L
Lynda Chin
Researcher at University of Texas MD Anderson Cancer Center
Publications - 127
Citations - 49829
Lynda Chin is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Melanoma & Cancer. The author has an hindex of 64, co-authored 126 publications receiving 40137 citations. Previous affiliations of Lynda Chin include Massachusetts Institute of Technology & Heidelberg University.
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Journal ArticleDOI
Absence of biallelic TCRγ deletion predicts early treatment failure in pediatric T-cell acute lymphoblastic leukemia
Alejandro Gutierrez,Suzanne E. Dahlberg,Donna Neuberg,Jianhua Zhang,Ruta Grebliunaite,Takaomi Sanda,Alexei Protopopov,Valeria Tosello,Jeffery L. Kutok,Richard S. Larson,Michael J. Borowitz,Mignon L. Loh,Adolfo A. Ferrando,Stuart S. Winter,Charles G. Mullighan,Lewis B. Silverman,Lynda Chin,Stephen P. Hunger,Stephen E. Sallan,A. Thomas Look +19 more
TL;DR: Lymphoblasts from children with T-ALL should be evaluated at diagnosis for deletion within the TCRgamma locus, and patients lacking biallelic deletion should be assigned to alternative therapy in the context of a prospective clinical trial.
Journal ArticleDOI
Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome
Simona Colla,Derrick Sek Tong Ong,Yamini Ogoti,Matteo Marchesini,Nipun A. Mistry,Karen Clise-Dwyer,Sonny Ang,Paola Storti,Paola Storti,Andrea Viale,Nicola Giuliani,Kathryn Ruisaard,Irene Ganan Gomez,Christopher A. Bristow,Marcos R. Estecio,David C. Weksberg,Yan Wing Ho,Baoli Hu,Giannicola Genovese,Piergiorgio Pettazzoni,Asha S. Multani,Shan Jiang,Sujun Hua,Michael Ryan,Alessandro Carugo,Luigi Nezi,Yue Wei,Hui Yang,Marianna D'Anca,Li Zhang,Sarah Gaddis,Ting Gong,James W. Horner,Timothy P. Heffernan,Philip Jones,Laurence J.N. Cooper,Han Liang,Hagop M. Kantarjian,Y. Alan Wang,Lynda Chin,Carlos Bueso-Ramos,Guillermo Garcia-Manero,Ronald A. DePinho +42 more
TL;DR: The genetic evidence that telomere dysfunction-induced DNA damage drives classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing the expression of mRNA splicing/processing genes, including SRSF2 is provided.
Journal ArticleDOI
Erratum: The somatic genomic landscape of glioblastoma (Cell (2013) 155 (462-477))
Cameron Brennan,Roel G.W. Verhaak,Aaron McKenna,Benito Campos,Houtan Noushmehr,Sofie R. Salama,Siyuan Zheng,Debyani Chakravarty,J. Zachary Sanborn,Samuel H. Berman,Rameen Beroukhim,Brady Bernard,Chang-Jiun Wu,Giannicola Genovese,Ilya Shmulevich,Jill S. Barnholtz-Sloan,Lihua Zou,Rahulsimham Vegesna,Sachet A. Shukla,Giovanni Ciriello,W. K. Yung,Wei Zhang,Carrie Sougnez,Tom Mikkelsen,Kenneth Aldape,Darell D. Bigner,Erwin G. Van Meir,Michael D. Prados,Andrew E. Sloan,Keith L. Black,Jennifer M. Eschbacher,Gaetano Finocchiaro,William A. Friedman,David W. Andrews,Abhijit Guha,Mary Iacocca,Brian P. O'Neill,Greg Foltz,Jerome Myers,Daniel J. Weisenberger,Robert Penny,Raju Kucherlapati,Charles M. Perou,D. Neil Hayes,Richard A. Gibbs,Marco A. Marra,Gordon B. Mills,Eric S. Lander,Paul T. Spellman,Rick K. Wilson,Chris Sander,John N. Weinstein,Matthew Meyerson,Stacey Gabriel,Peter W. Laird,David Haussler,Gad Getz,Lynda Chin +57 more
Journal ArticleDOI
Signaling From the Golgi: Mechanisms and Models for Golgi Phosphoprotein 3–Mediated Oncogenesis
Kenneth L. Scott,Lynda Chin +1 more
TL;DR: The fact that GOLPH3 has been implicated in protein trafficking, receptor recycling, and glycosylation points to potential links of these cellular processes to tumorigenesis, and how these processes may be deregulated and contribute to cancer pathogenesis and drug response will uncover new avenues for therapeutic intervention.
Journal ArticleDOI
Systematic Epigenomic Analysis Reveals Chromatin States Associated with Melanoma Progression
Petko Fiziev,Kadir C. Akdemir,John P. Miller,Emily Z. Keung,Neha S. Samant,Sneha Sharma,Christopher A. Natale,Christopher Terranova,Mayinuer Maitituoheti,Samirkumar B. Amin,Samirkumar B. Amin,Emmanuel Martinez-Ledesma,Mayura Dhamdhere,Jacob B. Axelrad,Amiksha Shah,Christine S. Cheng,Christine S. Cheng,Harshad S. Mahadeshwar,Sahil Seth,Michelle Craig Barton,Alexei Protopopov,Kenneth Y. Tsai,Michael A. Davies,Benjamin A. Garcia,Ido Amit,Lynda Chin,Lynda Chin,Jason Ernst,Kunal Rai +28 more
TL;DR: Restoration of acetylation levels on deacetylated loci by histone de acetylase (HDAC) inhibitors selectively blocked excessive proliferation in tumorigenic cells and human melanoma cells, suggesting functional roles of observed chromatin state transitions in driving hyperproliferative phenotype.