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Sarmila Majumder

Researcher at Ohio State University

Publications -  60
Citations -  5210

Sarmila Majumder is an academic researcher from Ohio State University. The author has contributed to research in topics: DNA methylation & Methyltransferase. The author has an hindex of 35, co-authored 55 publications receiving 4879 citations. Previous affiliations of Sarmila Majumder include McGill University & Florida State University College of Arts and Sciences.

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MicroRNA-221/222 Confers Tamoxifen Resistance in Breast Cancer by Targeting p27Kip1

TL;DR: This is the first study demonstrating a relationship between miR-221/222 expression and HER2/neu overexpression in primary breast tumors that are generally resistant to tamoxifen therapy, and provides the rationale for the application of altered expression of specific miRNAs as a predictive tamoxIFen-resistant breast cancer marker.
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Methylation mediated silencing of MicroRNA-1 gene and its role in hepatocellular carcinogenesis.

TL;DR: Up-regulation of several miR-1 targets including FoxP1, MET, and HDAC4 in primary human HCCs and down- regulation of their expression in 5-AzaC-treated HCC cells suggest their role in hepatocarcinogenesis.
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5-Aza-Deoxycytidine Induces Selective Degradation of DNA Methyltransferase 1 by a Proteasomal Pathway That Requires the KEN Box, Bromo-Adjacent Homology Domain, and Nuclear Localization Signal

TL;DR: Results demonstrate a unique mechanism for the selective degradation of DNMT1, the maintenance DNA methyltransferase, by well-known DNA-hypomethylating agents and indicate that covalent bond formation between the enzyme and 5-aza-CdR-incorporated DNA is not essential for enzyme degradation.
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Down-regulation of Micro-RNA-1 (miR-1) in Lung Cancer SUPPRESSION OF TUMORIGENIC PROPERTY OF LUNG CANCER CELLS AND THEIR SENSITIZATION TO DOXORUBICIN-INDUCED APOPTOSIS BY miR-1

TL;DR: It is reported that micro-RNA-1 (miR-1), abundant in the cardiac and smooth muscles, is expressed in the lung and is down-regulated in human primary lung cancer tissues and cell lines and has potential therapeutic application against lung cancers.
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TGFβ mediated upregulation of hepatic miR-181b promotes hepatocarcinogenesis by targeting TIMP3

TL;DR: Upregulation of miR-181b at early stages of feeding CDAA diet promotes hepatocarcinogenesis and enhanced resistance of HCC cells to the anticancer drug doxorubicin.