A study from the Division of Oncology, Department of Medicine/Pathology, Stanford University, Stanford, California, USA shows that “MYC through miR-17-92 Suppresses Specific Target Genes to Maintain Survival, Autonomous Proliferation…”
This study was published in the August 11, 2014 issue of Cancer Cell (The number 1 journal in basic cancer biology with an IF of ~27.238) by Prof. Felsher, Li, and others from the Division of Oncology, Department of Medicine/Pathology, Stanford University, Stanford, California, USA.
On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMD, reports here that: Therapeutic and Mechanistic insights into NIDDM drug-induced tumor suppression: Acarbose, the widely used drug in the treatment of NIDDM, inhibits tumorigenesis via up regulation of Sin3b, Hbp1, Suv420h1, Btg1 & BIM. This study suggests, for the first time, that acarbose, by up regulating its target genes, it may suppress the cancerous state of cells. Thereby, it may inhibit tumorigenesis. Together, this study suggests that pharmacological formulations encompassing “acarbose or its analogues“ may be used to treat c-myc-overexpressing tumors.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Web: http://genomediscovery.org
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
To cite: Boominathan, Therapeutic and Mechanistic insights into NIDDM drug-induced tumor suppression: Acarbose, the widely used drug in the treatment of NIDDM, inhibits tumorigenesis via up regulation of Sin3b, Hbp1, Suv420h1, Btg1 & BIM, Genome-2-Bio-Medicine Discovery center (GBMD), 25/08/2014, 7.51 am, http://genomediscovery.org
Courtesy: When you cite drop us a line at info@genomediscovery.org
* Research cooperation
