Jacqueline A. Lees

Affiliations: 
Biology Massachusetts Institute of Technology, Cambridge, MA, United States 
Area:
tumorigenicity
Website:
https://ki.mit.edu/people/faculty/lees
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"Jacqueline A. Lees"

Children

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Jeffrey Trimarchi grad student (Neurotree)
Ken Moberg grad student 1998 MIT
Christopher L. Sansam post-doc MIT (Neurotree)
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Publications

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Wilson MM, Weinberg RA, Lees JA, et al. (2020) Emerging Mechanisms by which EMT Programs Control Stemness. Trends in Cancer
Sharma S, Zhang T, Michowski W, et al. (2020) Targeting the cyclin-dependent kinase 5 in metastatic melanoma. Proceedings of the National Academy of Sciences of the United States of America
Dalin S, Sullivan MR, Lau AN, et al. (2019) Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance. Cancer Research
Ning JF, Stanciu M, Humphrey MR, et al. (2019) Myc targeted CDK18 promotes ATR and homologous recombination to mediate PARP inhibitor resistance in glioblastoma. Nature Communications. 10: 2910
Parisi T, Balsamo M, Gertler F, et al. (2018) The Rb tumor suppressor regulates epithelial cell migration and polarity. Molecular Carcinogenesis
Perez DE, Henle AM, Amsterdam A, et al. (2018) Uveal melanoma driver mutations in GNAQ/11 yield numerous changes in melanocyte biology. Pigment Cell & Melanoma Research
Roper J, Tammela T, Cetinbas NM, et al. (2018) Abstract B38: In vivo genome editing and organoid transplantation models of colorectal cancer and metastasis Cancer Research. 78
Guen VJ, Chavarria TE, Kröger C, et al. (2017) EMT programs promote basal mammary stem cell and tumor-initiating cell stemness by inducing primary ciliogenesis and Hedgehog signaling. Proceedings of the National Academy of Sciences of the United States of America
Guen VJ, Edvardson S, Fraenkel ND, et al. (2017) A homozygous deleterious CDK10 mutation in a patient with agenesis of corpus callosum, retinopathy, and deafness. American Journal of Medical Genetics. Part A
Braun CJ, Stanciu M, Boutz PL, et al. (2017) Coordinated Splicing of Regulatory Detained Introns within Oncogenic Transcripts Creates an Exploitable Vulnerability in Malignant Glioma. Cancer Cell
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