Introduction: What they say:
A study from the Institute of Genetics and Biophysics, CNR, Naples, Italy; and Department of Biochemistry, Biophysics and General Pathology, Second University of Naples, Naples, Italy shows that “miR-194-5p/BCLAF1 deregulation in AML tumorigenesis” This study was published in the 20 February 2017 issue of the journal “Leukemia” [One of the best journals in the field of “blood cancer biology” with an I.F of 12 plus] by Prof. Altuci, Dell’Aversana C, and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Combinatorial therapy for Acute Myeloid Leukemia: A pharmaceutical mixture encompassing Metformin and Navitoclax/ABT-263 (MAN) decreases the expression of BCLAF1, promotes differentiation of acute myeloid leukaemia cells, restores treatment responsiveness, increases therapeutic index of anticancer drugs, and promotes regression of AML via up-regulation of its target gene
From Significance of the study to Public health relevance:
Given that: (i) each year nearly 14 million people are diagnosed with cancer globally, and little more than half of them will die; (ii) cancer deaths globally are expected to be doubled by 2030; (iii) cancer treatment causes the highest economic loss compared to all the known causes of death worldwide; (iv) Acute myeloid leukemia is one of the most predominant leukemias among all adult leukemias; (v) each year about 10, 500 and 2900 new cases of AML are reported in the US and the UK, respectively; (vi) cure rates of AML ranges from 20-45% only, there is an urgent need to find: (i) a way to prevent an individual from being susceptible to cancer by strengthening his/her own immune system (Cancer immunotherapy); (ii) a cheaper alternative to the existing expensive anticancer drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and prevent metastatic progression and relapse of cancers.
What we infer from what they say:
Prof. Altucci’s research team has recently shown that MiRNA miR-194-5p: (1) inhibits BCL2-associated transcription factor 1 (BCLAF1) expression; (2) aids BCLAF1 in shuttling between nucleus and cytosol; (3) and its target gene BCLAF1 are commonly dysregulated in primary AMLs; (4) is induced in response to the HDAC inhibitor SAHA treatment, promotes differentiation, induces apoptosis and restores treatment responsiveness, suggesting that induction of miR-194-5p; and downregulation of its down-stream target gene BCLAF1 in AML cells may prevent AML progression.
From research findings to therapeutic opportunity :
A pharmaceutical mixture encompassing Metformin and Navitoclax/ABT-263 (MAN), by increasing the expression of its target genes, it may increase the expression of miR-194-5p (fig. 1). Thereby, it may: (i) decrease the expression of BCLAF1; (ii) aid BCLAF1 in shuttling between nucleus and Cytosol; (iii) promote differentiation of acute myeloid cells; (iv) restore treatment responsiveness; (v) increase therapeutic index of anticancer drugs; (vi) inhibit AML growth; and (vii) promote AML regression (fig.1).
Thus, pharmacological formulations encompassing “Metformin and Navitoclax(ABT-263), either alone or in combination with other known anticancer drugs,” (fig. 2), may be used to inhibit AML growth.
Details of the Research findings:
Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.
Undisclosed mechanistic information: How does a pharmaceutical mixture encompassing Metformin and Navitoclax (MAN) decrease the expression of BCLAF1?
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Citation: Boominathan, L., Combinatorial therapy for Acute Myeloid Leukemia: A pharmaceutical mixture encompassing Metformin and Navitoclax/ABT-263 (MAN) decreases the expression of BCLAF1, promotes differentiation of acute myeloid leukaemia cells, restores treatment responsiveness, increases therapeutic index of anticancer drugs, and promotes regression of AML via up-regulation of its target gene, 10/February/2019, 11.25 pm, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org
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