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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Mutant EGFR is required for maintenance of glioma growth in vivo, and its ablation leads to escape from receptor dependence
TL;DR: It is demonstrated that in vivo silencing of regulatable ΔEGFR with doxycycline attenuates glioma growth and that gliomas undergo selective pressure in vivo to employ alternative compensatory pathways to maintain aggressiveness in the event of EGFR silencing.
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Role of Epidermal Growth Factor Receptor Signaling in RAS-Driven Melanoma
Nabeel Bardeesy,Minjung Kim,Jin Xu,Ryung S. Kim,Qiong Shen,Marcus Bosenberg,Wing Hung Wong,Lynda Chin +7 more
TL;DR: This inducible tumor model system permits the identification and validation of alternative points of therapeutic intervention without neutralization of the primary genetic lesion, and genetic complementation and interference studies demonstrated that this signaling loop is essential to H-RASV12G-directed tumorigenesis.
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A Comparison of DNA Copy Number Profiling Platforms
Joel Greshock,Bin Feng,Cristina W. Nogueira,Elena Ivanova,Ilana Perna,Katherine L. Nathanson,Alexei Protopopov,Barbara L. Weber,Lynda Chin +8 more
TL;DR: A systematic comparison of five copy number profiling assays for their ability to detect 2-fold copy number gain and loss as well as focal high-amplitude CNAs concluded that the Agilent's 60-mer oligonucleotide microarray with probe design optimized for genomic hybridization offers the highest sensitivity and specificity, whereas Affymetrix's single nucleotide polymorphism microarray seems to offer better detection of CNAs in gene-poor regions.
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Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer
Beatrice Rondinelli,Beatrice Rondinelli,Dalia Rosano,Elena Antonini,Michela Frenquelli,Laura Montanini,Dachuan Huang,Simona Segalla,Kosuke Yoshihara,Samir B. Amin,Dejan Lazarevic,Roel G.W. Verhaak,P. Andrew Futreal,Luciano Di Croce,Lynda Chin,Davide Cittaro,Giovanni Tonon +16 more
TL;DR: The results shed light on a mechanism that underlies genomic instability in sporadic cancers and suggest that inactivation of JARID1C in renal cancer leads to heterochromatin disruption, genomic rearrangement, and aggressive ccRCCs.
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Dual Roles of RNF2 in Melanoma Progression
Kunal Rai,Kadir C. Akdemir,Lawrence N. Kwong,Petko Fiziev,Chang-Jiun Wu,Emily Z. Keung,Sneha Sharma,Neha S. Samant,Maura Williams,Jacob B. Axelrad,Amiksha Shah,Dong Yang,Elizabeth A. Grimm,Michelle Craig Barton,Denái R. Milton,Timothy P. Heffernan,James W. Horner,Suhendan Ekmekcioglu,Alexander J. Lazar,Jason Ernst,Lynda Chin +20 more
TL;DR: It is established that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms and oncogenic and prometastatic, and the notion that epigenetic regulators, such as R NF2, directly and functionally control powerful gene networks that are vital in multiple cancer processes is supported.