Full Text Journal Articles by
Author Sharmistha Sarkar

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Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma.

Mayinuer Maitituoheti, Emily Z Keung, Ming Tang, Liang Yan, Hunain Alam, Guangchun Han, Anand K Singh, Ayush T Raman, Christopher Terranova, Sharmistha Sarkar, Elias Orouji, Samir B Amin, Sneha Sharma, Maura Williams, Neha S Samant, Mayura Dhamdhere, Norman Zheng, Tara Shah, Amiksha Shah, Jacob B Axelrad, Nazanin E Anvar, Yu-Hsi Lin, Shan Jiang, Edward Q Chang, Davis R Ingram, Wei-Lien Wang, Alexander Lazar, Min Gyu Lee, Florian Muller, Linghua Wang, Haoqiang Ying, Kunal Rai,

Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma. Here, we identify KMT2D as a potent tumor suppressor in melanoma through an in vivo epigenome-focused pooled RNAi screen and confirm the finding by using a genetically engineered mouse model (GEMM) based on conditional and melanocyte-specific ... Read more >>

Cell Rep (Cell reports)
[2020, 33(3):108293]

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Telomere dysfunction activates YAP1 to drive tissue inflammation.

Deepavali Chakravarti, Baoli Hu, Xizeng Mao, Asif Rashid, Jiexi Li, Jun Li, Wen-Ting Liao, Elizabeth M Whitley, Prasenjit Dey, Pingping Hou, Kyle A LaBella, Andrew Chang, Guocan Wang, Denise J Spring, Pingna Deng, Di Zhao, Xin Liang, Zhengdao Lan, Yiyun Lin, Sharmistha Sarkar, Christopher Terranova, Yonathan Lissanu Deribe, Sarah E Blutt, Pablo Okhuysen, Jianhua Zhang, Eduardo Vilar, Ole Haagen Nielsen, Andrew Dupont, Mamoun Younes, Kalyani R Patel, Noah F Shroyer, Kunal Rai, Mary K Estes, Y Alan Wang, Alison A Bertuch, Ronald A DePinho,

Germline telomere maintenance defects are associated with an increased incidence of inflammatory diseases in humans, yet whether and how telomere dysfunction causes inflammation are not known. Here, we show that telomere dysfunction drives pATM/c-ABL-mediated activation of the YAP1 transcription factor, up-regulating the major pro-inflammatory factor, pro-IL-18. The colonic microbiome stimulates ... Read more >>

Nat Commun (Nature communications)
[2020, 11(1):4766]

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Bivalent and Broad Chromatin Domains Regulate Pro-metastatic Drivers in Melanoma

Christopher Terranova, Ming Tang, Mayinuer Maitituoheti, Ayush Raman, Jonathan Schulz, Samir Amin, Elias Orouji, Katarzyna Tomczak, Sharmistha Sarkar, Junna Oba, Caitlin Creasy, Chang-Jiun Wu, Dongyu Zhao, Kaifu Chen, Lauren Haydu, Wei-Lien Wang, Alexander Lazar, Scott Woodman, Chantale Bernatchez, Kunal Rai,

ABSTRACT Chromatin deregulation is an emerging hallmark of cancer. However, the extent of epigenetic aberrations during tumorigenesis and their relationship with genetic aberrations are poorly understood. Using ChIP-sequencing for enhancers (H3K27ac and H3K4me1), promoters (H3K4me3), active transcription (H3K79me2) and polycomb (H3K27me3) or heterochromatin (H3K9me3) repression we generated chromatin state profiles ... Read more >>

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Enhancer Reprogramming Confers Dependence on Glycolysis and IGF signaling in KMT2D Mutant Melanoma

Mayinuer Maitituoheti, Emily Keung, Ming Tang, Liang Yan, Hunain Alam, Guangchun Han, Ayush Raman, Christopher Terranova, Sharmistha Sarkar, Elias Orouji, Samir Amin, Sneha Sharma, Maura Williams, Neha Samant, Mayura Dhamdhere, Norman Zheng, Tara Shah, Amiksha Shah, Jacob Axelrad, Nazanin Anvar, Yu-Hsi Lin, Shan Jiang, Edward Chang, Davis Ingram, Wei-Lien Wang, Alexander Lazar, Min Gyu Lee, Florian Muller, Linghua Wang, Haoqiang Ying, Kunal Rai,

SUMMARY Epigenetic modifiers have emerged as important regulators of tumor progression. We identified histone methyltransferase KMT2D as a potent tumor-suppressor through an in vivo epigenome-focused pooled RNAi screen in melanoma. KMT2D harbors frequent somatic point mutations in multiple tumor types. How these events contribute to tumorigenesis and whether they impart ... Read more >>

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PRKCI promotes immune suppression in ovarian cancer.

Sharmistha Sarkar, Christopher A Bristow, Prasenjit Dey, Kunal Rai, Ruth Perets, Alejandra Ramirez-Cardenas, Shruti Malasi, Emmet Huang-Hobbs, Monika Haemmerle, Sherry Y Wu, Michael McGuire, Alexei Protopopov, Shan Jiang, Joyce F Liu, Michelle S Hirsch, Qing Chang, Alexander J Lazar, Anil K Sood, Ronny Drapkin, Ronald DePinho, Giulio Draetta, Lynda Chin,

A key feature of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification of the 3q26 locus harboring PRKC-ι (PRKCI). Here, we show that PRKCI is also expressed in early fallopian tube lesions, called serous tubal intraepithelial carcinoma. Transgenic mouse studies establish PRKCI as an ovarian cancer-specific oncogene. Mechanistically, we show ... Read more >>

Genes Dev. (Genes & development)
[2017, 31(11):1109-1121]

Cited: 11 times

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DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC.

Kunal Rai, Sharmistha Sarkar, Talmage J Broadbent, Matthew Voas, Kenneth F Grossmann, Lincoln D Nadauld, Somaye Dehghanizadeh, Fanuel T Hagos, Yumei Li, Rachel K Toth, Stephanie Chidester, Timothy M Bahr, W Evan Johnson, Brad Sklow, Randall Burt, Bradley R Cairns, David A Jones,

Although genome-wide hypomethylation is a hallmark of many cancers, roles for active DNA demethylation during tumorigenesis are unknown. Here, loss of the APC tumor suppressor gene causes upregulation of a DNA demethylase system and the concomitant hypomethylation of key intestinal cell fating genes. Notably, this hypomethylation maintained zebrafish intestinal cells ... Read more >>

Cell (Cell)
[2010, 142(6):930-942]

Cited: 49 times

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A two-step model for colon adenoma initiation and progression caused by APC loss.

Reid A Phelps, Stephanie Chidester, Somaye Dehghanizadeh, Jason Phelps, Imelda T Sandoval, Kunal Rai, Talmage Broadbent, Sharmistha Sarkar, Randall W Burt, David A Jones,

Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation. Using zebrafish and human cells, we show that homozygous loss of APC causes failed intestinal cell differentiation but that this occurs in the absence of nuclear beta-catenin and increased intestinal ... Read more >>

Cell (Cell)
[2009, 137(4):623-634]

Cited: 165 times

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