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1. Full Text Application of Cell-Free DNA Analysis to Cancer Treatment
by Corcoran, Ryan B and Chabner, Bruce A
Obstetrical & Gynecological Survey, ISSN 0029-7828, 04/2019, Volume 74, Issue 4, pp. 204 - 206
(Abstracted from N Engl J Med 2018;379(18):1754–1765)Tumor biopsies represent the standard for cancer diagnosis and the primary method for molecular testing to... 
Usage | Care and treatment | Biopsy | Genetic aspects | Nucleotide sequencing | Methods | DNA sequencing | Cancer
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2. Full Text Abstract SY10-01: Strategies to overcome resistance to MAPK inhibition
by Corcoran, Ryan B
Cancer Research, ISSN 0008-5472, 04/2013, Volume 73, Issue 8 Supplement, pp. SY10-01 - SY10-01
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3. Full Text Blood-Based Prediction of Tumor Relapse: The cfDNA Forecast
by Siravegna, Giulia and Corcoran, Ryan B
Cancer discovery, ISSN 2159-8274, 10/2018, Volume 8, Issue 10, pp. 1213 - 5
Khan and colleagues demonstrate how serial blood-based liquid biopsies integrated with imaging and mathematical modeling can accurately "forecast" the time to... 
EVOLUTION | THERAPY | ONCOLOGY | COLORECTAL-CANCER | DNA | ACQUIRED-RESISTANCE | LIQUID BIOPSIES | EGFR BLOCKADE
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4. Full Text Combined BRAF and MEK inhibition with dabrafenib and trametinib in BRAF V600-Mutant colorectal cancer
by Corcoran, Ryan B and Atreya, Chloe E and Falchook, Gerald S and Kwak, Eunice L and Ryan, David P and Bendell, Johanna C and Hamid, Omid and Messersmith, Wells A and Daud, Adil and Kurzrock, Razelle and Pierobon, Mariaelena and Sun, Peng and Cunningham, Elizabeth and Little, Shonda and Orford, Keith and Motwani, Monica and Bai, Yuchen and Patel, Kiran and Venook, Alan P and Kopetz, Scott
Journal of Clinical Oncology, ISSN 0732-183X, 12/2015, Volume 33, Issue 34, pp. 4023 - 4031
Purpose To evaluate dabrafenib, a selective BRAF inhibitor, combined with trametinib, a selective MEK inhibitor, in patients with BRAF V600-mutant metastatic... 
COLON-CANCER | MULTICENTER | GENE | ONCOLOGY | ADVANCED MELANOMA | MICROSATELLITE INSTABILITY | RAF | MUTATION | ACQUIRED-RESISTANCE | IMPROVED SURVIVAL | VEMURAFENIB | Microsatellite Instability | Prognosis | Follow-Up Studies | Colorectal Neoplasms - genetics | Humans | Middle Aged | Oximes - administration & dosage | Imidazoles - administration & dosage | Male | Pyridones - administration & dosage | Colorectal Neoplasms - drug therapy | Female | MAP Kinase Kinase 1 - antagonists & inhibitors | PTEN Phosphohydrolase - genetics | Mutation - genetics | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Biopsy | Proto-Oncogene Proteins B-raf - genetics | Mice | Pyrimidinones - administration & dosage | Colorectal Neoplasms - pathology | Neoplasm Staging | Cohort Studies | Index Medicus | Gic5 | ORIGINAL REPORTS | Gic7
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5. Full Text Expanded RAS: Refining the patient population
by Atreya, Chloe E and Corcoran, Ryan B and Kopetz, Scott
Journal of Clinical Oncology, ISSN 0732-183X, 03/2015, Volume 33, Issue 7, pp. 682 - 685
PANITUMUMAB | 1ST-LINE TREATMENT | CETUXIMAB | ONCOLOGY | PHASE-III | ACQUIRED-RESISTANCE | KRAS WILD-TYPE | MUTATIONS | FLUOROURACIL | METASTATIC COLORECTAL-CANCER | CHEMOTHERAPY | Leucovorin - administration & dosage | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Antineoplastic Combined Chemotherapy Protocols - administration & dosage | Humans | Antibodies, Monoclonal - therapeutic use | Membrane Proteins - analysis | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Bevacizumab | Polymerase Chain Reaction - methods | Organoplatinum Compounds - administration & dosage | Proto-Oncogene Proteins B-raf - analysis | Codon | Fluorouracil - administration & dosage | Antibodies, Monoclonal, Humanized - pharmacology | Proto-Oncogene Proteins - analysis | GTP Phosphohydrolases - analysis | Camptothecin - administration & dosage | Cetuximab | Molecular Targeted Therapy - methods | Camptothecin - analogs & derivatives | Antibodies, Monoclonal, Humanized - therapeutic use | Membrane Proteins - genetics | Antibodies, Monoclonal - pharmacology | Proto-Oncogene Proteins - genetics | ras Proteins - analysis | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | GTP Phosphohydrolases - genetics | Proto-Oncogene Proteins B-raf - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mutation | Index Medicus | To15 | Comments and Controversies | Gic5 | Gic7
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6. Full Text Abstract 3135: Pre-treatment p-EGFR levels in tumors from a genetically engineered mouse model of BRAFV600E colorectal cancer predict response to combined BRAF/EGFR inhibition
by Coffee, Erin M and Corcoran, Ryan B and Engelman, Jeffrey A
Cancer Research, ISSN 0008-5472, 10/2014, Volume 74, Issue 19 Supplement, pp. 3135 - 3135
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7. Full Text Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers
by Ebi, Hiromichi and Corcoran, Ryan B and Singh, Anurag and Chen, Zhao and Song, Youngchul and Lifshits, Eugene and Ryan, David P and Meyerhardt, Jeffrey A and Benes, Cyril and Settleman, Jeffrey and Wong, Kwok-Kin and Cantley, Lewis C and Engelman, Jeffrey A
Journal of Clinical Investigation, ISSN 0021-9738, 11/2011, Volume 121, Issue 11, pp. 4311 - 4321
Therapies inhibiting receptor tyrosine kinases (RTKs) are effective against some human cancers when they lead to simultaneous downregulation of PI3K/AKT and... 
CELL LUNG-CANCER | ANAPLASTIC LYMPHOMA KINASE | BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | GROWTH-FACTOR RECEPTOR | ONCOGENIC ACTIVATION | MUTATION STATUS | CYCLIN D1 | RAS | PHOSPHATIDYLINOSITOL 3-KINASE | ACQUIRED-RESISTANCE | Neoplasm Transplantation | RNA, Small Interfering - genetics | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Colorectal Neoplasms - genetics | Humans | Male | Transplantation, Heterologous | DNA Primers - genetics | Phosphatidylinositol 3-Kinases - metabolism | Gene Knockdown Techniques | MAP Kinase Signaling System | Base Sequence | Colorectal Neoplasms - drug therapy | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Colorectal Neoplasms - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | ras Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | Class I Phosphatidylinositol 3-Kinases | Mice, Nude | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Colorectal Neoplasms - pathology | Apoptosis | Tyrosine | Care and treatment | Gene mutations | Colorectal cancer | Cellular signal transduction | Genetic aspects | Research | Diagnosis | Properties | Genetic regulation | Identification and classification | Index Medicus | Abridged Index Medicus
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8. Full Text Resistance to checkpoint blockade therapy through inactivation of antigen presentation
by Sade-Feldman, Moshe and Jiao, Yunxin J and Chen, Jonathan H and Rooney, Michael S and Barzily-Rokni, Michal and Eliane, Jean-Pierre and Bjorgaard, Stacey L and Hammond, Marc R and Vitzthum, Hans and Blackmon, Shauna M and Frederick, Dennie T and Hazar-Rethinam, Mehlika and Nadres, Brandon A and Van Seventer, Emily E and Shukla, Sachet A and Yizhak, Keren and Ray, John P and Rosebrock, Daniel and Livitz, Dimitri and Adalsteinsson, Viktor and Getz, Gad and Duncan, Lyn M and Li, Bo and Corcoran, Ryan B and Lawrence, Donald P and Stemmer-Rachamimov, Anat and Boland, Genevieve M and Landau, Dan A and Flaherty, Keith T and Sullivan, Ryan J and Hacohen, Nir
Nature Communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 1136 - 11
Treatment with immune checkpoint blockade (CPB) therapies often leads to prolonged responses in patients with metastatic melanoma, but the common mechanisms of... 
PLATFORM | METASTATIC MELANOMA | CTLA-4 BLOCKADE | PEMBROLIZUMAB | GENOMICS | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | CANCER-IMMUNOTHERAPY | MUTATIONS | TUMORS | Humans | Mice, Inbred C57BL | Antibodies, Monoclonal - therapeutic use | Antigen Presentation - genetics | Melanoma - pathology | CTLA-4 Antigen - immunology | Loss of Heterozygosity | Mice, Knockout | Neoplasms, Experimental - pathology | Point Mutation | Drug Resistance, Neoplasm - genetics | Neoplasm Metastasis | Animals | Melanoma - genetics | Melanoma - drug therapy | Neoplasms, Experimental - genetics | Female | Antigen Presentation - drug effects | Programmed Cell Death 1 Receptor - immunology | Neoplasms, Experimental - drug therapy | Antibodies, Monoclonal - immunology | beta 2-Microglobulin - genetics | Drug Resistance, Neoplasm - drug effects | Antigen presentation | Deactivation | PD-1 protein | Melanoma | Metastasis | Inactivation | Patients | Metastases | Heterozygosity | CTLA-4 protein | Major histocompatibility complex | Immune checkpoint | Loss of heterozygosity | Mutation | Target acquisition | Index Medicus
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9. Integrating Biomarkers and Targeted Therapy Into Colorectal Cancer Management
by Lieu, Christopher H and Corcoran, Ryan B and Overman, Michael J
American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting, 01/2019, Volume 39, p. 207
There have been substantial advances in the treatment of metastatic colorectal cancer (mCRC) over the past 15 years. Molecular characteristics of mCRC and... 
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10. Full Text Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients
by Siravegna, Giulia and Mussolin, Benedetta and Buscarino, Michela and Corti, Giorgio and Cassingena, Andrea and Crisafulli, Giovanni and Ponzetti, Agostino and Cremolini, Chiara and Amatu, Alessio and Lauricella, Calogero and Lamba, Simona and Hobor, Sebastijan and Avallone, Antonio and Valtorta, Emanuele and Rospo, Giuseppe and Medico, Enzo and Motta, Valentina and Antoniotti, Carlotta and Tatangelo, Fabiana and Bellosillo, Beatriz and Veronese, Silvio and Budillon, Alfredo and Montagut, Clara and Racca, Patrizia and Marsoni, Silvia and Falcone, Alfredo and Corcoran, Ryan B and Di Nicolantonio, Federica and Loupakis, Fotios and Siena, Salvatore and Sartore-Bianchi, Andrea and Bardelli, Alberto
Nature Medicine, ISSN 1078-8956, 07/2015, Volume 21, Issue 7, pp. 795 - 801
Colorectal cancers (CRCs) evolve by a reiterative process of genetic diversification and clonal evolution. The molecular profile of CRC is routinely assessed... 
MEDICINE, RESEARCH & EXPERIMENTAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | SENSITIVE DETECTION | DRUG-RESISTANCE | NUCLEIC-ACIDS | CELL BIOLOGY | KRAS MUTATIONS | HETEROGENEITY | DROPLET DIGITAL PCR | MELANOMA | THERAPY | FREE TUMOR DNA | Antibodies - therapeutic use | Receptor, Epidermal Growth Factor - genetics | Receptor, Epidermal Growth Factor - immunology | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Colorectal Neoplasms - blood | Antibodies, Neoplasm - blood | Colorectal Neoplasms - genetics | Humans | Proto-Oncogene Proteins - genetics | Antineoplastic Agents - therapeutic use | Mutation - genetics | Antibodies - pharmacology | Drug Resistance, Neoplasm - genetics | DNA, Neoplasm - blood | Colorectal Neoplasms - drug therapy | Alleles | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Clone Cells | Colorectal Neoplasms - pathology | Clonal Evolution | Index Medicus
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11. Full Text Hedgehog Signal Transduction by Smoothened: Pharmacologic Evidence for a 2-Step Activation Process
by Rajat Rohatgi and Ljiljana Milenkovic and Ryan B. Corcoran and Matthew P. Scott
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2009, Volume 106, Issue 9, pp. 3196 - 3201
The Hedgehog (Hh) signaling pathway controls growth, cell fate decisions, and morphogenesis during development. Damage to Hh transduction machinery can lead to... 
Hedgehogs | 3T3 cells | NIH 3T3 cells | Genes | Cell lines | Fluorescence | Ligands | Inhibitory concentration 50 | Genetic mutation | Cilia | Developmental signaling | Primary cilium | Transport | Hedgehog inhibitor | primary cilium | INHIBITION | MULTIDISCIPLINARY SCIENCES | CYCLOPAMINE | RECEPTOR | developmental signaling | transport | MUTATIONS | INTRAFLAGELLAR TRANSPORT | BINDING | Cell Line | Animals | Receptors, G-Protein-Coupled - metabolism | Signal Transduction | Receptors, Cell Surface - deficiency | Hedgehog Proteins - metabolism | Receptors, Cell Surface - metabolism | Mice | Receptors, G-Protein-Coupled - genetics | Patched Receptors | Mice, Knockout | Receptors, Cell Surface - genetics | Physiological aspects | Genetic aspects | Cellular signal transduction | Research | Drug therapy | Cancer | Membrane proteins | Proteins | Signal transduction | Molecules | Rodents | DNA damage | Cells | Index Medicus | Biological Sciences
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12. Full Text BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation
by Corcoran, Ryan B and Dias-Santagata, Dora and Bergethon, Kristin and Iafrate, A. John and Settleman, Jeffrey and Engelman, Jeffrey A
Science Signaling, ISSN 1945-0877, 11/2010, Volume 3, Issue 149, pp. ra84 - ra84
Oncogenic BRAF mutations are found in several tumor types, including melanomas and colorectal cancers. Tumors with BRAF mutations have increased... 
LUNG-CANCER | GEFITINIB | MELANOMA | BCR-ABL | ADENOCARCINOMAS | GROWTH | SENSITIVITY | KINASE INHIBITORS | CARCINOMA | EGFR | CELL BIOLOGY | RNA, Small Interfering - genetics | Humans | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | In Situ Hybridization, Fluorescence | DNA Primers - genetics | Sequence Analysis, DNA | Blotting, Western | Mutation, Missense - genetics | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Mitogen-Activated Protein Kinase Kinases - metabolism | Drug Resistance, Neoplasm - genetics | Analysis of Variance | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Inhibitory Concentration 50 | Benzimidazoles - pharmacology | Gene Amplification - genetics | Phosphorylation - drug effects | Drug Resistance, Neoplasm - physiology | Index Medicus
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13. Full Text Oxysterols Stimulate Sonic Hedgehog Signal Transduction and Proliferation of Medulloblastoma Cells
by Ryan B. Corcoran and Matthew P. Scott
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2006, Volume 103, Issue 22, pp. 8408 - 8413
Sterol synthesis is required for Sonic hedgehog (Shh) signal transduction. Errors in Shh signal transduction play important roles in the formation of human... 
Signal transduction | Cell growth | Sterols | Genes | Cell lines | Fibroblasts | Cholesterols | Cells | Steroids | Tumors | Smoothened | Sterol synthesis pathway | Cholesterol | Patched | Cancer | HOMEOSTASIS | smoothened | MULTIDISCIPLINARY SCIENCES | sterol synthesis pathway | HMG-COA REDUCTASE | CHOLESTEROL MODIFICATION | IDENTIFICATION | SMALL-MOLECULE INHIBITOR | GENE | PATHWAY | patched | cholesterol | CYCLOPAMINE | cancer | MICE | MUTATIONS | Cell Line | Cell Proliferation | Receptors, G-Protein-Coupled - metabolism | Signal Transduction | Sterols - chemistry | Medulloblastoma - metabolism | Sterols - biosynthesis | Hedgehog Proteins | Animals | Medulloblastoma - pathology | Smoothened Receptor | Oxygen - chemistry | Trans-Activators - genetics | Trans-Activators - metabolism | Mice | Molecular Structure | Research | Studies | Chemical synthesis | Index Medicus | Biological Sciences
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14. Full Text TORC1 suppression predicts responsiveness to RAF and MEK inhibition in BRAF-mutant melanoma
by Corcoran, Ryan B and Rothenberg, Stephen Michael and Hata, Aaron N and Faber, Anthony C and Piris, Adriano and Nazarian, Rosalynn M and Brown, Ronald D and Godfrey, Jason T and Winokur, Daniel and Walsh, John and Mino-Kenudson, Mari and Maheswaran, Shyamala and Settleman, Jeffrey and Wargo, Jennifer A and Flaherty, Keith T and Haber, Daniel A and Engelman, Jeffrey A
Science Translational Medicine, ISSN 1946-6234, 07/2013, Volume 5, Issue 196, pp. 196ra98 - 196ra98
RAF and MEK (mitogen-activated or extracellular signal-regulated protein kinase kinase) inhibitors are effective in treating patients with BRAF-mutant... 
TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | Melanoma - enzymology | Extracellular Signal-Regulated MAP Kinases - metabolism | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase Kinases - metabolism | Multiprotein Complexes - metabolism | Melanoma - genetics | Indoles - pharmacology | Phosphorylation - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Down-Regulation - drug effects | Mutation - genetics | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Sulfonamides - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Ribosomal Protein S6 - metabolism | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Mice | Protein Kinase Inhibitors - pharmacology | MEDICINE, RESEARCH & EXPERIMENTAL | CELL BIOLOGY | Index Medicus
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15. Full Text A combinatorial strategy for treating KRAS-mutant lung cancer
by Manchado, Eusebio and Manchado, Eusebio and Weissmueller, Susann and Weissmueller, Susann and Morris, John P and Morris, John P and Chen, Chi-Chao and Chen, Chi-Chao and Wullenkord, Ramona and Wullenkord, Ramona and Lujambio, Amaia and Lujambio, Amaia and de Stanchina, Elisa and De Stanchina, Elisa and Poirier, John T and Poirier, John T and Gainor, Justin F and Gainor, Justin F and Corcoran, Ryan B and Corcoran, Ryan B and Engelman, Jeffrey A and Engelman, Jeffrey A and Rudin, Charles M and Rudin, Charles M and Rosen, Neal and Rosen, Neal and Lowe, Scott W and Lowe, Scott W
Nature, ISSN 0028-0836, 2016, Volume 534, Issue 7609, pp. 647 - 651
Therapeutic targeting of KRAS-mutant lung adenocarcinoma represents a major goal of clinical oncology. KRAS itself has proved difficult to inhibit, and the... 
COLON-CANCER | SELECTIVE INHIBITOR | POTENT | FEEDBACK ACTIVATION | MEK INHIBITION | MODELS | RAS | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | MEDIATED REACTIVATION | RECEPTOR TYROSINE KINASE | Molecular targeted therapy | Care and treatment | Cell death | Lung cancer | Methods | Cancer cells | Phosphorylation | Chemotherapy | Inhibitor drugs | Mutation | Drug resistance | Tumors | Index Medicus
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16. Full Text Synthetic Lethal Interaction of Combined BCL-XL and MEK Inhibition Promotes Tumor Regressions in KRAS Mutant Cancer Models
by Corcoran, Ryan B and Cheng, Katherine A and Hata, Aaron N and Faber, Anthony C and Ebi, Hiromichi and Coffee, Erin M and Greninger, Patricia and Brown, Ronald D and Godfrey, Jason T and Cohoon, Travis J and Song, Youngchul and Lifshits, Eugene and Hung, Kenneth E and Shioda, Toshi and Dias-Santagata, Dora and Singh, Anurag and Settleman, Jeffrey and Benes, Cyril H and Mino-Kenudson, Mari and Wong, Kwok-Kin and Engelman, Jeffrey A
Cancer Cell, ISSN 1535-6108, 01/2013, Volume 23, Issue 1, pp. 121 - 128
KRAS is the most commonly mutated oncogene, yet no effective targeted therapies exist for KRAS mutant cancers. We developed a pooled shRNA-drug screen strategy... 
PATHWAYS | GENE-EXPRESSION SIGNATURE | APOPTOSIS | CELLS | ACTIVATION | RAS ONCOGENE | K-RAS | ONCOLOGY | SENSITIVITY | RESISTANCE | INDUCTION | CELL BIOLOGY | Aniline Compounds - pharmacology | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Antineoplastic Agents - therapeutic use | Sulfonamides - pharmacology | Neoplasms - drug therapy | Animals | Neoplasms - genetics | Sulfonamides - therapeutic use | bcl-X Protein - antagonists & inhibitors | Benzimidazoles - pharmacology | Antineoplastic Agents - pharmacology | Mice | Aniline Compounds - therapeutic use | MAP Kinase Kinase Kinases - antagonists & inhibitors | Benzimidazoles - therapeutic use | Drug Screening Assays, Antitumor | Proto-Oncogene Proteins p21(ras) - metabolism | Proteins | Care and treatment | Lung cancer | Analysis | Genes | Genetically modified organisms | Cancer | Protein binding | Index Medicus
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17. Full Text STAT3 plays a critical role in KRAS-induced pancreatic tumorigenesis
by Corcoran, Ryan B and Contino, Gianmarco and Deshpande, Vikram and Tzatsos, Alexandros and Conrad, Claudius and Benes, Cyril H and Levy, David E and Settleman, Jeffrey and Engelman, Jeffrey A and Bardeesy, Nabeel
Cancer Research, ISSN 0008-5472, 07/2011, Volume 71, Issue 14, pp. 5020 - 5029
The STAT3 transcription factor is an important regulator of stem cell self-renewal, cancer cell survival, and inflammation. In the pancreas, STAT3 is... 
TRANSFORMATION | ACTIVATION | MITOCHONDRIAL STAT3 | JAK2 INHIBITOR | ONCOLOGY | DUCTAL ADENOCARCINOMA | EPIDERMAL-GROWTH-FACTOR | SERINE PHOSPHORYLATION | CANCER | CELL-LINE | SIGNAL TRANSDUCER | Genetic Predisposition to Disease | Phosphorylation | Pancreatic Neoplasms - metabolism | Humans | Transcriptional Activation | Carcinoma, Pancreatic Ductal - metabolism | Mice, Transgenic | Pancreatic Neoplasms - genetics | Precancerous Conditions - metabolism | Mice, SCID | Cell Transformation, Neoplastic - metabolism | Precancerous Conditions - genetics | Carcinoma, Pancreatic Ductal - genetics | Animals | Cell Transformation, Neoplastic - genetics | Cell Line, Tumor | Mice | Genes, ras | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Index Medicus | mouse models | gp130 | Pancreatic intraepithelial neoplasia | Pancreatic cancer | STAT3
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