Small molecule-based therapy for p53-deficient tumors: IAPP (Amylin) suppresses the expression of oncomiR-17-92 and induces regression of p53-mutated human tumors via up regulation of its target gene, 11/May/2015, 23.54

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A recent study from the Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [3] Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [4] Metastasis Research Center, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA shows that“IAPP-driven metabolic reprogramming induces regression of p53-deficient tumours in vivo.” This study was published in the 29 January  2015 issue of the Journal “Nature” (the no.1 journal in Science with an impact factor of 42) by Prof. Flores ER, Venkatanarayan A and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that:  Small molecule-based therapy for p53-deficient tumors: IAPP (Amylin) suppresses the expression of oncomiR-17-92 and induces regression of p53-mutated human tumors via up regulation of its target gene 

Significance:  Cancer suppressor p53 is mutated in more than 50% of cancers of different origin, while its pathway is altered in about 80% of tumors. This study suggests a therapeutic strategy as to how p53-deficient or mutant p53 expressing human cancers can be cured by activating its homologous protein such as TAp73.

Although IAPP has been shown to induce regression of p53-deficient tumours in vivo, the mechanistic basis of which remains unclear.  This study suggests, for the first time, that IAPP (Amylin), by increasing the expression of its target gene, it may decrease the expression of oncomiR 17-92. Thereby, it may induce regression of p53-mutated human tumors. Thus, pharmacological formulations encompassing IAPP or its analogues  can be used to inhibit the progression of p53-deficient human tumors.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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CitationBoominathan,  Small molecule-based therapy for p53-deficient tumors: IAPP (Amylin) suppresses the expression of oncomiR-17-92 and induces regression of p53-mutated human tumors via up regulation of its target gene, 11/May/2015, 23.54, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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Undisclosed information: How IAPP (Amylin)  suppresses the expression of oncomiR-17-92

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