Publisher: Smart Science and Technology LLC   (Total: 3 journals)

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Cancer Cell & Microenvironment
Number of Followers: 9  

  This is an Open Access Journal Open Access journal
ISSN (Print) 2331-0928
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  • Cellular Homeostasis or Tumorigenesis: USP7 Playing the Double Agent

    • Authors: Mrinal Kanti Ghosh; Bhaskar Basu, Gouranga Saha, Shreyasee Ghatak Choudhury
      Abstract: The ubiquitin specific protease USP7/HAUSP is a major deubiquitinase that acts upon a wide spectrum of substrate proteins. Deubiquitination by USP7 generally leads to stabilization of substrates and their rescue from proteasomal degradation, but can also lead to alteration in their intracellular localization and activity. On the basis of its substrate proteins, USP7 has been shown to regulate processes involved in both the maintenance of homeostasis and the promotion of tumorigenesis. USP7, so far does not seem to be a dedicated regulator for either of these cellular phenomena, instead the relative abundance of a particular set of substrates over another being the factor that decides towards which phenomena it will be monopolized. The onset of cancer unfortunately creates an abundance of pro-oncogenic substrates, and this leads to a drastic monopolization of USP7 function towards the enhancement of further pro-oncogenic signaling.
      PubDate: 2020-04-04
      Issue No: Vol. 5 (2020)
       
  • Role of Monoamine oxidase A (MAO-A) in cancer progression and metastasis

    • Authors: Ashish Bhattacharjee; Pritam Biswas, Sukhamoy Dhabal, Payel Das, Pradip Das, Surbhi Swaroop, Tuhina Prasad, Dhanalakshmi J, Indhumathi S
      Abstract: Monoamine oxidase A (MAO-A) is a flavoenzyme that catalyzes biogenic amines into the corresponding aldehydes by oxidative deamination. Although MAO-A is primarily associated with depression and antisocial behaviour, dysregulation of MAO-A has been associated with neurodegenerative diseases and cardiovascular disorders. Moreover, the contribution of MAO-A in the resolution of inflammation is well established. Recent reports reveal the unanticipated role of MAO-A in tumorigenesis. In this review we provide informations that MAO-A is involved in the progression and metastasis of many different cancer cells including prostate cancer, colorectal cancer, hepatocellular carcinoma and lung cancer. We further discuss the regulatory mechanisms that control tumorigenesis, progression and metastasis in these different type of cancer cells. Altogether these informations indicate that MAO-A can be a general therapeutic target in cancer treatment. 
      PubDate: 2020-04-04
      Issue No: Vol. 5 (2020)
       
  • Scaling up to study brca2: the zeppelin zebrafish mutant reveals a role
           for brca2 in embryonic development of kidney mesoderm

    • Authors: Bridgette E. Drummond; Rebecca Ann Wingert
      Abstract: Specialized renal epithelial cells known as podocytes are essential components of the filtering structures within the kidney that coordinate the process of removing waste from the bloodstream. Podocyte loss initiates many human kidney diseases as it triggers subsequent damage to the kidney, leading to progressive loss of function that culminates with end stage renal failure. Podocyte morphology, function and gene expression profiles are well conserved between zebrafish and humans, making the former a relevant model to study podocyte development and model kidney diseases. Recently, we reported that whole genome sequencing of the zeppelin (zep) zebrafish mutant, which exhibits podocyte abrogation, revealed that the causative lesion for this defect was a splicing mutation in the breast cancer 2, early onset (brca2) gene. This was a surprising and novel discovery, as previous research on brca2/BRCA2 in a number of vertebrate animal models had not implicated an explicit role for this gene in kidney mesoderm development. Interestingly, the abrogation of the podocyte lineage in zep mutants was also accompanied by the formation of a larger interrenal (IR) gland, which is analogous to the adrenal gland in mammals, and suggested a fate switch between the renal and interrenal mesodermal derivatives. Mirroring these findings, knockdown of brca2 also recapitulated the loss of podocytes and increased IR populace. In addition, brca2 overexpression was sufficient to partially rescue podocytes in zep mutants, and induced ectopic podocyte formation in wild-type embryos. Interestingly, immunofluorescence studies indicated that zep mutants had elevated P-h2A.X levels, suggesting that DNA repair is dysfunctional in these animals and contributes to the zep phenotype. Moving forward, this unique zebrafish mutant provides a new model to further explore how brca2 contributes to the development of tissues including the kidney mesoderm—roles which may have implications for renal diseases as well.
      PubDate: 2020-04-04
      Issue No: Vol. 5 (2020)
       
  • Metastatic Malignant Thymoma to the Abdomen

    • Authors: Saju Joseph
      Abstract: Thymoma is a rare neoplasm of thymic epithetical cells that has the ability to spread by local extension. While metastases are most commonly confined to the pleura, pericardium and diaphragm, cases of abdominal metastases have been reported. In a recent publication [ref 7], we conducted a SEER database and literature review to identify cases of malignant thymoma (MT) and abdominal metastases, demonstrating an increasing overall incidence of MT with a significant male predominance. Additionally, we suggested routine screening for all MT patients as roughly 50% of abdominal metastasis cases presented as asymptomatic, as well as a multimodal treatment approach for those with metastatic MT to the abdomen. In this highlight, we briefly present the evidence for a rising rate of MT, review reported cases of abdominal metastasis, and emphasize the need for a multimodal treatment approach.  
      PubDate: 2020-04-04
      Issue No: Vol. 5 (2020)
       
 
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Publisher: Smart Science and Technology LLC   (Total: 3 journals)

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Heriot-Watt University
Edinburgh, EH14 4AS, UK
Email: journaltocs@hw.ac.uk
Tel: +00 44 (0)131 4513762
 


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