Destabilization of NOXA mRNA as a common resistance mechanism to targeted therapies

[1]  J. A. Hendricks,et al.  Discovery of Mcl-1-specific inhibitor AZD5991 and preclinical activity in multiple myeloma and acute myeloid leukemia , 2018, Nature Communications.

[2]  Sean P. Brown,et al.  Exploiting MCL1 Dependency with Combination MEK + MCL1 Inhibitors Leads to Induction of Apoptosis and Tumor Regression in KRAS-Mutant Non-Small Cell Lung Cancer. , 2018, Cancer discovery.

[3]  Steven J. M. Jones,et al.  Oncogenic Signaling Pathways in The Cancer Genome Atlas. , 2018, Cell.

[4]  J. Arribas,et al.  Coamplification of miR-4728 protects HER2-amplified breast cancers from targeted therapy , 2018, Proceedings of the National Academy of Sciences.

[5]  J. Montero,et al.  Why do BCL-2 inhibitors work and where should we use them in the clinic? , 2017, Cell Death and Differentiation.

[6]  P. Blackshear,et al.  An Ancient Family of RNA-Binding Proteins: Still Important! , 2017, Trends in biochemical sciences.

[7]  A. Letai,et al.  Blastic Plasmacytoid Dendritic Cell Neoplasm Is Dependent on BCL2 and Sensitive to Venetoclax. , 2017, Cancer discovery.

[8]  A. Strasser,et al.  The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models , 2016, Nature.

[9]  A. Letai,et al.  iBH3: simple, fixable BH3 profiling to determine apoptotic priming in primary tissue by flow cytometry , 2016, Biological chemistry.

[10]  D. Green A BH3 Mimetic for Killing Cancer Cells , 2016, Cell.

[11]  A. Letai,et al.  Mitochondria-Judges and Executioners of Cell Death Sentences. , 2016, Molecular cell.

[12]  David L. Vaux,et al.  Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies , 2016, Nature Reviews Cancer.

[13]  T. Kipps,et al.  Targeting BCL2 with Venetoclax in Relapsed Chronic Lymphocytic Leukemia. , 2016, The New England journal of medicine.

[14]  E. Felip,et al.  BIM and mTOR expression levels predict outcome to erlotinib in EGFR-mutant non-small-cell lung cancer , 2015, Scientific Reports.

[15]  A. Chanan-Khan,et al.  Safety and Efficacy of Venetoclax (ABT-199/GDC-0199) in Combination with Bortezomib and Dexamethasone in Relapsed/Refractory Multiple Myeloma: Phase 1b Results , 2015 .

[16]  R. Sullivan,et al.  Overexpression of Mcl-1 confers resistance to BRAFV600E inhibitors alone and in combination with MEK1/2 inhibitors in melanoma , 2015, Oncotarget.

[17]  Xin Lu,et al.  MCL-1 Is a Key Determinant of Breast Cancer Cell Survival: Validation of MCL-1 Dependency Utilizing a Highly Selective Small Molecule Inhibitor , 2015, Molecular Cancer Therapeutics.

[18]  Karen Cichowski,et al.  Drug-Induced Death Signaling Strategy Rapidly Predicts Cancer Response to Chemotherapy , 2015, Cell.

[19]  R. Sullivan,et al.  Clinical Profiling of BCL-2 Family Members in the Setting of BRAF Inhibition Offers a Rationale for Targeting De Novo Resistance Using BH3 Mimetics , 2014, PloS one.

[20]  C. Garbe,et al.  Dacarbazine with or without oblimersen (a Bcl-2 antisense oligonucleotide) in chemotherapy-naive patients with advanced melanoma and low–normal serum lactate dehydrogenase: ‘The AGENDA trial’ , 2014, Melanoma research.

[21]  Ben S. Wittner,et al.  Abstract 4832: Isolation and molecular characterization of circulating melanoma cells , 2014 .

[22]  M. Skobe,et al.  Anti-apoptotic BCL-2 proteins govern cellular outcome following B-RAFV600E inhibition and can be targeted to reduce resistance , 2014, Oncogene.

[23]  E. Felip,et al.  The Impact of EGFR T790M Mutations and BIM mRNA Expression on Outcome in Patients with EGFR-Mutant NSCLC Treated with Erlotinib or Chemotherapy in the Randomized Phase III EURTAC Trial , 2014, Clinical Cancer Research.

[24]  John W. Adams,et al.  Obatoclax Mesylate, a Pan–Bcl-2 Inhibitor, in Combination with Docetaxel in a Phase 1/2 Trial in Relapsed Non–Small-Cell Lung Cancer , 2014, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[25]  N. Rosen,et al.  Tumor adaptation and resistance to RAF inhibitors , 2013, Nature Medicine.

[26]  A. King,et al.  Dabrafenib; Preclinical Characterization, Increased Efficacy when Combined with Trametinib, while BRAF/MEK Tool Combination Reduced Skin Lesions , 2013, PloS one.

[27]  K. Flaherty,et al.  Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma. , 2013, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[28]  Jun S. Song,et al.  Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF. , 2013, Cancer cell.

[29]  D. Schadendorf,et al.  A genome-scale RNA interference screen implicates NF1 loss in resistance to RAF inhibition. , 2013, Cancer discovery.

[30]  Jun S. Song,et al.  BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that confers resistance to BRAF inhibition , 2013, Proceedings of the National Academy of Sciences.

[31]  P. Hersey,et al.  The BH3-mimetic ABT-737 sensitizes human melanoma cells to apoptosis induced by selective BRAF inhibitors but does not reverse acquired resistance. , 2013, Carcinogenesis.

[32]  Travis J Cohoon,et al.  Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models. , 2013, Cancer cell.

[33]  A. Aplin,et al.  BH3-only protein silencing contributes to acquired resistance to PLX4720 in human melanoma , 2012, Cell Death and Differentiation.

[34]  Jane Fridlyand,et al.  Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors , 2012, Nature.

[35]  T. Golub,et al.  Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion , 2012, Nature.

[36]  M. Nöthen,et al.  A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer , 2012, Nature Medicine.

[37]  Z. Nikolovska-Coleska,et al.  Inhibitors of the anti-apoptotic Bcl-2 proteins: a patent review , 2012, Expert opinion on therapeutic patents.

[38]  S. Nelson,et al.  Melanoma whole exome sequencing identifies V600EB-RAF amplification-mediated acquired B-RAF inhibitor resistance , 2012, Nature Communications.

[39]  D. Bar-Sagi,et al.  RAS oncogenes: weaving a tumorigenic web , 2011, Nature Reviews Cancer.

[40]  Tom Misteli,et al.  RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E) , 2011, Nature.

[41]  S. Digumarthy,et al.  BIM expression in treatment-naive cancers predicts responsiveness to kinase inhibitors. , 2011, Cancer discovery.

[42]  A. Hauschild,et al.  Improved survival with vemurafenib in melanoma with BRAF V600E mutation. , 2011, The New England journal of medicine.

[43]  N. Mazure,et al.  Constitutive ERK activity induces downregulation of tristetraprolin, a major protein controlling interleukin8/CXCL8 mRNA stability in melanoma cells. , 2011, American journal of physiology. Cell physiology.

[44]  Sarat Chandarlapaty,et al.  AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity. , 2011, Cancer cell.

[45]  Damien Kee,et al.  Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. , 2010, Cancer cell.

[46]  B. Taylor,et al.  The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner , 2010, Proceedings of the National Academy of Sciences.

[47]  P. Blackshear,et al.  The RNA-binding zinc-finger protein tristetraprolin regulates AU-rich mRNAs involved in breast cancer-related processes , 2010, Oncogene.

[48]  A. Gemma,et al.  F1000 highlights , 2010 .

[49]  C. Sander,et al.  V600EBRAF is associated with disabled feedback inhibition of RAF–MEK signaling and elevated transcriptional output of the pathway , 2009, Proceedings of the National Academy of Sciences.

[50]  R. Kofler,et al.  Noxa: at the tip of the balance between life and death , 2008, Oncogene.

[51]  M. McMahon,et al.  Oncogenic BRAFV600E inhibits BIM expression to promote melanoma cell survival , 2008, Pigment cell & melanoma research.

[52]  Mihaela Zavolan,et al.  Comparative Analysis of mRNA Targets for Human PUF-Family Proteins Suggests Extensive Interaction with the miRNA Regulatory System , 2008, PloS one.

[53]  A. D. Van den Abbeele,et al.  Major response to imatinib mesylate in KIT-mutated melanoma. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[54]  Seamus J. Martin,et al.  Expression and purification of recombinant annexin V for the detection of membrane alterations on apoptotic cells. , 2008, Methods.

[55]  A. Letai,et al.  Diagnosing and exploiting cancer's addiction to blocks in apoptosis , 2008, Nature Reviews Cancer.

[56]  James T. Elder,et al.  A novel BH3 mimetic reveals a mitogen-activated protein kinase-dependent mechanism of melanoma cell death controlled by p53 and reactive oxygen species. , 2006, Cancer research.

[57]  J. Arthur,et al.  Posttranslational Regulation of Tristetraprolin Subcellular Localization and Protein Stability by p38 Mitogen-Activated Protein Kinase and Extracellular Signal-Regulated Kinase Pathways , 2006, Molecular and Cellular Biology.

[58]  H. Lane,et al.  ERBB receptors and cancer: the complexity of targeted inhibitors , 2005, Nature Reviews Cancer.

[59]  Brian J. Smith,et al.  Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. , 2005, Molecular cell.

[60]  H. Cao Expression, purification, and biochemical characterization of the antiinflammatory tristetraprolin: a zinc-dependent mRNA binding protein affected by posttranslational modifications. , 2004, Biochemistry.

[61]  S. Gabriel,et al.  EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.

[62]  Patricia L. Harris,et al.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.

[63]  P. Blackshear,et al.  Expression and purification of recombinant tristetraprolin that can bind to tumor necrosis factor-α mRNA and serve as a substrate for mitogen-activated protein kinases , 2003 .

[64]  A. Nicholson,et al.  Mutations of the BRAF gene in human cancer , 2002, Nature.

[65]  Anuradha Roy,et al.  Patent Review , 2002, Combinatorial chemistry & high throughput screening.

[66]  S. Hirota,et al.  Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. , 1998, Science.

[67]  M J Thompson,et al.  Phosphorylation of Tristetraprolin, a Potential Zinc Finger Transcription Factor, by Mitogen Stimulation in Intact Cells and by Mitogen-activated Protein Kinase in Vitro(*) , 1995, The Journal of Biological Chemistry.

[68]  N. Kato,et al.  Molecular cloning and characterization of a cDNA for a novel phorbol-12-myristate-13-acetate-responsive gene that is highly expressed in an adult T-cell leukemia cell line , 1990, Journal of virology.

[69]  Erin M. Coffee,et al.  mTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1. , 2014, Cancer discovery.

[70]  A. McKenna,et al.  The genetic landscape of clinical resistance to RAF inhibition in metastatic melanoma. , 2014, Cancer discovery.

[71]  A. Aplin,et al.  Downregulation of Noxa by RAF/MEK inhibition counteracts cell death response in mutant B-RAF melanoma cells. , 2012, American journal of cancer research.

[72]  J. Pouysségur,et al.  Implication of the ERK pathway on the post-transcriptional regulation of VEGF mRNA stability. , 2010, Methods in molecular biology.

[73]  P. Blackshear,et al.  Expression and purification of recombinant tristetraprolin that can bind to tumor necrosis factor-alpha mRNA and serve as a substrate for mitogen-activated protein kinases. , 2003, Archives of biochemistry and biophysics.