Search Results - "CHU, Gerald C"
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Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer
Published in Cell (03-07-2014)“…Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal…”
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Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism
Published in Nature communications (03-07-2017)“…Pancreatic ductal adenocarcinoma is a notoriously difficult-to-treat cancer and patients are in need of novel therapies. We have shown previously that these…”
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Oncogenic Kras Maintains Pancreatic Tumors through Regulation of Anabolic Glucose Metabolism
Published in Cell (27-04-2012)“…Tumor maintenance relies on continued activity of driver oncogenes, although their rate-limiting role is highly context dependent. Oncogenic Kras mutation is…”
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4
Oncogenic Kras drives invasion and maintains metastases in colorectal cancer
Published in Genes & development (15-02-2017)“…Human colorectal cancer (CRC) is a major cause of cancer mortality and frequently harbors activating mutations in the gene. To understand the role of oncogenic…”
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5
Telomerase Reactivation following Telomere Dysfunction Yields Murine Prostate Tumors with Bone Metastases
Published in Cell (02-03-2012)“…To determine the role of telomere dysfunction and telomerase reactivation in generating pro-oncogenic genomic events and in carcinoma progression, an inducible…”
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Animal Models of Human Prostate Cancer: The Consensus Report of the New York Meeting of the Mouse Models of Human Cancers Consortium Prostate Pathology Committee
Published in Cancer research (Chicago, Ill.) (01-05-2013)“…Animal models, particularly mouse models, play a central role in the study of the etiology, prevention, and treatment of human prostate cancer. While tissue…”
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GLI1 is regulated through Smoothened-independent mechanisms in neoplastic pancreatic ducts and mediates PDAC cell survival and transformation
Published in Genes & development (01-01-2009)“…Pancreatic ductal adenocarcinoma (PDAC) is characterized by the deregulation of the hedgehog signaling pathway. The Sonic Hedgehog ligand (Shh), absent in the…”
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8
p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation
Published in Nature (23-10-2008)“…Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM…”
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Stromal biology of pancreatic cancer
Published in Journal of cellular biochemistry (01-07-2007)“…The genetic paradigm of cancer, focused largely on sequential molecular aberrations and associated biological impact in the neoplastic cell compartment of…”
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10
Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer
Published in Genes & development (15-11-2006)“…SMAD4 is inactivated in the majority of pancreatic ductal adenocarcinomas (PDAC) with concurrent mutational inactivation of the INK4A/ARF tumor suppressor…”
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11
Context-Dependent Transformation of Adult Pancreatic Cells by Oncogenic K-Ras
Published in Cancer cell (06-11-2009)“…Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies. To investigate the cellular origin(s) of this cancer, we determined the…”
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Proinvasion Metastasis Drivers in Early-Stage Melanoma Are Oncogenes
Published in Cancer cell (12-07-2011)“…Clinical and genomic evidence suggests that the metastatic potential of a primary tumor may be dictated by prometastatic events that have additional oncogenic…”
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13
Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma
Published in Proceedings of the National Academy of Sciences - PNAS (06-12-2011)“…Preclinical trials in mice represent a critical step in the evaluation of experimental therapeutics. Genetically engineered mouse models (GEMMs) represent a…”
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14
Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation
Published in Proceedings of the National Academy of Sciences - PNAS (18-03-2008)“…The Sin3-histone deacetylase (HDAC) corepressor complex is conserved from yeast to humans. Mammals possess two highly related Sin3 proteins, mSin3A and mSin3B,…”
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Mutant N-RAS protects colorectal cancer cells from stress-induced apoptosis and contributes to cancer development and progression
Published in Cancer discovery (01-03-2013)“…N-RAS is one member of a family of oncoproteins that are commonly mutated in cancer. Activating mutations in NRAS occur in a subset of colorectal cancers, but…”
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16
Genomic alterations link Rho family of GTPases to the highly invasive phenotype of pancreas cancer
Published in Proceedings of the National Academy of Sciences - PNAS (09-12-2008)“…Pancreas ductal adenocarcinoma (PDAC) is a highly lethal cancer that typically presents as advanced, unresectable disease. This invasive tendency, coupled with…”
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Feedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development
Published in Cancer cell (01-04-2008)“…We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM),…”
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Ott1 (Rbm15) Is Essential for Placental Vascular Branching Morphogenesis and Embryonic Development of the Heart and Spleen
Published in Molecular and Cellular Biology (01-01-2009)“…Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley…”
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Autophagy is critical for pancreatic tumor growth and progression in tumors with p53 alterations
Published in Cancer discovery (01-08-2014)“…Pancreatic ductal adenocarcinoma is refractory to available therapies. We have previously shown that these tumors have elevated autophagy and that inhibition…”
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Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma
Published in Nature medicine (01-10-2012)“…NRAS-driven melanomas have limited therapeutic options. Combining genetically engineered models and oncogenic signaling inhibitors with rational…”
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