo situation.
      Citation: Journal of Carcinogenesis 2012 11(1):18-18
      PubDate: Wed,28 Nov 2012
      DOI: 10.4103/1477-3163.104007
      Issue No: Vol. 11, No. 1 (2012)
       
  • Advances in bronchoscopy for lung cancer

    • Authors: Samjot Singh Dhillon, Elisabeth U Dexter
      Pages: 19 - 19
      Abstract: Samjot Singh Dhillon, Elisabeth U Dexter
      Journal of Carcinogenesis 2012 11(1):19-19
      Bronchoscopic techniques have seen significant advances in the last decade. The development and refinement of different types of endobronchial ultrasound and navigation systems have led to improved diagnostic yield and lung cancer staging capabilities. The complication rate of these minimally invasive procedures is extremely low as compared to traditional transthoracic needle biopsy and surgical sampling. These advances augment the safe array of methods utilized in the work up and management algorithms of lung cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):19-19
      PubDate: Mon,31 Dec 2012
      DOI: 10.4103/1477-3163.105337
      Issue No: Vol. 11, No. 1 (2012)
       
  • Hope for progress after 40 years of futility? Novel approaches in the
           treatment of advanced stage III and IV non-small-cell-lung cancer:
           Stereotactic body radiation therapy, mediastinal lymphadenectomy, and
           novel systemic therapy

    • Authors: Simon Fung Kee Fung, Graham W Warren, Anurag K Singh
      Pages: 20 - 20
      Abstract: Simon Fung Kee Fung, Graham W Warren, Anurag K Singh
      Journal of Carcinogenesis 2012 11(1):20-20
      Non-small-cell lung cancer (NSCLC) remains a leading cause of cancer mortality. The majority of patients present with advanced (stage III-IV) disease. Such patients are treated with a variety of therapies including surgery, radiation, and chemotherapy. Despite decades of work, however, overall survival in this group has been resistant to any substantial improvement. This review briefly details the evolution to the current standard of care for advanced NSCLC, advances in systemic therapy, and novel techniques (stereotactic body radiation therapy [SBRT], and transcervical extended mediastinal lymphadenectomy [TEMLA] or video-assisted mediastinal lymphadenectomy [VAMLA]) that have been used in localized NSCLC. The utility of these techniques in advanced stage therapy and potential methods of combining these novel techniques with systemic therapy to improve survival are discussed.
      Citation: Journal of Carcinogenesis 2012 11(1):20-20
      PubDate: Mon,31 Dec 2012
      DOI: 10.4103/1477-3163.105340
      Issue No: Vol. 11, No. 1 (2012)
       
  • Advances in lung cancer surgery

    • Authors: Mark W Hennon, Sai Yendamuri
      Pages: 21 - 21
      Abstract: Mark W Hennon, Sai Yendamuri
      Journal of Carcinogenesis 2012 11(1):21-21
      The last few years have witnessed an explosion of the use of minimally invasive techniques for the detection, diagnosis, and treatment of all stages of lung cancer. The use of these techniques has improved the risk-benefit ratio of surgery and has made it more acceptable to patients considering lung surgery. They have also facilitated the delivery of multi-modality therapy to patients with advanced lung cancer. This review article summarizes current surgical techniques that represent the "cutting edge" of thoracic surgery for lung cancer.
      Citation: Journal of Carcinogenesis 2012 11(1):21-21
      PubDate: Mon,31 Dec 2012
      DOI: 10.4103/1477-3163.105341
      Issue No: Vol. 11, No. 1 (2012)
       
  • Inhibitory effects of meju prepared with mixed starter cultures on
           azoxymethane and dextran sulfate sodium-induced colon carcinogenesis in
           mice

    • Authors: Ji-Kang Jeong, Hee-Kyung Chang, Kun-Young Park
      Pages: 13 - 13
      Abstract: Ji-Kang Jeong, Hee-Kyung Chang, Kun-Young Park
      Journal of Carcinogenesis 2012 11(1):13-13
      Backgrounds: Meju is the main ingredient and the starter culture of traditional Korean fermented soybean foods; these fermented soybean products are well-known for their various health benefits, including anticancer effects. We developed the grain-type meju using probiotic mixed starter cultures to improve the qualities and functionalities of fermented soybean products, as well as the meju itself. In this study, the inhibitory effects of the grain-type meju were investigated in azoxymethane (AOM) and dextran sulfate sodium (DSS)-induced colon carcinogenesis mice model. Materials and Methods: AOM and DSS colon carcinogenesis was induced in female C57BL/6 mice and meju was orally administered for 4 weeks. The body weight, colon length, and colon weight of mice were determined, and colonic tissues were histologically observed. The serum levels of proinflammatory cytokines and the levels of inflammation- and apoptosis-related genes in colonic tissue were also analyzed. Results: The administration of meju using probiotic mixed starter cultures ameliorated the symptoms of colon cancer and reduced number of neoplasia, and reduced serum proinflammatory cytokine levels and iNOS and COX-2 expression levels in colonic tissue. It increased Bax and reduced Bcl-2 expression levels and increased p21 and p53 expression in colonic tissues. Conclusion: The meju showed inhibitory effects on the progression of colon cancer induced by AOM and DSS by ameliorating the symptoms of colon cancer, reducing the number of neoplasias and regulating proinflammatory cytokine levels and the expressions of inflammation- and apoptosis-related genes in the colonic tissue.
      Citation: Journal of Carcinogenesis 2012 11(1):13-13
      PubDate: Mon,1 Jan 1900
      DOI: 10.4103/1477-3163.100404
      Issue No: Vol. 11, No. 1 (1900)
       
 
 
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