LKB1 inactivation sensitizes non-small cell lung cancer to pharmacological aggravation of ER stress.

[1]  Takla Griss,et al.  Loss of the tumor suppressor LKB1 promotes metabolic reprogramming of cancer cells via HIF-1α , 2014, Proceedings of the National Academy of Sciences.

[2]  Travis J Cohoon,et al.  Metabolic and functional genomic studies identify deoxythymidylate kinase as a target in LKB1-mutant lung cancer. , 2013, Cancer discovery.

[3]  Bei Liu,et al.  The role of endoplasmic reticulum stress in maintaining and targeting multiple myeloma: a double-edged sword of adaptation and apoptosis , 2013 .

[4]  R. Kaufman,et al.  ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death , 2013, Nature Cell Biology.

[5]  A. Schönthal Pharmacological targeting of endoplasmic reticulum stress signaling in cancer. , 2013, Biochemical pharmacology.

[6]  Liu Wei,et al.  LKB1 inactivation dictates therapeutic response of non-small cell lung cancer to the metabolism drug phenformin. , 2013, Cancer cell.

[7]  J. Schlesselman,et al.  A phase I dose-escalation trial of 2-deoxy-d-glucose alone or combined with docetaxel in patients with advanced solid tumors , 2013, Cancer Chemotherapy and Pharmacology.

[8]  A. Jemal,et al.  Cancer statistics, 2013 , 2013, CA: a cancer journal for clinicians.

[9]  M. Herlyn,et al.  Control of tumor bioenergetics and survival stress signaling by mitochondrial HSP90s. , 2012, Cancer cell.

[10]  S. Weroha,et al.  Oncogenic pathways, molecularly targeted therapies, and highlighted clinical trials in non-small-cell lung cancer (NSCLC). , 2012, Clinical lung cancer.

[11]  C. Kingsley,et al.  Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion. , 2012, The American journal of pathology.

[12]  C. Perou,et al.  LKB1/STK11 inactivation leads to expansion of a prometastatic tumor subpopulation in melanoma. , 2012, Cancer cell.

[13]  M. Rosen,et al.  A Phase I Trial of the HIV Protease Inhibitor Nelfinavir with Concurrent Chemoradiotherapy for Unresectable Stage IIIA/IIIB Non-small Cell Lung Cancer: A Report of Toxicities and Clinical Response , 2012, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[14]  Andrew L. Kung,et al.  A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response , 2012, Nature.

[15]  Jennifer B Dennison,et al.  Dual Inhibition of Tumor Energy Pathway by 2-Deoxyglucose and Metformin Is Effective against a Broad Spectrum of Preclinical Cancer Models , 2011, Molecular Cancer Therapeutics.

[16]  J. Flickinger,et al.  Failure rates and patterns of recurrence in patients with resected N1 non-small-cell lung cancer. , 2011, International journal of radiation oncology, biology, physics.

[17]  Leah E. Mechanic,et al.  Frequent homozygous deletion of the LKB1/STK11 gene in non-small cell lung cancer , 2011, Oncogene.

[18]  F. R. Papa,et al.  Signaling cell death from the endoplasmic reticulum stress response. , 2011, Current opinion in cell biology.

[19]  B. Viollet,et al.  Phosphorylation of ULK1 (hATG1) by AMP-Activated Protein Kinase Connects Energy Sensing to Mitophagy , 2011, Science.

[20]  Ioannis Mylonas,et al.  Tamoxifen enhances the cytotoxic effects of nelfinavir in breast cancer cells , 2010, Breast Cancer Research.

[21]  L. Dick,et al.  Building on bortezomib: second-generation proteasome inhibitors as anti-cancer therapy. , 2010, Drug discovery today.

[22]  F. R. Papa,et al.  IRE1α Kinase Activation Modes Control Alternate Endoribonuclease Outputs to Determine Divergent Cell Fates , 2009, Cell.

[23]  R. Shaw,et al.  The LKB1–AMPK pathway: metabolism and growth control in tumour suppression , 2009, Nature Reviews Cancer.

[24]  Chin-Lee Wu,et al.  mTOR and HIF-1α-mediated tumor metabolism in an LKB1 mouse model of Peutz-Jeghers syndrome , 2009, Proceedings of the National Academy of Sciences.

[25]  K. Coon,et al.  Expression of LKB1 tumor suppressor in non-small cell lung cancer determines sensitivity to 2-deoxyglucose. , 2009, The Journal of thoracic and cardiovascular surgery.

[26]  S. Kridel,et al.  Preferential cytotoxicity of bortezomib toward hypoxic tumor cells via overactivation of endoplasmic reticulum stress pathways. , 2008, Cancer research.

[27]  Brian H. Dunford-Shore,et al.  Somatic mutations affect key pathways in lung adenocarcinoma , 2008, Nature.

[28]  Kwok-Kin Wong,et al.  Loss of Lkb1 provokes highly invasive endometrial adenocarcinomas. , 2008, Cancer research.

[29]  Thomas C. Chen,et al.  HIV-1 protease inhibitors nelfinavir and atazanavir induce malignant glioma death by triggering endoplasmic reticulum stress. , 2007, Cancer research.

[30]  A. Lane,et al.  Under normoxia, 2-deoxy-d-glucose elicits cell death in select tumor types not by inhibition of glycolysis but by interfering with N-linked glycosylation , 2007, Molecular Cancer Therapeutics.

[31]  D. Neil Hayes,et al.  LKB1 modulates lung cancer differentiation and metastasis , 2007, Nature.

[32]  Johnathan C. Maher,et al.  Differential toxic mechanisms of 2-deoxy-D-glucose versus 2-fluorodeoxy-D-glucose in hypoxic and normoxic tumor cells. , 2007, Antioxidants & redox signaling.

[33]  P. Walter,et al.  Signal integration in the endoplasmic reticulum unfolded protein response , 2007, Nature Reviews Molecular Cell Biology.

[34]  J. Uddin,et al.  Calcium-activated endoplasmic reticulum stress as a major component of tumor cell death induced by 2,5-dimethyl-celecoxib, a non-coxib analogue of celecoxib , 2007, Molecular Cancer Therapeutics.

[35]  M. Katze,et al.  Cotranslocational Degradation Protects the Stressed Endoplasmic Reticulum from Protein Overload , 2006, Cell.

[36]  F. Urano,et al.  Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress , 2006, Molecular and Cellular Biology.

[37]  M. Katze,et al.  Cotranslocational Degradation Protects the Stressed Endoplasmic Reticulum from Protein Overload , 2006, Cell.

[38]  Amy S. Lee The ER chaperone and signaling regulator GRP78/BiP as a monitor of endoplasmic reticulum stress. , 2005, Methods.

[39]  L. Hendershot,et al.  The role of the unfolded protein response in tumour development: friend or foe? , 2004, Nature Reviews Cancer.

[40]  A. Cooper,et al.  Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death. , 2004, Molecular cell.

[41]  Bengt Bergman,et al.  Cisplatin-based adjuvant chemotherapy in patients with completely resected non-small-cell lung cancer. , 2004, The New England journal of medicine.

[42]  N. Savaraj,et al.  2-Deoxy-d-glucose Increases the Efficacy of Adriamycin and Paclitaxel in Human Osteosarcoma and Non-Small Cell Lung Cancers In Vivo , 2004, Cancer Research.

[43]  R. Paules,et al.  An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. , 2003, Molecular cell.

[44]  J. Ohnishi,et al.  ER stress induces caspase-8 activation, stimulating cytochrome c release and caspase-9 activation. , 2003, Experimental cell research.

[45]  Ronald A. DePinho,et al.  Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation , 2002, Nature.

[46]  T. Jacks,et al.  Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. , 2001, Genes & development.

[47]  Xiaozhong Wang,et al.  Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153) , 1996, Molecular and cellular biology.

[48]  J. Haveman,et al.  Clonogenic assay of cells in vitro , 2006, Nature Protocols.

[49]  J. M. Arbeit,et al.  Selective depletion of tumor ATP by 2-deoxyglucose and insulin, detected by 31P magnetic resonance spectroscopy. , 1992, Cancer research.

[50]  N. Dubrawsky Cancer statistics , 1989, CA: a cancer journal for clinicians.