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Meyerson, Matthew

https://orcid.org/0000-0002-9133-8108

Mayo Clinic

Broad Institute

Citations 4

TP63 Fusions Drive Enhancer Rewiring, Lymphomagenesis, and Dependence on EZH2
Wu, Gongwei , Liu, Jihe , Heavican‐Foral, Tayla B. , Yang, Lu, Chen, Renee , Jones, M. , Xu, Ran , Jain, Salvia , Leahy, Catharine, Jones, Kristen L. , Stevenson, Kristen E. , Wu, Wenchao, Louissaint, Abner , Debaize, Lydie , Chan, Wing C. , Sui, Shannan Ho, Ng, Samuel Y., Chen, chun-Wei David, Weinstock, David M. , Jones, Marcus K , Yoshida, Noriaki , Zhang, Xiaoyang , Heavican, Tayla B., Liu, Huiyun , Nelson, Geoffrey M. , Nirmal, Ajit J , Feldman, Andrew L. , Meyerson, Matthew , Adelman, Karen , Brown, Myles

Blood | November 28, 2022 | Volume: 140 | Issue: Supplement 1 | Pages: 1696-1697

10.1182/blood-2022-163368 Get It

Genomic aberrations in cervical adenocarcinomas in Hong Kong Chinese women
Chung, Tony K.H. , Hummelen, Paul Van , Chan, Paul K.S. , Cheung, Tak Hong , Yim, So Fan, Yu, Mei , MacConaill, Laura E. , Doran, Graeme, Pedamallu, Chandra Sekhar , Ojesina, Akinyemi I. , Wong, Raymond R.Y., Wang, Vivian W., Freeman, Samuel S. , Lau, Tat‐San , Kwong, Joseph , Chan, Loucia Kit Ying , May, Taymaa , Esselen, Katharine M. , Elias, Kevin M. , Smith, David I., Crum, Christopher P. , Meyerson, Matthew , Berkowitz, Ross S. , Wong, Yick Fu, Ducar, Matthew D. , Thorner, Aaron R. , Fromer, Menachem , Worley, Michael J. , Lawrence, Michael S. , Getz, Gad , Smith, David I., Elias, Kevin M

International Journal of Cancer | January 28, 2015 | Volume: 137 | Issue: 4 | Pages: 776-783

10.1002/ijc.29456 Get It

Summary Statement: Novel Agents in the Treatment of Lung Cancer: Advances in Epidermal Growth Factor Receptor-Targeted Agents
Lynch, Thomas J. , Adjei, Alex A. , Bunn, Paul A. , Engelman, Jeffrey A. , Haber, Daniel A. , Heymach, John V. , Jänne, Pasi A. , Johnson, Bruce E. , Johnson, David H. , Lilenbaum, Rogério, Sandler, Alan B., Sequist, Lecia V. , Settleman, Jeffrey , Wong, Kwok‐Kin , Hart, Carol S. , Eisen, Tim G , Goss, Glenwood D. , Meyerson, Matthew , Heymach, John V

Clinical Cancer Research | July 20, 2006 | Volume: 12 | Issue: 14 | Pages: 4365s-4371s

10.1158/1078-0432.ccr-06-1005 Get It

Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors
Milne, Thomas A. , Hughes, Christina M., Lloyd, Ricardo V., Rozenblatt–Rosen, Orit , Schnepp, Robert W. , Krankel, Cynthia, LiVolsi, Virginia A. , Gibbs, Denise , Hua, Xianxin , Hess, Jay L. , Yang, Zhaohai , Dou, Yali , Roeder, Robert G. , Meyerson, Matthew

Proceedings of the National Academy of Sciences | January 7, 2005 | Volume: 102 | Issue: 3 | Pages: 749-754

10.1073/pnas.0408836102 Get It

Mutations in the MEN1 gene are associated with the multiple endocrine neoplasia syndrome type 1 (MEN1), which is characterized by parathyroid hyperplasia and tumors of the pituitary and pancreatic islets. The mechanism by which MEN1 acts as a tumor suppressor is unclear. We have recently shown that menin, the MEN1 protein product, interacts with mixed lineage leukemia (MLL) family proteins in a histone methyltransferase complex including Ash2, Rbbp5, and WDR5. Here, we show that menin directly regulates expression of the cyclin-dependent kinase inhibitors p27 Kip1 and p18 Ink4c . Menin activates transcription by means of a mechanism involving recruitment of MLL to the p27 Kip1 and p18 Ink4c promoters and coding regions. Loss of function of either MLL or menin results in down-regulation of p27 Kip1 and p18 Ink4c expression and deregulated cell growth. These findings suggest that regulation of cyclin-dependent kinase inhibitor transcription by cooperative interaction between menin and MLL plays a central role in menin's activity as a tumor suppressor.