ORCID Profile
0000-0002-3736-8621
Current Organisation
All India Institute of Medical Sciences
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Publisher: Springer Science and Business Media LLC
Date: 22-06-2020
DOI: 10.1038/S43018-020-0080-0
Abstract: Cancer cells adapt their metabolic activities to support growth and proliferation. However, increased activity of metabolic enzymes is not usually considered an initiating event in the malignant process. Here, we investigate the possible role of the enzyme serine hydroxymethyltransferase-2 (SHMT2) in lymphoma initiation.
Publisher: American Association for the Advancement of Science (AAAS)
Date: 19-06-2091
DOI: 10.1126/SCITRANSLMED.AAV5599
Abstract: Frequently observed DNA copy number gains of TCF4 in ABC-like DLBCL promote immunoglobulin expression and are targetable by BET inhibition.
Publisher: Springer Science and Business Media LLC
Date: 05-10-2020
Publisher: American Association for Cancer Research (AACR)
Date: 03-2020
DOI: 10.1158/2159-8290.CD-19-0116
Abstract: We have leveraged the molecular characterization of different types of CREBBP mutations to define a rational approach for targeting these mutations through selective inhibition of HDAC3. This represents an attractive therapeutic avenue for targeting synthetic vulnerabilities in CREBBP-mutant cells in tandem with promoting antitumor immunity. This article is highlighted in the In This Issue feature, p. 327
Publisher: Elsevier BV
Date: 06-2019
Publisher: Cold Spring Harbor Laboratory
Date: 19-06-2019
DOI: 10.1101/674259
Abstract: B-cell non-Hodgkin’s lymphoma (B-NHL) encompasses multiple clinically and phenotypically distinct subtypes of malignancy with unique molecular etiologies. Common subtypes of B-NHL such as diffuse large B-cell lymphoma (DLBCL) have been comprehensively interrogated at the genomic level. But rarer subtypes such as mantle cell lymphoma (MCL) remain sparsely characterized. Furthermore, multiple B-NHL subtypes have thus far not been comprehensively compared using the same methodology to identify conserved or subtype-specific patterns of genomic alterations. Here, we employed a large targeted hybrid-capture sequencing approach encompassing 380 genes to interrogate the genomic landscapes of 685 B-NHL tumors at high depth including DLBCL, MCL, follicular lymphoma (FL), and Burkitt lymphoma (BL). We identified conserved hallmarks of B-NHL that were deregulated in the majority of tumor from each subtype, including the frequent genetic deregulation of the ubiquitin proteasome system (UPS). In addition, we identified subtype-specific patterns of genetic alterations, including clusters of co-occurring mutations and DNA copy number alterations. The cumulative burden of mutations within a single cluster were more discriminatory of B-NHL subtypes than in idual mutations, implicating likely patterns of genetic cooperation that contribute to disease etiology. We therefore provide the first cross-sectional analysis of mutations and DNA copy number alterations across major B-NHL subtypes and a framework of co-occurring genetic alterations that deregulate genetic hallmarks and likely cooperate in lymphomagenesis.
Location: United States of America
Location: No location found
No related grants have been discovered for NEERAJ JAIN.