Satavisha Roy

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.

TL;DR: It is concluded that PRMT5 is critical to EBV-driven B-cell transformation and maintenance of the malignant phenotype, and thatPRMT5 inhibition shows promise as a novel therapeutic approach for B- cell lymphomas.

TL;DR: It is shown that miR-221 and -222 are up-regulated in tamoxifen-resistant MCF-7 (OHTR) cells and Her2-positive human breast tumors when compared with Her2 negative tumors, and corresponding anti-miRs can be used to render these tumors responsive to tamoxIFen.

TL;DR: A specific miR signature for the tamoxifen- resistant breast cancer and an important cell cycle inhibitor target of the altered miR, which could be used as a prognostic marker for the drug-resistant breast cancer.

TL;DR: A key role is suggested of PRMT5 and the two methylated histones in regulating rRNA promoter activity in Epstein Barr virus‐ transformed primary B‐cells and HeLa cells responding to serum‐regulated growth.