We’re especially interested in determining what roles microRNAs and ncRNAs play in the genesis and development of human melanomas.
Dr. Perera investigates the molecular mechanisms by which non-coding RNA might affect melanoma and prostate cancer development in humans.
Dr. Perera received his Ph.D. in molecular genetics from Moscow State University, Russia, and was a postdoctoral fellow at MIT.
The functional characterization of long noncoding RNA SPRY4-IT1 in human melanoma cells.
Mazar J, Zhao W, Khalil AM, Lee B, Shelley J, Govindarajan SS, Yamamoto F, Ratnam M, Aftab MN, Collins S, Finck BN, Han X, Mattick JS, Dinger ME, Perera RJ
Oncotarget. 2014 Oct 15;5(19):8959-69
Long noncoding RNAs as putative biomarkers for prostate cancer detection.
Lee B, Mazar J, Aftab MN, Qi F, Shelley J, Li JL, Govindarajan S, Valerio F, Rivera I, Thurn T, Tran TA, Kameh D, Patel V, Perera RJ
J Mol Diagn. 2014 Nov;16(6):615-26
Genome-wide methylated CpG island profiles of melanoma cells reveal a melanoma coregulation network.
Li JL, Mazar J, Zhong C, Faulkner GJ, Govindarajan SS, Zhang Z, Dinger ME, Meredith G, Adams C, Zhang S, Mattick JS, Ray A, Perera RJ
Sci Rep. 2013;3:2962
The melanoma-upregulated long noncoding RNA SPRY4-IT1 modulates apoptosis and invasion.
Khaitan D, Dinger ME, Mazar J, Crawford J, Smith MA, Mattick JS, Perera RJ
Cancer Res. 2011 Jun 1;71(11):3852-62
The regulation of miRNA-211 expression and its role in melanoma cell invasiveness.
Mazar J, DeYoung K, Khaitan D, Meister E, Almodovar A, Goydos J, Ray A, Perera RJ
PLoS One. 2010;5(11):e13779
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Vascular smooth muscle LRP6 limits arteriosclerotic calcification in diabetic LDLR-/- mice by restraining noncanonical Wnt signals.
Cheng SL, Ramachandran B, Behrmann A, Shao JS, Mead M, Smith C, Krchma K, Bello Arredondo Y, Kovacs A, Kapoor K, Brill LM, Perera R, Williams BO, Towler DA
Circ Res. 2015 Jul 3;117(2):142-56
Ranjan Perera's Research Focus
Skin Cancer and Melanoma, Prostate Cancer
Prostate cancer and metastatic melanoma are both difficult cancers to detect early, and once detected late they are nearly always impossible to cure, causing mortality within three years despite surgery and conventional therapies. To find effective treatment it is imperative to understand the biology of these aggressive cancers. Our recent research has provided a novel direction in the biology of these cancers - that abnormal patterns of regulation of certain non-coding RNA (ncRNA) and microRNA genes determine aggressiveness of these cancers. Our genome-wide studies have found evidence for abnormal epigenetic processes, rather than direct gene mutations, that lead to such abnormal ncRNA/miRNA regulation. These findings support an unorthodox approach to investigating such cancers in that epigenetic rather than mutational processes might be the important underlying molecular mechanism behind these aggressive cancers. Therefore, novel therapeutic approaches might be in order. However, much more remains to be understood in this direction. Specifically, the genome-wide systems biology approaches to dissect the epigenetic processes that become abnormal when aggressive prostate cancer and melanoma initiates, rather than the reductionist "gene-by-gene" classical approaches, are urgently necessary. We have embarked upon a systems biology initiative to investigate the role of epigenetic regulation of ncRNA/miRNA expression in these cancers, and now propose to extend this initiative from the laboratory ultimately to the bedside of patients.
About Ranjan Perera
Ranjan Perera, Ph.D., most recently held faculty positions at Mercer University’s School of Medicine as an Associate Professor and Director of Genomics and R&D at Anderson Cancer Institute at Memorial Health Medical Center. Prior to his academic affiliations, he held positions at several major biotech and pharmaceutical companies, including ISIS Pharmaceuticals and Invitrogen Corporation. He received his Ph.D. in molecular genetics from Moscow State University, Russia and University of Gent, Belgium. He completed his postdoctoral studies in gene targeting and DNA recombination at Massachusetts Institute of Technology (MIT).