Dr Boominathan’s Scientific caliber
- First, Dr Boominathan had predicted on May 30, 2008 that p53 homologue p63 could regulate microRNA processing (Evidence: email sent on 30.5.2008-Gmail- p63 is a regulator of miRNA processing May 30, 2008, 1.39 a.m- (no subject); Proposal p63 is a regulator of microRNA processing complex (1)). This was one of the first evidences favoring a role for the tumor suppressor p53 homologue p63 in microRNA processing. In an astonishing coincidence (?), Miyazono K’s group (University of Tokyo, Japan) has published a scientific paper entitled “Modulation of microRNA processing by p53″ http://www.ncbi.nlm.nih.gov/pubmed/19626115 on July 23, 2009—nearly a year after (July 23, 2009) the date of prediction (May 30, 2008) made by Dr Boominathan—in the Journal “Nature” (No.1 journal in Science)
- Second, Dr Boominathan had proposed on June 13/14, 2008 that the tumor suppressor p53, p14/p19ARF & INK4a could function as negative regulators of stem cell proliferation and reprogramming (Evidence: email sent on 13/14.6.2008-Model p73.63 regulates selfrenewal and reprogramming June 13, 2008; Email-Gmail- Model p53 p63 p73 regulates stem cell renewal, June 14, 2008 10.32 a.m). In a rare and an astonishing coincidence (?), four different groups—led by the 2012 Noble prize winner Shinya Yamanaka (Center for iPS Cells Research and Application, Kyoto University, Kyoto, Japan), Belmonte JC (The Salk Institute for Biological Studies, La Jolla, California, USA), Hochedlinger K (HHMI at MGH,(MIT) Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, and Department of Stem Cell and Regenerative Biology, Harvard University and Harvard Medical School, Boston, Massachusetts, USA.,) & Serrano M (Spanish National Cancer Research Center (CNIO), Madrid, Spain)—from different parts of the world have published back-to-back papers—Suppression of induced pluripotent stem cell generation by the p53–p21 pathway http://www.ncbi.nlm.nih.gov/pubmed/19668191; Linking the p53 tumour suppressor pathway to somatic cell reprogramming http://www.ncbi.nlm.nih.gov/pubmed?term=Linking%20the%20p53%20tumour%20suppressor%20pathway%20to%20somatic%20cell%20reprogramming; Immortalization eliminates a roadblock during cellular reprogramming into iPS cells http://www.ncbi.nlm.nih.gov/pubmed?term=Immortalization%20eliminates%20a%20roadblock%20during%20cellular%20reprogramming%20into%20iPS%20cells; and The Ink4/Arf locus is a barrier for iPS cell reprogramming http://www.ncbi.nlm.nih.gov/pubmed?term=The%20Ink4%2FArf%20locus%20is%20a%20barrier%20for%20iPS%20cell%20reprogramming–Nature advance online publication 9 August 2009— in “Nature”. These papers were published nearly a year and three months after ( 9 August 2009) the date of prediction (June 13/14, 2008) made by Dr Boominathan.
- Third, Dr Boominathan had proposed on June 13, 2008 that the DNp63 could function as regulators of stem cell proliferation and reprogramming (Evidence: email sent on 13.6.2008-Model p73.63 regulates selfrenewal and reprogramming, June 13, 2008). In a rare and an astonishing coincidence, Lin’s group has published a paper entitled “DNp73 improves generation efficiency of human induced pluripotent stem cells” http://www.ncbi.nlm.nih.gov/pubmed/22449255 in BMC Cell Biol on Mar 26, 2012 (Volume 13:9). This paper was published nearly three years and three months after (Mar 26, 2012) the date of prediction (June 13, 2008) made by Dr Boominathan.
- Fourth, Dr Boominathan had proposed on May 30, 2008 that the tumor suppressor p63 could regulate the expression of Dicer, the microRNA-processing enzyme (Evidence: email sent on 30.5.2008-Gmail-p63 is a regulator of miRNA processing, May 30, 2008, 1.39 a.m- (no subject); Proposal p63 is a regulator of microRNA processing complex (1)). Subsequently, Dr Boominathan has proposed a role for TAp63 in inhibiting metastasis through induction of Dicer and miRNAs (Boominathan L, 12th, May, PloS One 2010 http://www.ncbi.nlm.nih.gov/pubmed/20485546). In a rare and an astonishing coincidence (?), Su X & Elsa Flores have published a paper entitled TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs http://www.ncbi.nlm.nih.gov/pubmed/20962848 in “Nature” (Nature. 2010 Oct 21; 467 (7318):986-90). This paper was published nearly two years and five months (Oct 21, 2010) after the date of prediction (May 30, 2008/May 12, 2010) made by Dr Boominathan.
- Fifth, Dr Boominathan had proposed in the manuscript submitted to Annual review of Biochemistry for review on July 26, 2009 that Hypoxia induced factors (HIFs)-induced Oct4, Sox-2, Nanog and c-Myc may promote Stem cell renewal. Remarkably, in a rare and an astonishing coincidence (?), on August 27, 2009, the 2012 Nobel laureate Shinya Yamanaka (Japan)’s group has published a paper entitled “Hypoxia enhances the generation of induced pluripotent stem cells” in Cancer Stem Cell (5-Year Impact Factor: 27.494)
- Sixth, Dr Boominathan had proposed on June 16, 2006 (and 10, December, 2011) that the p63 could play a role in insulin resistance, diabetes and obesity (Invention disclosure document(June 16, 2006) can be provided upon request). Remarkably, in a rare and an astonishing coincidence (?), on Oct 3, 2012, Su X and Flores ER (The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.) have published a paper entitled TAp63 Is a Master Transcriptional Regulator of Lipid and Glucose Metabolism in Cell Metabolism (5 year impact factor:17.770) ( http://www.ncbi.nlm.nih.gov/pubmed/23040072). This paper was published nearly six years and four months (Oct 3, 2012) after the date of invention disclosure document (June 16, 2006) made by Dr Boominathan.
- Seventh, GBMD’s Chief-Scientist Dr Boominathan had proposed on March 23, 2013 (and in a number of other dates in 2012 and 2013–http://genomediscovery.org/molecular-insights-into-pain-mechanism-p53p63p73-regulates-pain-perception-via-targeting-sodium-channel-voltage-gated-type-xi-%CE%B1-subunit-14november2013-5-41-am/; http://genomediscovery.org/insights-into-pain-mechanism-tumor-suppressor-p53-increases-cox-2-expression-and-prostaglandin-e2-pge2-production/; http://genomediscovery.org/hyperalgesia-p53p63p73-controls-the-severity-and-duration-of-inflammatory-pain-responses-5november2013-6-38-am/; http://genomediscovery.org/molecular-insights-into-pain-mechanism-p53-suppresses-mechanical-hyperalgesia-in-mice-via-induction-of-its-target-mirna-30september2013-7-10-am/; http://genomediscovery.org/assigning-new-function-to-an-old-pain-reliever-diclofenac-activates-a-number-of-tumor-suppressor-mirnas-by-repressing-its-target-gene-2august2013-10-41-am/ http://genomediscovery.org/assigning-new-function-to-an-old-pain-reliever-diclofenac-activates-a-number-of-tumor-suppressor-mirnas-by-repressing-its-target-gene-2august2013-10-41-am/; http://genomediscovery.org/p53p63p73-functions-as-regulators-of-pain-tolerance-6july2012/; http://genomediscovery.org/p63p73-senses-temperature-pain-and-itching-30january2013/) that p63/p73 regulates thermal and neuropathic pain [http://genomediscovery.org/p63p73-regulates-thermal-and-neuropathic-pain-23march2013-21-56/]. Evidently, on Nov 4, 2013, Niklison-Chirou MV and Melino G (from Toxicology Unit, Medical Research Council, Leicester, United Kingdom) have published a paper in the high profile journal PNAS stating that “p73 null mice have impairments in the peripheral nervous system with reduced thermal sensitivity, axon number, and myelin thickness” (http://www.ncbi.nlm.nih.gov/pubmed/24190996). However, it is important to understand that this research paper was published nearly one year and four months (Nov 4, 2013) later from the date of publication made by Dr L Boominathan. This serves as a strong supporting evidence for the fact that Dr L Boominathan’s scientific mind/idea matches with the best in the world.
- Eighth, GBMD’s Chief-Scientist Dr Boominathan had proposed on October 22, 2013 that p53 suppresses nucleoside diphosphate linked moiety X-type motif 1 (NUDT1 or MTH1) via up regulation of its target gene; and Resveratrol suppresses nucleoside diphosphate linked moiety X-type motif 1 (NUDT1 or MTH1) via up regulation of its target gene (http://genomediscovery.org/p53-suppresses-nucleoside-diphosphate-linked-moiety-x-type-motif-1-nudt1-or-mth1-via-up-regulation-of-its-target-gene-22october2013-7-21-am/; http://genomediscovery.org/resveratrol-suppresses-nucleoside-diphosphate-linked-moiety-x-type-motif-1-nudt1-or-mth1-via-up-regulation-of-its-target-gene-22october2013-7-23-am/). Together, this data suggest that the most mutated gene in human cancer and the potent tumor suppressor gene known as of today p53 and its activator Resveratrol suppress the expression of MTH1/NUDT1 to inhibit cancer progression. Evidently, Prof Helleday & Gad h (from Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden), on Apr 10, 2014, have published a paper in the Number one journal in Science “Nature” stating that “MTH1 inhibition eradicates cancer by preventing sanitation of the dNTP pool” (http://www.ncbi.nlm.nih.gov/pubmed/24190996). In the same issue of the Journal Nature, Prof Supertif Furga and Huber have published a paper stating that “Stereospecific targeting of MTH1 … as an anticancer strategy (http://www.ncbi.nlm.nih.gov/pubmed/24695225).” However, it is important to understand that these research papers were published nearly six months (Apr 10, 2014) later from the date of publication made by Dr L Boominathan. This serves as a strong supporting evidence for the fact that Dr L Boominathan’s scientific mind/idea matches with the best in the world.
- Ninth, GBMD’s Chief-Scientist Dr Boominathan had published on 3rd September 2014 that “Vitamin-based therapy for DM: ATRA (a derivative of Vitamin-A) increases the expression of a positive regulator of insulin transcription, NeuroD1 via down regulation of its target gene. Furthermore, he suggested, for the first time, that: ATRA, by increasing the expression of its target gene, it may decrease the expression of a number of stress responsive proteins. Thereby, it may increase the expression of an activator of insulin transcription, NeuroD1. Given this, physicians may consider prescribing ATRA to treat DM [http://genomediscovery.org/insights-into-the-treatment-of-stress-induced-t2d-atra-a-derivative-of-vitamin-a-increases-the-expression-of-a-positive-regulator-of-insulin-transcription-neurod1-via-down-regulation-of-its-target/].” In support of the findings published by Dr Boominathan, Prof. Lorraine J. Gudas, Steven E. Trasino and others (from Weill Cornell Medical College, United States; & McMaster University, Canada) have published a paper in the journal Journal of Biological chemistry, on December 1, 2014, stating that Vitamin A Deficiency Causes Hyperglycemia and Loss of Pancreatic β-Cell Mass. However, it is important to understand that this research paper was published nearly three months (Dec 1, 2014) later from the date of publication made by Dr L Boominathan, suggesting that Dr L Boominathan’s/GBMD’s therapeutic mind/idea matches with the best in the world.
- Tenth, GBMD’s Chief-Scientist Dr Boominathan had published on 6th June ’13 that “p63/p73/p53 regulates the expression of telomere-associated protein TRF2 through its target miRNAs (http://genomediscovery.org/p63p73p53-regulates-telomere-associated-protein-trf2-through-its-target-mirnas-6june2013-15-40/).” In support of the finding published by Dr Boominathan, Prof. Songyang Z, Dr. Luo Z and others (from Key Laboratory of Gene Engineering of the Ministry of Education, Key Laboratory of Reproductive Medicine of Guangdong Province, School of Life Sciences and the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510275, China) have published a paper in the journal Aging Cell (the no.1 journal in aging), on 6th March, 2015, stating that Mir-23a induces telomere dysfunction and cellular senescence by inhibiting TRF2 expression. It is important to remember that Mir-23a is a transcriptional target of p53/p63/p73. Further, it is important to understand that this research paper was published nearly nine months (March 6, 2015) later from the date of publication made by Dr L Boominathan, suggesting that Dr L Boominathan’s/GBMD’s therapeutic mind/idea matches with the best in the world.
- Eleventh, GBMD’s Chief-Scientist Dr Boominathan had published on 8th September ’13 that “BRCA1 suppresses Sirtuin 1 expression through its target gene, 8/September/2013, 7.12 am (http://genomediscovery.org/brca1-suppresses-sirtuin-1-expression-through-its-target-gene-8september2013-7-12-am/).” In line with the finding published by Dr Boominathan, Prof. Yang Q, Dr. Li and others (from Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China) have published a paper in the journal “Scientific Reports”, on 17th October, 2014, stating that “A novel crosstalk between BRCA1 and sirtuin 1 in ovarian cancer.” It is important to understand that this research paper was published in “Scientific Reports” nearly thirteen months later from the date of publication made by Dr L Boominathan, suggesting that Dr L Boominathan’s/GBMD’s scientific mind/idea matches with the best in the world.
- For the viewer’s kind information, less than 10% of Professors in the United States of America (USA) publish three Nature papers in a career spanning for about forty years. Furthermore, less than 0.1% of Professors in India publish a paper in Nature in a career spanning for about 35 years. A scientific report in the number one Journal Nature will get a permanent faculty position in abroad and in any of the best research institutes/universities in India, including All India Institute of Medical Sciences (AIIMS), Indian Institute of Science (IISc), National Center for Biological Sciences (NCBS), Central for Cellular and Molecular Biology (CCMB), Tata Institute of Fundamental research (TIFR), Indian Institute of Technologies (IITs) etc. Unfortunately, Dr Boominathan has lost the credit and recognition for three Nature papers in a span of one-and-half-a-years itself. Not only this, but on numerous occasions—what is quoted above with evidences gives only the glimpse of Dr Boominathan’s scientific caliber—Dr Boominathan had the idea (for the research findings published in high impact journals in biological/medical sciences), but did not get a chance to publish it. Needless to mention, Dr Boominathan’s scientific mind matches with the best of the best scientists/researchers/faculties–at Harvard University, Massachusetts Institute of Technology (MIT),Yale, Stanford, Caltech etc., (USA); Cambridge, Oxford, Imperial etc., ( UK)— in the world.
- Having realized his talent as a front line researcher/scientist, Dr Boominathan has started a drug discovery center and an educational institute namely GBMD and B-MERIIT, respectively. The GBMD aims to provide bio-medical/pharma/therapeutic/clinical ideas to scientists; and to develop miRNA therapeutics, while B-MERIIT aims to offer innovative educational programs.
- GBMD Chief Scientist Dr Boominathan PhD., had posted 7,000+ Bio-medical/pharma/therapeutic/clinical ideas (as of March, 2015) in the website http://genomediscovery.org/category/ideas/ with the noble intention to (i) serve science relentlessly; and (ii) take the science forward at the faster rate so that patients who suffer from diseases can be cured faster. Dr Boominathan was the first one in the world to provide an innovative research solution to ongoing research in the field of Biology/p53/p63/p73/cancer biology/Bio-Medicine. Considering that every idea proposed is based on scientific evidence/logic/literature, each of them will become a research manuscript in the coming years. Besides, some of the ideas posted provide guidelines for a new direction of research. If every scientist, who views the idea, sites Dr Boominathan’s contribution towards the idea, then he will become one of the most prolific Scientist recognized throughout the world. Placing high hope on the integrity of scientists/faculty members/researchers, who view the ideas for no cost, there is a good chance that this could indeed be true. This selfless effort is indeed appreciated by scientists/researchers/faculties, who visit Dr Boominathan company’s website regularly, from more than ninety eight nations.
- Dr L Boominathan had followed the works of Noble laureates (Profs. Schekman Randy, Sudhof C Thomas, Shinya Yamanaka, Gurdon JB, Phil Sharp, David Baltimore, Elizabeth H. Blackburn, Carol W Greider, Beutler A Bruce, Ferid & Varmus H) and posted numerous ideas related to their work (>180 ideas, as of March, 2015; http://genomediscovery.org/ideas/nobel-laureates-work-tracked-by-gbmd/).
- Dr Boominathan has served as a faculty member in Pondicherry Central university, India. He had earlier been invited to attend the interview (Feb, 2012) for an Associate Professor position (Interview letter for Associate Professor position from Pondicherry Central University.jpg). Dr Boominathan is eligible to be considered for a Professor position, as per University Grants Commission (UGC) regulations. The UGC regulation (2011) states that faculty members who obtain an “academic performance indicator” score of 300 and 400 are eligible to be considered for Associate Professor and Professor positions, respectively. Dr Boominathan has an impressive score of 900 above. Besides, Dr Boominathan is eligible to be considered for Professorship as an outstanding Professional. Given that Dr L Boominathan has posted/published 7,000+ Bio-medical/pharma/therapeutic/clinical ideas (as of February, 2015), a credit shared by no other bio-scientist/Professor in the world, this should not be surprising.