Publisher: BMC (Biomed Central)   (Total: 316 journals)

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Showing 1 - 200 of 316 Journals sorted alphabetically
Acta Neuropathologica Communications     Open Access   (Followers: 1, SJR: 2.683, CiteScore: 5)
Acta Veterinaria Scandinavica     Open Access   (Followers: 1, SJR: 0.655, CiteScore: 1)
Addiction Science & Clinical Practice     Open Access   (Followers: 8, SJR: 1.224, CiteScore: 3)
Advances in Rheumatology     Open Access   (Followers: 2)
Advances in Simulation     Open Access   (Followers: 6)
Agriculture & Food Security     Open Access   (Followers: 17, SJR: 0.575, CiteScore: 2)
AIDS Research and Therapy     Open Access   (Followers: 15, SJR: 1.08, CiteScore: 2)
Algorithms for Molecular Biology     Open Access   (Followers: 4, SJR: 1.333, CiteScore: 2)
Allergy, Asthma and Clinical Immunology     Open Access   (Followers: 27, SJR: 0.732, CiteScore: 2)
Alzheimer's Research & Therapy     Open Access   (Followers: 4, SJR: 2.449, CiteScore: 6)
Animal Biotelemetry     Open Access   (Followers: 1, SJR: 1.067, CiteScore: 2)
Annals of Clinical Microbiology and Antimicrobials     Open Access   (Followers: 15, SJR: 1.104, CiteScore: 3)
Annals of General Psychiatry     Open Access   (Followers: 28, SJR: 0.784, CiteScore: 2)
Annals of Occupational and Environmental Medicine     Open Access   (Followers: 13, SJR: 0.452, CiteScore: 1)
Annals of Surgical Innovation and Research     Open Access   (Followers: 3, SJR: 0.328, CiteScore: 1)
Antimicrobial Resistance and Infection Control     Open Access   (Followers: 13, SJR: 1.573, CiteScore: 3)
Applied Cancer Research     Open Access   (Followers: 3)
Archives of Physiotherapy     Open Access   (Followers: 15)
Archives of Public Health     Open Access   (Followers: 12, SJR: 1.244, CiteScore: 3)
Arthritis Research & Therapy     Open Access   (Followers: 16, SJR: 2.154, CiteScore: 4)
Asthma Research and Practice     Open Access   (Followers: 2)
Basic and Clinical Andrology     Open Access   (SJR: 0.564, CiteScore: 2)
Behavioral and Brain Functions     Open Access   (Followers: 3, SJR: 0.986, CiteScore: 3)
Big Data Analytics     Open Access   (Followers: 31)
BioData Mining     Open Access   (Followers: 5, SJR: 0.982, CiteScore: 2)
Bioelectronic Medicine     Open Access   (Followers: 1)
Biological Procedures Online     Open Access   (SJR: 1.352, CiteScore: 4)
Biological Research     Open Access   (Followers: 1, SJR: 0.654, CiteScore: 2)
Biology Direct     Open Access   (Followers: 10, SJR: 1.694, CiteScore: 3)
Biology of Mood & Anxiety Disorders     Open Access   (Followers: 6)
Biology of Sex Differences     Open Access   (Followers: 2, SJR: 1.902, CiteScore: 4)
Biomarker Research     Open Access   (Followers: 3)
Biomaterials Research     Open Access   (Followers: 6, SJR: 0.735, CiteScore: 3)
Biomedical Dermatology     Open Access  
BioMedical Engineering OnLine     Open Access   (Followers: 8, SJR: 0.542, CiteScore: 2)
BioPsychoSocial Medicine     Open Access   (Followers: 8, SJR: 0.416, CiteScore: 1)
Biotechnology for Biofuels     Open Access   (Followers: 9, SJR: 1.899, CiteScore: 6)
BMC Anesthesiology     Open Access   (Followers: 17, SJR: 0.807, CiteScore: 2)
BMC Biochemistry     Open Access   (Followers: 15, SJR: 0.708, CiteScore: 2)
BMC Bioinformatics     Open Access   (Followers: 195, SJR: 1.479, CiteScore: 2)
BMC Biology     Open Access   (Followers: 64, SJR: 3.842, CiteScore: 5)
BMC Biomedical Engineering     Open Access  
BMC Biophysics     Open Access   (Followers: 3, SJR: 0.682, CiteScore: 2)
BMC Biotechnology     Open Access   (Followers: 17, SJR: 1.012, CiteScore: 3)
BMC Cancer     Open Access   (Followers: 33, SJR: 1.464, CiteScore: 3)
BMC Cardiovascular Disorders     Open Access   (Followers: 22, SJR: 0.909, CiteScore: 2)
BMC Chemical Engineering     Open Access  
BMC Clinical Pathology     Open Access   (Followers: 7, SJR: 1.141, CiteScore: 3)
BMC Complementary and Alternative Medicine     Open Access   (Followers: 19, SJR: 0.858, CiteScore: 3)
BMC Dermatology     Open Access   (Followers: 13, SJR: 0.796, CiteScore: 2)
BMC Developmental Biology     Open Access   (Followers: 14, SJR: 1.43, CiteScore: 2)
BMC Ear, Nose and Throat Disorders     Open Access   (Followers: 1, SJR: 0.653, CiteScore: 2)
BMC Ecology     Open Access   (Followers: 23, SJR: 1.076, CiteScore: 2)
BMC Emergency Medicine     Open Access   (Followers: 20, SJR: 0.572, CiteScore: 1)
BMC Endocrine Disorders     Open Access   (Followers: 8, SJR: 0.965, CiteScore: 2)
BMC Energy     Open Access  
BMC Evolutionary Biology     Open Access   (Followers: 72, SJR: 1.656, CiteScore: 3)
BMC Family Practice     Open Access   (Followers: 15, SJR: 1.137, CiteScore: 2)
BMC Gastroenterology     Open Access   (Followers: 15, SJR: 1.231, CiteScore: 3)
BMC Genetics     Open Access   (Followers: 31, SJR: 1.16, CiteScore: 3)
BMC Genomics     Open Access   (Followers: 91, SJR: 2.11, CiteScore: 4)
BMC Geriatrics     Open Access   (Followers: 16, SJR: 1.257, CiteScore: 3)
BMC Health Services Research     Open Access   (Followers: 18, SJR: 1.151, CiteScore: 2)
BMC Hematology     Open Access   (Followers: 6, SJR: 0.545, CiteScore: 1)
BMC Immunology     Open Access   (Followers: 11, SJR: 0.993, CiteScore: 3)
BMC Infectious Diseases     Open Access   (Followers: 21, SJR: 1.576, CiteScore: 3)
BMC Intl. Health and Human Rights     Open Access   (Followers: 6, SJR: 1.006, CiteScore: 2)
BMC Materials     Open Access   (Followers: 2)
BMC Medical Education     Open Access   (Followers: 49, SJR: 0.765, CiteScore: 2)
BMC Medical Ethics     Open Access   (Followers: 22, SJR: 1.016, CiteScore: 2)
BMC Medical Genetics     Open Access   (Followers: 8, SJR: 1.109, CiteScore: 2)
BMC Medical Genomics     Open Access   (Followers: 5, SJR: 1.688, CiteScore: 3)
BMC Medical Imaging     Open Access   (Followers: 10, SJR: 0.536, CiteScore: 2)
BMC Medical Informatics and Decision Making     Open Access   (Followers: 25, SJR: 0.812, CiteScore: 2)
BMC Medical Physics     Open Access   (Followers: 7)
BMC Medical Research Methodology     Open Access   (Followers: 9, SJR: 2.221, CiteScore: 3)
BMC Medicine     Open Access   (Followers: 14, SJR: 4.219, CiteScore: 7)
BMC Microbiology     Open Access   (Followers: 16, SJR: 1.242, CiteScore: 3)
BMC Molecular and Cell Biology     Open Access   (Followers: 48, SJR: 1.277, CiteScore: 3)
BMC Molecular Biology     Open Access   (Followers: 199, SJR: 1.216, CiteScore: 2)
BMC Musculoskeletal Disorders     Open Access   (Followers: 27, SJR: 0.951, CiteScore: 2)
BMC Nephrology     Open Access   (Followers: 8, SJR: 1.098, CiteScore: 3)
BMC Neurology     Open Access   (Followers: 22, SJR: 1.006, CiteScore: 2)
BMC Neuroscience     Open Access   (Followers: 17, SJR: 1.12, CiteScore: 2)
BMC Nursing     Open Access   (Followers: 27, SJR: 0.766, CiteScore: 2)
BMC Nutrition     Open Access   (Followers: 11)
BMC Obesity     Open Access   (Followers: 8)
BMC Ophthalmology     Open Access   (Followers: 17, SJR: 0.921, CiteScore: 2)
BMC Oral Health     Open Access   (Followers: 7, SJR: 0.867, CiteScore: 2)
BMC Palliative Care     Open Access   (Followers: 37, SJR: 1.105, CiteScore: 2)
BMC Pediatrics     Open Access   (Followers: 17, SJR: 1.278, CiteScore: 2)
BMC Pharmacology     Open Access   (Followers: 2)
BMC Pharmacology & Toxicology     Open Access   (Followers: 7, SJR: 0.785, CiteScore: 2)
BMC Physiology     Open Access   (Followers: 4, SJR: 0.936, CiteScore: 2)
BMC Plant Biology     Open Access   (Followers: 17, SJR: 1.887, CiteScore: 4)
BMC Pregnancy and Childbirth     Open Access   (Followers: 22, SJR: 1.427, CiteScore: 3)
BMC Proceedings     Full-text available via subscription   (Followers: 1, SJR: 0.302, CiteScore: 1)
BMC Psychiatry     Open Access   (Followers: 38, SJR: 1.346, CiteScore: 3)
BMC Psychology     Open Access   (Followers: 19, SJR: 0.817, CiteScore: 2)
BMC Public Health     Open Access   (Followers: 199, SJR: 1.337, CiteScore: 3)
BMC Pulmonary Medicine     Open Access   (Followers: 5, SJR: 1.373, CiteScore: 3)
BMC Research Notes     Open Access   (Followers: 4, SJR: 0.691, CiteScore: 2)
BMC Rheumatology     Open Access   (Followers: 3)
BMC Sports Science, Medicine and Rehabilitation     Open Access   (Followers: 35, SJR: 0.926, CiteScore: 2)
BMC Structural Biology     Open Access   (Followers: 8, SJR: 1.024, CiteScore: 2)
BMC Surgery     Open Access   (Followers: 10, SJR: 0.693, CiteScore: 2)
BMC Systems Biology     Open Access   (Followers: 14, SJR: 1.109, CiteScore: 2)
BMC Urology     Open Access   (Followers: 14, SJR: 0.853, CiteScore: 2)
BMC Veterinary Research     Open Access   (Followers: 20, SJR: 0.934, CiteScore: 2)
BMC Women's Health     Open Access   (Followers: 14, SJR: 0.931, CiteScore: 2)
BMC Zoology     Open Access   (Followers: 1)
BMJ Evidence-Based Medicine     Hybrid Journal   (Followers: 4)
Borderline Personality Disorder and Emotion Dysregulation     Open Access   (Followers: 10)
Breast Cancer Research     Open Access   (Followers: 21, SJR: 3.026, CiteScore: 6)
Burns & Trauma     Open Access   (Followers: 13)
CABI Agriculture and Bioscience     Open Access   (Followers: 2)
Cancer & Metabolism     Open Access   (Followers: 7)
Cancer Cell Intl.     Open Access   (Followers: 7, SJR: 1.13, CiteScore: 3)
Cancer Communications     Open Access  
Cancer Convergence     Open Access   (Followers: 1)
Cancer Imaging     Open Access   (Followers: 3, SJR: 1.012, CiteScore: 3)
Cancer Nanotechnology     Open Access   (Followers: 2, SJR: 1.168, CiteScore: 4)
Cancers of the Head & Neck     Open Access   (Followers: 3)
Canine Genetics and Epidemiology     Open Access   (Followers: 1)
Carbon Balance and Management     Open Access   (Followers: 5, SJR: 0.977, CiteScore: 2)
Cardio-Oncology     Open Access  
Cardiovascular Diabetology     Open Access   (Followers: 10, SJR: 2.157, CiteScore: 5)
Cardiovascular Ultrasound     Open Access   (Followers: 5, SJR: 0.812, CiteScore: 2)
Cell Communication and Signaling     Open Access   (Followers: 2, SJR: 2.211, CiteScore: 4)
Cell Division     Open Access   (Followers: 1, SJR: 2.445, CiteScore: 4)
Cellular & Molecular Biology Letters     Hybrid Journal   (Followers: 3)
Cerebellum & Ataxias     Open Access   (Followers: 1)
Chemistry Central J.     Open Access   (Followers: 5, SJR: 0.607, CiteScore: 3)
Child and Adolescent Psychiatry and Mental Health     Open Access   (Followers: 28, SJR: 0.901, CiteScore: 2)
Chinese Medicine     Open Access   (Followers: 2, SJR: 0.57, CiteScore: 2)
Chinese Neurosurgical J.     Open Access  
Chiropractic & Manual Therapies     Open Access   (Followers: 5, SJR: 0.599, CiteScore: 2)
Cilia     Open Access   (SJR: 0.732, CiteScore: 1)
Clinical and Molecular Allergy     Open Access   (Followers: 5, SJR: 0.933, CiteScore: 3)
Clinical and Translational Allergy     Open Access   (Followers: 2, SJR: 1.425, CiteScore: 4)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 22)
Clinical Epigenetics     Open Access   (Followers: 11, SJR: 2.435, CiteScore: 5)
Clinical Hypertension     Open Access   (Followers: 5)
Clinical Sarcoma Research     Open Access  
Conflict and Health     Open Access   (Followers: 8, SJR: 1.851, CiteScore: 3)
Contraception and Reproductive Medicine     Open Access   (Followers: 2)
COPD Research and Practice     Open Access   (Followers: 1, SJR: 0.755, CiteScore: 2)
Cost Effectiveness and Resource Allocation     Open Access   (Followers: 5, SJR: 0.888, CiteScore: 2)
Critical Care     Open Access   (Followers: 70, SJR: 2.48, CiteScore: 5)
Current Opinion in Molecular Therapeutics     Full-text available via subscription   (Followers: 13)
Diabetology & Metabolic Syndrome     Open Access   (Followers: 7, SJR: 0.943, CiteScore: 2)
Diagnostic and Prognostic Research     Open Access  
Diagnostic Pathology     Open Access   (Followers: 13, SJR: 0.818, CiteScore: 2)
Disaster and Military Medicine     Open Access   (Followers: 5)
Emerging Themes in Epidemiology     Open Access   (Followers: 13, SJR: 1.003, CiteScore: 2)
Energy, Sustainability and Society     Open Access   (Followers: 16, SJR: 0.607, CiteScore: 2)
Environmental Health     Open Access   (Followers: 13, SJR: 1.662, CiteScore: 4)
Environmental Health and Preventive Medicine     Open Access   (Followers: 4, SJR: 0.5, CiteScore: 1)
Environmental Microbiome     Open Access   (SJR: 0.768, CiteScore: 2)
Epigenetics & Chromatin     Open Access   (Followers: 8, SJR: 3.767, CiteScore: 5)
European J. of Medical Research     Open Access   (Followers: 1, SJR: 0.55, CiteScore: 1)
European Review of Aging and Physical Activity     Open Access   (Followers: 11, SJR: 1.308, CiteScore: 4)
Experimental & Translational Stroke Medicine     Open Access   (Followers: 9, SJR: 0.98, CiteScore: 3)
Experimental Hematology & Oncology     Open Access   (Followers: 4, SJR: 0.842, CiteScore: 2)
ExRNA     Open Access  
Eye and Vision     Open Access   (Followers: 1)
Fertility Research and Practice     Open Access   (Followers: 2)
Fibrogenesis & Tissue Repair     Open Access   (SJR: 1.531, CiteScore: 4)
Fisheries and Aquatic Sciences     Open Access   (Followers: 2, SJR: 0.199, CiteScore: 0)
Flavour     Open Access   (Followers: 3)
Fluids and Barriers of the CNS     Open Access   (Followers: 2, SJR: 2.054, CiteScore: 5)
Frontiers in Zoology     Open Access   (Followers: 9, SJR: 1.597, CiteScore: 3)
Genes and Environment     Open Access   (Followers: 1, SJR: 0.516, CiteScore: 1)
Genetics Selection Evolution     Open Access   (Followers: 7, SJR: 1.745, CiteScore: 4)
Genome Biology     Open Access   (Followers: 38)
Genome Medicine     Open Access   (Followers: 7, SJR: 4.537, CiteScore: 7)
Global Health Research and Policy     Open Access   (Followers: 4)
Globalization and Health     Open Access   (Followers: 8, SJR: 1.262, CiteScore: 2)
Gut Pathogens     Full-text available via subscription   (Followers: 5, SJR: 1.066, CiteScore: 3)
Gynecologic Oncology Research and Practice     Open Access   (Followers: 1)
Harm Reduction J.     Open Access   (SJR: 1.445, CiteScore: 3)
Head & Face Medicine     Open Access   (Followers: 1, SJR: 0.62, CiteScore: 2)
Health and Quality of Life Outcomes     Open Access   (Followers: 15, SJR: 1.069, CiteScore: 3)
Health Research Policy and Systems     Open Access   (Followers: 15, SJR: 1.11, CiteScore: 2)
Hereditary Cancer in Clinical Practice     Open Access   (Followers: 2, SJR: 0.848, CiteScore: 2)
Hereditas     Open Access   (Followers: 1, SJR: 0.278, CiteScore: 1)
Human Genomics     Open Access   (Followers: 3, SJR: 1.501, CiteScore: 3)
Human Resources for Health     Open Access   (Followers: 11, SJR: 1.301, CiteScore: 2)
Immunity & Ageing     Open Access   (Followers: 10, SJR: 1.218, CiteScore: 3)
Implementation Science     Open Access   (Followers: 21, SJR: 2.443, CiteScore: 4)
Implementation Science Communications     Open Access   (Followers: 3)
Infectious Agents and Cancer     Open Access   (SJR: 0.855, CiteScore: 2)
Infectious Diseases of Poverty     Open Access   (Followers: 1, SJR: 1.212, CiteScore: 3)
Inflammation and Regeneration     Open Access   (Followers: 2)
Intl. Breastfeeding J.     Open Access   (Followers: 26, SJR: 0.913, CiteScore: 3)
Intl. J. for Equity in Health     Open Access   (Followers: 7, SJR: 1.04, CiteScore: 2)
Intl. J. of Behavioral Nutrition and Physical Activity     Open Access   (Followers: 30, SJR: 2.626, CiteScore: 6)
Intl. J. of Health Geographics     Open Access   (Followers: 7, SJR: 1.385, CiteScore: 3)
Intl. J. of Mental Health Systems     Open Access   (Followers: 7, SJR: 0.721, CiteScore: 2)
Intl. J. of Pediatric Endocrinology     Open Access   (Followers: 10)

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Similar Journals
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Biomarker Research
Number of Followers: 3  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2050-7771
Published by BMC (Biomed Central) Homepage  [316 journals]
  • Advances in targeted therapy for acute myeloid leukemia

    • Abstract: Abstract Acute myeloid leukemia (AML) is a clonal malignancy characterized by genetic heterogeneity due to recurrent gene mutations. Treatment with cytotoxic chemotherapy has been the standard of care for more than half of a century. Although much progress has been made toward improving treatment related mortality rate in the past few decades, long term overall survival has stagnated. Exciting developments of gene mutation-targeted therapeutic agents are now changing the landscape in AML treatment. New agents offer more clinical options for patients and also confer a more promising outcome. Since Midostaurin, a FLT3 inhibitor, was first approved by US FDA in 2017 as the first gene mutation-targeted therapeutic agent, an array of new gene mutation-targeted agents are now available for AML treatment. In this review, we will summarize the recent advances in gene mutation-targeted therapies for patients with AML.
      PubDate: 2020-05-20
       
  • Characterization of novel dual tandem CD19/BCMA chimeric antigen receptor
           T cells to potentially treat multiple myeloma

    • Abstract: Background Treatment with chimeric antigen receptor (CAR)-engineered T cells directed against the B-cell maturation antigen (BCMA) promoted transient recovery from multiple myeloma (MM). However, the absence of this antigen on immature plasma cells may limit the efficacy of this modality and facilitate relapse. The purpose of this study is to characterize a novel CAR that includes both a single-chain variable fragment (scFv)-BCMA and an scFv-CD19 in tandem orientation (tan-CAR) in an attempt to target both BCMA and CD19 expression on MM cells. Method The scFv sequences from the anti-CD19 antibody FMC63 and the anti-BCMA antibody C11D5.3 were ligated in tandem with transmembrane and T-cell signaling domains to generate the tan-CAR construct. Specificity and efficacy of activated tan-CAR T cells were analyzed using in vitro proliferation, cytokine release, and cytolysis assays. We also evaluated the in vivo efficacy with a xenograft mouse model that included target tumor cells that expressed CD19 or BCMA and compared the results to those obtained with conventional CAR T cells. Results The in vitro studies revealed specific activation of tan-CAR T cells by K562 cells that overexpressed CD19 and/or BCMA. Cell proliferation, cytokine release, and cytolytic activity were all comparable to the responses of single scFv CAR T cells. Importantly, in vivo studies of tan-CAR T cells revealed specific inhibition of tumor growth in the mouse xenograft model that included cells expressing both CD19 and BCMA. Systemic administration of tan-CAR T cells resulted in complete tumor remission, in contrast to the reduced efficacies of BCMA-CAR T and CD19-CAR T alone in this setting. Conclusion We report the successful design and execution of novel tan-CAR T cells that promote significant anti-tumor efficacy against both CD19 and BCMA antigen-positive tumor cells in vitro and in vivo. The data from this study reveal a novel strategy that may help to reduce the rate of relapse in the treatment with single scFv-CAR T cells.
      PubDate: 2020-05-13
       
  • Trends and projections of kidney cancer incidence at the global and
           

    • Abstract: Background Identifying the temporal trends of kidney cancer (KC) incidence in both the past and the future at the global and national levels is critical for KC prevention. Methods We retrieved annual KC case data between 1990 and 2017 from the Global Burden of Disease (GBD) online database. The average annual percentage change (AAPC) was used to quantify the temporal trends of KC age-standardized incidence rates (ASRs) from 1990 to 2017. Bayesian age-period-cohort models were used to predict KC incidence through 2030. Results Worldwide, the number of newly diagnosed KC cases increased from 207.3 thousand in 1990 to 393.0 thousand in 2017. The KC ASR increased from 4.72 per 100,000 to 4.94 per 100,000 during the same period. Between 2018 and 2030, the number of KC cases is projected to increase further to 475.4 thousand (95% highest density interval [HDI] 423.9, 526.9). The KC ASR is predicted to decrease slightly to 4.46 per 100,000 (95% HDI 4.06, 4.86). A total of 90, 2, and 80 countries or territories are projected to experience increases, remain stable, and experience decreases in KC ASR between 2018 and 2030, respectively. In most developed countries, the KC incidence is forecasted to decrease irrespective of past trends. In most developing countries, the KC incidence is predicted to increase persistently through 2030. Conclusions KC incidence is predicted to decrease in the next decade, and this predicted decrease is mainly driven by the decreases in developed countries. More attention should be placed on developing countries.
      PubDate: 2020-05-13
       
  • Circulating long non-coding RNA GAS5 (growth arrest-specific transcript 5)
           as a complement marker for the detection of malignant mesothelioma using
           liquid biopsies

    • Abstract: Background For the detection of malignant mesothelioma additional markers are needed besides the established panel consisting of calretinin and mesothelin. The aim of this study was the identification and verification of long non-coding RNAs (lncRNAs) as complementing circulating markers. Methods Candidate lncRNAs were identified in silico using previously published RNA expression profiles and verified using quantitative PCR (qPCR) in mesothelioma cell lines as well as human plasma samples from mesothelioma patients and asbestos-exposed controls. Results GAS5 (growth arrest-specific transcript 5) as a single marker is marked by a low sensitivity of 14%, but the combination of GAS5 with calretinin and mesothelin increased the panel’s sensitivity from 64 to 73% at a predefined specificity of 97%. Circulating GAS5 is not affected by pleurectomy before blood collection, age, or smoking status. Conclusions GAS5 is verified as an appropriate circulating marker for the supplement of calretinin and mesothelin to detect malignant mesothelioma. Although the sensitivity of GAS5 is too low for the use as a single marker, the addition of GAS5 as a third marker improves the performance of the established marker panel. The benefit of GAS5 for the detection of malignant mesothelioma at early stages needs to be validated in a prospective study.
      PubDate: 2020-05-13
       
  • Biomarkers in individualized management of chimeric antigen receptor T
           cell therapy

    • Abstract: Abstract The development of chimeric antigen receptor (CAR) T cell immunotherapy has achieved promising results, both in clinical studies and in commercial products for patients with hematologic malignancies. Despite high remission rates of CAR-T cell therapy in previously untreatable, refractory and/or relapsed patients, several challenges in CAR-T therapy remain to be overcome, especially in integrating such therapies into personalized disease management approaches. Given the unique characteristics of CAR-T therapy, it is particularly urgent to identify biomarkers to maximize their clinical benefits. This systematic review summarizes clinically relevant biomarkers that may help individualized disease management in patients receiving CAR-T cell therapy in terms of toxicity warning, efficacy prediction and relapse monitoring. We summarize data from 18 clinical trials, including traditional indicators like cytokines, biochemical proteins, tumor burden, as well as potential novel indicators such as CAR-T cell expansion and persistency. The establishment of a biomarker-based system aimed at individualized management is recommended to guide better clinical application of CAR-T products.
      PubDate: 2020-05-11
       
  • Successful treatment of acute B lymphoblastic leukemia relapse in the skin
           and testicle by anti-CD19 CAR-T with IL-6 knocking down: a case report

    • Abstract: Background Extramedullary relapse is an important cause of treatment failure among patients with acute lymphoblastic leukemia (ALL). This type of relapse is commonly observed in the central nervous system, while it is rare in the testicles and skin. Chimeric antigen receptor-modified T cell (CAR-T) therapy targeting CD19 has shown to be a beneficial treatment approach for relapsed/refractory B cell acute lymphoblasticleukemia (r/r B-ALL). Yet, few studies have reported data regarding the treatment of extramedullary B-ALL relapse, especially both in skin and testicle, with CAR-T therapy. Case presentation Here we reported a single case of a patient with relapsed B-ALL in skin and testicle who was successfully treated by the shRNA-IL6-modified anti-CD19 CAR-T(ssCAR-T-19) therapy. A 29-year-old man with relapsed B-ALL in skin and testicle was enrolled in clinal trial involving the shRNA-IL6-modified anti-CD19 CAR-T(ssCAR-T-19) therapy (ClinicalTrials.gov number, NCT03919240). The patient had toxicity consistent with the grade 1 cytokine release syndrome. Conclusions ssCART-19 therapy may be used to effectively eliminate infiltrating leukemia cells in the skin and testicle with mild toxicity, which could be a much safer approach to bridge allo-HSCT, thus further improving the patient’s outcome. Trial registration ClinicalTrials.gov number, NCT03919240, Registered 18 April 2019, retrospectively registered.
      PubDate: 2020-05-06
       
  • Overexpressed immunoglobulin-like transcript (ILT) 4 in lung
           adenocarcinoma is correlated with immunosuppressive T cell subset
           infiltration and poor patient outcomes

    • Abstract: Background The poor response to current PD-1/PD-L1 inhibitors in lung cancer patients requires development of novel immunotargets. Immunoglobulin-like transcript (ILT)4 is an immunosuppressive molecule mainly expressed in myeloid innate cells. Recent studies showed that ILT4 was highly expressed in multiple malignant cells and regulated tumor biologies including proliferation, invasion and metastasis. However, the immunomodulatory role of tumor cell-derived ILT4 is unclear. Here we aimed to analyze the correlation of tumor cell ILT4 expression with T cell infiltration and subset distribution, illustrate ILT4-regulated immunosuppressive microenvironment, and raise tumor cell-derived ILT4 as a novel immunotherapeutic target and prognostic biomarker for lung adenocarcinoma (LUAD) patients. Methods We collected the tissue samples and corresponding clinicopathological data from 216 primary LUAD patients. Using immunohistochemical staining and public database analyses we investigated the relationship between ILT4 expression and different T cell subset density as well as patient outcomes. Results Enriched ILT4 expression in tumor cells of LUAD tissues indicated reduced T cell infiltration in the tumor microenvironment (TME), advanced diseases and poor patient overall survival (OS). Further T cell subset analyses revealed that ILT4 expression was correlated with decreased CD8+T cell and increased Treg frequency in both cancer nest and stroma, but not with altered CD4+T cell frequency. High ILT4 level combined with low CD8+T cell/high Treg density predicted markedly poorer clinical outcomes compared with any of these biomarkers alone. Conclusions Tumor cell-derived ILT4 is correlated with immunosuppressive T cell subset infiltration and poor clinical outcomes, and might be a potential immunotherapeutic target and prognostic biomarker for LUAD patients. Combined ILT4 expression and CD8+ T cell/Treg frequency in tumor infiltrating lymphocytes (TILs) are stronger predictors for patient outcomes.
      PubDate: 2020-04-29
       
  • TBL1XR1 mutation predicts poor outcome in primary testicular diffuse large
           B-cell lymphoma patients

    • Abstract: Abstract Primary testicular lymphoma (PTL), often appearing as focal masses in the scrotum and epididymides, is the most frequent testicular tumor in aged men. Although MYD88 and CD79B mutations were the most common genetic alterations observed, the gene mutation landscape of PTL remains poorly defined. In this study, we identified 1326 mutations involving 311 genes or regions in 90 PTL patients through next-generation sequencing (NGS). PTL patients with the TBL1XR1 mutation, irrespective of treatment therapy, had an inferior overall survival (OS) than TBL1XR1 WT (wild type) patients (p = 0.045). Moreover, patients with this mutation, treated with a CHOP regimen (CTX 750 mg/m2 iv, d1,8 ADM 50 mg/m2 iv, d1 VCR 1.4 mg/m2 iv, d1 PDN 100 mg/m2 po d1–5), had a poorer OS (p = 0.019). In addition, such patients were prone to have a more intensive infiltration of tumors (p = 0.025, x2 = 4.890). Thus, we speculated that patients with a TBL1XR1 mutation have poorer prognosis, partly due to greater invasion and infiltration of tumors. Our results suggest that the TBL1XR1 mutation can be used as an indicator to predict the prognosis of PTL and can be employed as a promising new target for treatment of PTL in the future.
      PubDate: 2020-04-17
       
  • The predictive value of tumor mutation burden for immune checkpoint
           inhibitors therapy in non-small cell lung cancer is affected by
           patients’ age

    • Abstract: Abstract High tumor mutation burden (TMB), which is associated with increased tumor immunogenicity, has been identified to predict improved response to immune checkpoint inhibitors (ICIs) therapy in non-small cell lung cancer (NSCLC). As host immunity is also significant to eliminate cancer cells, however, its clinical impact on cancer immunotherapy is still largely unknown. Here we explored the influence of age, which is an important characteristic to evaluate immune response of patients, on TMB-based predictive system for ICIs therapy in NSCLC. Our results showed that high TMB was capable of predicting better durable clinical benefit (DCB) in agelow group, while it was insignificant in agehigh group. Besides, the predictive power of TMB for progression-free survival (PFS) and overall survival (OS) was better in agelow group than in agehigh group. Our study illustrated that the predictive value of TMB for ICIs therapy was better in young patients than in elderly patients in NSCLC.
      PubDate: 2020-04-09
       
  • LncRNA profile study reveals a seven-lncRNA signature predicts the
           prognosis of patients with colorectal cancer

    • Abstract: Background The prognosis of colorectal cancer (CRC) is still challenging to evaluate or predict. Recently, long non-coding RNAs (lncRNAs) have been found to play an important role in tumorigenesis and prognosis, however, few lncRNAs have been identified in CRC progression. We aimed to establish a lncRNA signature to improve prognosis prediction of CRC. Methods In the present study, we profiled lncRNA expression with a lncRNA-mining approach in two CRC data sets from Gene Expression Ominus (GEO) (GSE39582, N = 557 and GSE17538, N = 200). LncRNAs were analyzed to determine a prognostic signature by Cox regression and Robust likelihood-based survival model. We identified seven lncRNAs that significantly associated with the disease free survival (DFS) in the training group. A risk score formula was constructed to evaluate the performance of this lncRNA panel. Results A seven-lncRNA signature was established to predict prognosis of CRC patients. The prognostic value of this signature was verified in the training group, internal validation group and external validation cohort, respectively. Receiver operating characteristic (ROC) analysis suggested a powerful discrimination ability of the seven-gene signature. Finally, Cox regression analyzed this signature as an independent influencing factor and subsequent pathway or network analysis implicated a potential mechanism of these lncRNAs. Conclusions In summary, the seven-lncRNA signature we identified can effectively classify patients. This risk score model could serve as an independent biomarker to predict prognosis of CRC patients.
      PubDate: 2020-02-28
       
  • The mir-767-105 cluster: a crucial factor related to the poor prognosis of
           hepatocellular carcinoma

    • Abstract: Abstract MiRNAs have been widely reported as the therapeutic target for hepatocellular carcinoma (HCC). However, mirna clusters, as the more impressive tumor regulatory factors, have received little attention. By deeply digging the Cancer Genome Atlas (TCGA) database, we aimed to explore the vital mirna cluster that regulated the poor prognosis of HCC. The results showed that the upregulation of mirna cluster-767-105 in HCC was the most significant, compared with the non-tumor tissues. Besides, high expression of all three members of the cluster was positively correlated with poor prognosis of HCC and the resistance of sorafenib. Cox analysis proved that all the three mirnas were independent prognostic factors, while the mir-767 was the most compelling (HR value 8.388, 95%CI 2.524–27.897). The higher expression of the three-mirna signature also significantly indicated the worse prognosis. Through bioinformatics analysis, we screened their common potential target genes, which were highly correlated with tumor regulation. These results supported that the mirna cluster-767-105 promoted the poor outcome of HCC and could be a robust target for the therapy of HCC patients.
      PubDate: 2020-02-13
       
  • Using toponomics to characterize phenotypic diversity in alveolar
           macrophages from male mice treated with exogenous SP-A1

    • Abstract: Background We used the Toponome Imaging System (TIS) to identify “patterns of marker expression”, referred to here as combinatorial molecular phenotypes (CMPs) in alveolar macrophages (AM) in response to the innate immune molecule, SP-A1. Methods We compared 114 AM from male SP-A deficient mice. One group (n = 3) was treated with exogenous human surfactant protein A1 (hSP-A1) and the other with vehicle (n = 3). AM obtained by bronchoalveolar lavage were plated onto slides and analyzed using TIS to study the AM toponome, the spatial network of proteins within intact cells. With TIS, each slide is sequentially immunostained with multiple FITC-conjugated antibodies. Images are analyzed pixel-by-pixel identifying all of the proteins within each pixel, which are then designated as CMPs. CMPs represent organized protein clusters postulated to contribute to specific functions. Results 1) We compared identical CMPs in KO and SP-A1 cells and found them to differ significantly (p = 0.0007). Similarities between pairs of markers in the two populations also differed significantly (p < 0.0001). 2) Focusing on the 20 most abundant CMPs for each cell, we developed a method to generate CMP “signatures” that characterized various groups of cells. Phenotypes were defined as cells exhibiting similar signatures of CMPs. i) AM were extremely diverse and each group contained cells with multiple phenotypes. ii) Among the 114 AM analyzed, no two cells were identical. iii) However, CMP signatures could distinguish among cell subpopulations within and between groups. iv) Some cell populations were enriched with SP-A1 treatment, some were more common without SP-A1, and some seemed not to be influenced by the presence of SP-A1. v) We also found that AM were more diverse in mice treated with SP-A1 compared to those treated with vehicle. Conclusions AM diversity is far more extensive than originally thought. The increased diversity of SP-A1-treated mice points to the possibility that SP-A1 enhances or activates several pathways in the AM to better prepare it for its innate immune functions and other functions shown previously to be affected by SP-A treatment. Future studies may identify key protein(s) responsible for CMP integrity and consequently for a given function, and target it for therapeutic purposes.
      PubDate: 2020-02-13
       
  • Increased PD-1+Tim-3+ exhausted T cells in bone marrow may influence the
           clinical outcome of patients with AML

    • Abstract: Background Altered expression of T cell immune inhibitory receptors may result in immunosuppression and associate with the poor prognosis of leukemia patients in which the leukemic bone marrow (BM) microenvironment may contribute to such immunosuppression. We found higher numbers of programmed death-1 (PD-1) + exhausted T cells in peripheral blood (PB) from acute myeloid leukemia (AML) patients. To investigate the leukemic BM influence on immunosuppression, we further compared the distributions of PD-1 and T cell immunoglobulin mucin-3 (Tim-3) and the exhausted T cell phenotype in PB and BM from AML patients and characterized their relationship with clinical outcome. Methods PB and BM samples from 15 patients with newly diagnosed AML were collected and analyzed for the expression of PD-1, Tim-3, CD244, and CD57 on CD3+, CD4+, and CD8+ T cells by multicolor flow cytometry. Results The proportions of PD-1 + CD3+ and PD-1 + CD8+ T cells were significantly higher in BM compared with PB. Similarly, higher PD-1 + CD244 + CD3+ and PD-1 + CD244 + CD8+ T cells were found in BM, and an increased tendency for PD-1 + CD244 + CD4+ T cells was also detected in this group. In contrast, increased Tim-3 + CD4+/Tim-3 + CD244 + CD4+ T cells were predominant in BM compared with PB, but there was no statistically significant difference in Tim-3 + CD8+ T cells. Moreover, PD-1 and Tim-3 double-positive CD3+/CD4+/CD8+ T cells were significantly increased in the BM group. In addition, a higher proportion of PD-1 + Tim-3 + CD3+ T cells in the BM and PD-1 + Tim-3 + CD4+ T cells in PB was detected in non-complete remission (NCR) compared with complete remission (CR) patients after first-cycle chemotherapy. Conclusions Upregulation of PD-1 and Tim-3 and the exhausted phenotype of CD4+ and CD8+ T cells in the BM of AML patients may contribute to mediating the leukemic immunosuppressive microenvironment, and increased PD-1 + Tim-3+ CD8+ T cells may be related to T cell dysfunction in AML, which may influence clinical outcome.
      PubDate: 2020-02-13
       
  • Identification of pAKT as a pharmacodynamic marker for MER kinase in human
           melanoma G361 cells

    • Abstract: Background The MER signaling pathway represents an attractive therapeutic target for human cancers. Growth arrest–specific protein 6 (GAS6)–induced MER phosphorylation is often unstable and difficult to detect without pervanadate pretreatment in human cancer cells, posing a challenge for the development of selective MER kinase inhibitors. Here, we identified phosphorylated AKT (pAKT) as a specific pharmacodynamic marker for MER kinase inhibitors in human melanoma G361 cells. Methods The expression of MER, TYRO3, and AXL were profiled among multiple human cancer cells. To determine whether they play a role in the activation of pAKT, MER and TYRO3 were selectively depleted by small, interfering RNA knockdown. In addition, using AKT phosphorylation as a readout, a high-throughput cell-based assay was established in G361 cells for evaluation of the potency of potential inhibitors of MER pathway activation. Results We demonstrated that high levels of MER and TYRO3, but not AXL, were expressed in G361 cells. In these cells, pAKT was induced by GAS6 treatment, which could be reversed by AXL/MER inhibitors. We showed that GAS6-induced pAKT is only dependent on MER kinase, but not TYRO3, in G361 cells. Furthermore, we observed a correlation in potency between inhibition of pAKT in G361 cells and pMER in MER-overexpressing Ba/F3 cells by these inhibitors. Conclusions In summary, we have demonstrated that GAS6-induced pAKT is a possible pharmacodynamic marker for the inhibition of MER kinase, and we have successfully developed a cell-based functional assay for screening small-molecule inhibitors of MER kinase for potential therapeutic utility in treating GAS6/MER-deregulated human cancers.
      PubDate: 2020-02-04
       
  • PSCA is a target of chimeric antigen receptor T cells in gastric cancer

    • Abstract: Background Gastric cancer is a deadly malignancy and is a prognostically unfavorable entity with restricted therapeutic strategies available. Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein widely expressed in bladder, prostate, and pancreatic cancers. Existing studies have thoroughly recognized the availability of utilizing anti-PSCA CAR-T cells in the treatment of metastatic prostate cancer and non-small-cell lung cancer. However, no previous study has investigated the feasibility of using anti-PSCA CAR-T cells to treat gastric cancer, irrespective of the proven expression of PSCA on the gastric cancer cell surface. Methods We determined the expression of PSCA in several primary tumor tissues and constructed third-generation anti-PSCA CAR-T cells. We then incubated anti-PSCA CAR-T cells and GFP-T cells with target tumor cell lines at E:T ratios of 2:1, 1:1, 1:2, and 1:4 to evaluate the therapeutic efficacy of anti-PSCA CAR-T cells in vitro. We also assayed canonical T cell activation markers after coculturing anti-PSCA CAR-T cells with target cell lines by flow cytometry. The detection of a functional cytokine profile was carried out via enzyme-linked immunosorbent assays. We then evaluated the antitumor activity of anti-PSCA CAR-T cells in vivo by establishing two different xenograft GC mouse models. Results Anti-PSCA CAR-T cells exhibited upregulated activation markers and increased cytokine production profiles related to T cell cytotoxicity in an antigen-dependent manner. Moreover, anti-PSCA CAR-T cells exhibited robust anti-tumor cytotoxicity in vitro. Importantly, we demonstrated that anti-PSCA CAR-T cells delivered by peritumoral injection successfully stunted tumor progression in vivo. However, intravenous administration of anti-PSCA CAR-T cells failed to reveal any therapeutic improvements. Conclusions Our findings corroborated the feasibility of anti-PSCA CAR-T cells and their efficacy against gastric cancer, implicating the potential of applying anti-PSCA CAR-T cells to treat GC patients in the clinic.
      PubDate: 2020-01-28
       
  • Novel immunomodulatory drugs and neo-substrates

    • Abstract: Abstract Thalidomide, lenalidomide and pomalidomide are immunomodulatory drugs (IMiDs) effective in the treatment of multiple myeloma, myelodysplastic syndrome (MDS) with deletion of chromosome 5q and other hematological malignancies. Recent studies showed that IMiDs bind to CRBN, a substrate receptor of CRL4 E3 ligase, to induce the ubiquitination and degradation of IKZF1 and IKZF3 in multiple myeloma cells, contributing to their anti-myeloma activity. Similarly, lenalidomide exerts therapeutic efficacy via inducing ubiquitination and degradation of CK1α in MDS with deletion of chromosome 5q. Recently, novel thalidomide analogs have been designed for better clinical efficacy, including CC-122, CC-220 and CC-885. Moreover, a number of neo-substrates of IMiDs have been discovered. Proteolysis-targeting chimeras (PROTACs) as a class of bi-functional molecules are increasingly used as a strategy to target otherwise intractable cellular protein. PROTACs appear to have broad implications for novel therapeutics. In this review, we summarized new generation of immunomodulatory compounds, their potential neo-substrates, and new strategies for the design of novel PROTAC drugs.
      PubDate: 2020-01-09
       
  • LOX family and ZFPM2 as novel diagnostic biomarkers for malignant pleural
           mesothelioma

    • Abstract: Background Malignant pleural mesothelioma (MPM) is a rare and aggressive cancer that develops in the pleural and outer layer of tissues surrounding the lungs. MPM is primarily caused by occupational exposure to asbestos and results in a poor prognosis. Effective therapeutics as well as early diagnostics for the MPM are still lacking. To identify potential diagnostic biomarkers for MPM, we performed bioinformatics analysis of public database. Methods Utilizing databases from Cancer Cell Line Encyclopedia (CCLE) and Gene Expression Omnibus (GEO), we identified several potential candidates that could act as MPM biomarkers. We carried out additional molecular analyses of these potential markers using MPM patient tissue samples via quantitative polymerase chain reaction. Results We identified Lysyl oxidase (LOX), Lysyl oxidase homologs 1&2 (LOXL1& LOXL2) Zinc Finger Protein, FOG Family Member 2 (ZFPM2) as potential diagnostic biomarkers for MPM. In this study, we found that the LOX family and ZFPM2 showed comparable diagnostic ability to Fibulin-3 or mesothelin (MSLN) and would be better potential biomarkers than Sulfatase 1 (SULF1), Thrombospondin 2 (THBS2) and Cadherin 11 (CDH11). Conclusions LOX family and ZPFM2 were identified as novel MPM diagnostic biomarkers which could strengthen MPM clinical diagnostic capabilities.
      PubDate: 2020-01-08
       
  • Immune biomarkers in thymic epithelial tumors: expression patterns,
           prognostic value and comparison of diagnostic tests for PD-L1

    • Abstract: Background Immunotherapy is currently under investigation in B3 Thymoma (TB3) and Thymic Carcinoma (TC). PD-L1 expression has been evaluated on a limited number of patients with selected antibodies. We aimed to analyze cohort of TB3 and TC with a panel of antibodies to assess the prevalence of PD-L1 expression, its prognostic value and to set up a reproducible test. Methods We retrospectively studied 103 patients samples of FFPE histologically confirmed TB3 (n = 53) and TC (n = 50) by expert pathologists within the RYTHMIC national network. We compared PD-L1, PD1, CD8 and PD-L2 expression and performed correlation with tumor types and patients outcomes. Four PD-L1 antibodies were tested, three of them validated as companion tests in lung cancer, one tested on two automates on whole section of tumors. We evaluated the percentage and intensity of both epithelial and immune stained cells. Results TB3 epithelial cells had a higher and more diffuse expression of PD-L1 than TC regardless the antibodies tested (p < 0.0001). Three out of four antibodies targeting PD-L1 tested on the DAKO autostainer gave similar staining. Concordance between antibodies was lower for PD-L1 staining on immune cells with no significant difference between TB3 and TC except on E1L3N antibody. PD-L2 antibody stained no tumor epithelial cells. High PD-L1 expression was correlated with a better overall survival for TB3 and was not correlated with tumor staging. Conclusion Frequent PD-L1 expression, particularly in TB3, paves the way for immunotherapy in TET (Thymic Epithelial Tumor). Otherwise, we have set up three reproducible LDT (laboratory-developed test) for four PD-L1 antibodies.
      PubDate: 2019-12-04
       
  • Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase
           inhibitors for EGFR-mutant lung cancer

    • Abstract: Abstract EGFR-tyrosine kinase inhibitors (EGFR-TKIs) have achieved remarkable outcomes in the treatment of patients with EGFR-mutant non-small-cell lung cancer, but acquired resistance is still the main factor restricting their long-term use. In addition to the T790 M mutation of EGFR, amplification of the MET (or c-MET) gene has long been recognized as an important resistance mechanism for first- or second-generation EGFR-TKIs. Recent studies suggest that a key mechanism of acquired resistance to third-generation EGFR-TKIs (such as osimertinib) may be MET amplification and/or protein overactivation, especially when they are used as a first-line treatment. Therefore, in patients resistant to first-generation EGFR-TKIs caused by MET amplification and/or protein overactivation, the combination of osimertinib with MET or MEK inhibitors may be considered.
      PubDate: 2019-11-21
       
  • Clinical significance of stromal ER and PR expression in periampullary
           adenocarcinoma

    • Abstract: Background Tamoxifen treatment has previously been reported to confer life-prolonging effects in patients with advanced pancreatic cancer, and most evidently so in women. None of these trials did however include biomarkers, and the relevance of female hormone signaling in pancreatic or other periampullary adenocarcinoma remains largely unexplored. The aim of this study was to examine the extent and potential clinical significance of estrogen receptor-α (ER) and progesterone receptor (PR) expression in pancreatic and other periampullary cancers. Methods ER and PR expression was examined using immunohistochemistry on tissue microarrays with primary tumors from a retrospective consecutive cohort of 175 patients with resected periampullary adenocarcinoma, with long-term clinical follow-up. Non-parametric and Chi square tests were applied to examine the associations of stromal ER and PR expression with patient and tumor characteristics. Kaplan-Meier analysis and log rank test were applied to illustrate survival differences in relation to ER and PR expression. Cox regression proportional hazards models were applied to examine the associations between investigative factors and risk of death and recurrence, and to test for interactions between KRAS mutation status and hormone receptor expression in relation to survival. Results Expression of both ER and PR was more frequent in the tumor-associated stroma than in the epithelium. A significant prognostic interaction, independent of tumor morphology, was found between stromal PR expression and KRAS mutation status in relation to both overall and recurrence-free survival (pinteraction = 0.026 and pinteraction = 0.005), in particular in women (pinteraction = 0.002 and pinteraction = 0.005). Specifically, stromal PR expression was associated with a prolonged survival in patients with KRAS-mutated tumors, whereas the opposite was seen for KRAS wild-type tumors. The prognostic value of ER positivity was limited to the subgroup of women with tumors of pancreatic origin. Conclusions These results demonstrate that stromal PR rather than ER expression, together with KRAS mutation status, provides long-term prognostic information in patients with periampullary adenocarcinoma. Further study into the mechanistic basis for these observations may unveil important clues to the pathogenesis of these cancers and open up for the discovery of novel treatment options.
      PubDate: 2019-11-19
       
 
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