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Anthony G. Letai, MD, PhD


Medical Oncology

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Physician

  • Physician
  • Professor of Medicine, Harvard Medical School

Centers/Programs

Clinical Interests

  • Leukemias

Contact Information

  • Appointments617-632-6140
  • Office Phone Number617-632-2348
  • Fax617-582-8160

Bio

Dr. Letai received his MD and PhD from the University of Chicago. He completed his residency in internal medicine at Brigham and Women's Hospital, and a fellowship in hematology and oncology at DFCI. He did his postdoctoral research training in the laboratory of Dr. Stanley Korsmeyer. Dr. Letai's research focuses on the mechanisms by which cancer cells evade death, and on the application of that knowledge to the selective killing of cancer cells. He joined the faculty of DFCI and Harvard Medical School in 2004.

Board Certification:

  • Medical Oncology, 2001

Fellowship:

  • Dana-Farber/Partners CancerCare, Hematology/Oncology

Residency:

  • Brigham and Women's Hospital, Internal Medicine

Medical School:

  • University of Chicago

Recent Awards:

  • Leukemia and Lymphoma Society Scholar Award 2008
  • American Society of Clinical Investigation, Elected Member 2009
  • V Scholar Award 2005
  • Smith Family New Investigator 2004
  • Kimmel Scholar Award 2005

Research

Dysregulation of Death Pathways in Cancer

The cells of the body are constructed so that if they become sufficiently damaged or abnormal, programmed cell death, or apoptosis, rapidly eliminates them before they can cause any harm. Cancer cells, which bear many abnormalities, apparently have found ways to escape this death sentence. One way that cancer cells escape death is via the overexpression of antideath proteins in the BCL-2 family. We are investigating how these antideath proteins might be selectively targeted in cancer cells. Using a combination of mouse models, protein biochemistry, and mitochondrial and cellular studies, we have determined conditions under which cancer and normal cells are susceptible to inhibition of BCL-2 family function. We are collaborating with biotechnology and pharmaceutical firms to bring small-molecule BCL-2 antagonists to clinical trial here at Dana-Farber. Most likely, the novel strategy of BCL-2 antagonism will first be tested in chronic lymphocytic leukemia, small-cell lung cancer, and non-Hodgkin's lymphoma. If these trials are successful, the strategy of BCL-2 antagonism may find wide application in other human cancers.We also investigate more fundamental questions about how interactions among BCL-2 family proteins govern death and survival in normal and cancer cells. We explore how these proteins participate in a wide range of death signals, growth factor withdrawal, and chemotherapy.

Apoptotic Blocks in Primary Non-Hodgkin B Cell Lymphomas Identified by BH3 Profiling. Cancers (Basel). 2021 Feb 28; 13(5).
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Multiple screening approaches reveal HDAC6 as a novel regulator of glycolytic metabolism in triple-negative breast cancer. Sci Adv. 2021 Jan; 7(3).
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An Autochthonous Mouse Model of Myd88- and BCL2-Driven Diffuse Large B-cell Lymphoma Reveals Actionable Molecular Vulnerabilities. Blood Cancer Discov. 2021 Jan; 2(1):70-91.
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Navitoclax enhances the effectiveness of EGFR-targeted antibody-drug conjugates in PDX models of EGFR-expressing triple-negative breast cancer. Breast Cancer Res. 2020 11 30; 22(1):132.
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Reduced Mitochondrial Apoptotic Priming Drives Resistance to BH3 Mimetics in Acute Myeloid Leukemia. Cancer Cell. 2020 Dec 14; 38(6):872-890.e6.
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Aneuploidy increases resistance to chemotherapeutics by antagonizing cell division. Proc Natl Acad Sci U S A. 2020 12 01; 117(48):30566-30576.
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Venetoclax with azacitidine or decitabine in patients with newly diagnosed acute myeloid leukemia: Long term follow-up from a phase 1b study. Am J Hematol. 2021 02 01; 96(2):208-217.
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Combined EZH2 and Bcl-2 inhibitors as precision therapy for genetically defined DLBCL subtypes. Blood Adv. 2020 10 27; 4(20):5226-5231.
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Azacitidine and Venetoclax in Previously Untreated Acute Myeloid Leukemia. N Engl J Med. 2020 08 13; 383(7):617-629.
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Leukemia Cell of Origin Influences Apoptotic Priming and Sensitivity to LSD1 Inhibition. Cancer Discov. 2020 Oct; 10(10):1500-1513.
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High-throughput dynamic BH3 profiling may quickly and accurately predict effective therapies in solid tumors. Sci Signal. 2020 06 16; 13(636).
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Increased mitochondrial apoptotic priming with targeted therapy predicts clinical response to re-induction chemotherapy. Am J Hematol. 2020 03; 95(3):245-250.
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Destabilization of NOXA mRNA as a common resistance mechanism to targeted therapies. Nat Commun. 2019 11 14; 10(1):5157.
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DNA methyltransferase inhibition overcomes diphthamide pathway deficiencies underlying CD123-targeted treatment resistance. J Clin Invest. 2019 11 01; 129(11):5005-5019.
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Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies. Cancer Cell. 2019 10 14; 36(4):369-384.e13.
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Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer. Mol Cancer Res. 2019 11; 17(11):2281-2293.
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Prohibitin is a prognostic marker and therapeutic target to block chemotherapy resistance in Wilms' tumor. JCI Insight. 2019 08 08; 4(15).
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MYC paralog-dependent apoptotic priming orchestrates a spectrum of vulnerabilities in small cell lung cancer. Nat Commun. 2019 08 02; 10(1):3485.
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Prediction of venetoclax activity in precursor B-ALL by functional assessment of apoptosis signaling. Cell Death Dis. 2019 07 29; 10(8):571.
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BH3 profiling discriminates on-target small molecule BH3 mimetics from putative mimetics. Cell Death Differ. 2020 03; 27(3):999-1007.
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Patterns of substrate affinity, competition, and degradation kinetics underlie biological activity of thalidomide analogs. Blood. 2019 07 11; 134(2):160-170.
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Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins. Nat Rev Mol Cell Biol. 2019 03; 20(3):175-193.
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MCL1 and DEDD Promote Urothelial Carcinoma Progression. Mol Cancer Res. 2019 06; 17(6):1294-1304.
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Biomarker-driven strategy for MCL1 inhibition in T-cell lymphomas. Blood. 2019 02 07; 133(6):566-575.
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PRC2 loss induces chemoresistance by repressing apoptosis in T cell acute lymphoblastic leukemia. J Exp Med. 2018 12 03; 215(12):3094-3114.
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Venetoclax combined with decitabine or azacitidine in treatment-naive, elderly patients with acute myeloid leukemia. Blood. 2019 01 03; 133(1):7-17.
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Targeted inhibition of PI3Ka/d is synergistic with BCL-2 blockade in genetically defined subtypes of DLBCL. Blood. 2019 01 03; 133(1):70-80.
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Splicing modulation sensitizes chronic lymphocytic leukemia cells to venetoclax by remodeling mitochondrial apoptotic dependencies. JCI Insight. 2018 10 04; 3(19).
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BCL-2 inhibition in AML: an unexpected bonus? Blood. 2018 09 06; 132(10):1007-1012.
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Phosphorylation switches Bax from promoting to inhibiting apoptosis thereby increasing drug resistance. . 2018 09; 19(9).
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PPM1D-truncating mutations confer resistance to chemotherapy and sensitivity to PPM1D inhibition in hematopoietic cells. Blood. 2018 09 13; 132(11):1095-1105.
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Metabolomic and BH3 profiling of esophageal cancers: novel assessment methods for precision therapy. BMC Gastroenterol. 2018 Jun 22; 18(1):94.
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Statins enhance efficacy of venetoclax in blood cancers. Sci Transl Med. 2018 06 13; 10(445).
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Targeting B-Cell Lymphoma 2: A Lethal Shortcut in Del(17p) Chronic Lymphocytic Leukemia. J Clin Oncol. 2018 07 01; 36(19):1991-1993.
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Diminished apoptotic priming and ATM signalling confer a survival advantage onto aged haematopoietic stem cells in response to DNA damage. Nat Cell Biol. 2018 04; 20(4):413-421.
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MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia. Cancer Discov. 2018 04; 8(4):478-497.
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Iterative optimization yields Mcl-1-targeting stapled peptides with selective cytotoxicity to Mcl-1-dependent cancer cells. Proc Natl Acad Sci U S A. 2018 01 30; 115(5):E886-E895.
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Safety and preliminary efficacy of venetoclax with decitabine or azacitidine in elderly patients with previously untreated acute myeloid leukaemia: a non-randomised, open-label, phase 1b study. Lancet Oncol. 2018 02; 19(2):216-228.
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ER Stress Signaling Promotes the Survival of Cancer "Persister Cells" Tolerant to EGFR Tyrosine Kinase Inhibitors. Cancer Res. 2018 02 15; 78(4):1044-1057.
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Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis. Sci Transl Med. 2017 Dec 13; 9(420).
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Found in Translation: How Preclinical Research Is Guiding the Clinical Development of the BCL2-Selective Inhibitor Venetoclax. Cancer Discov. 2017 12; 7(12):1376-1393.
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Overcoming mutational complexity in acute myeloid leukemia by inhibition of critical pathways. Sci Transl Med. 2017 Oct 25; 9(413).
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BCL-XL directly modulates RAS signalling to favour cancer cell stemness. Nat Commun. 2017 10 24; 8(1):1123.
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Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma. Nat Med. 2017 Nov; 23(11):1342-1351.
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Inhibition of USP10 induces degradation of oncogenic FLT3. Nat Chem Biol. 2017 Dec; 13(12):1207-1215.
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Functional precision cancer medicine-moving beyond pure genomics. Nat Med. 2017 Sep 08; 23(9):1028-1035.
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Epistatic mutations in PUMA BH3 drive an alternate binding mode to potently and selectively inhibit anti-apoptotic Bfl-1. Elife. 2017 06 08; 6.
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Synergistic interactions with PI3K inhibition that induce apoptosis. Elife. 2017 05 31; 6.
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Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection. Elife. 2017 04 20; 6.
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Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages. Nature. 2017 03 16; 543(7645):428-432.
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Complementary dynamic BH3 profiles predict co-operativity between the multi-kinase inhibitor TG02 and the BH3 mimetic ABT-199 in acute myeloid leukaemia cells. Oncotarget. 2017 Mar 07; 8(10):16220-16232.
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Bruton's tyrosine kinase inhibition increases BCL-2 dependence and enhances sensitivity to venetoclax in chronic lymphocytic leukemia. Leukemia. 2017 10; 31(10):2075-2084.
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Developmental Regulation of Mitochondrial Apoptosis by c-Myc Governs Age- and Tissue-Specific Sensitivity to Cancer Therapeutics. Cancer Cell. 2017 01 09; 31(1):142-156.
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Tight Sequestration of BH3 Proteins by BCL-xL at Subcellular Membranes Contributes to Apoptotic Resistance. Cell Rep. 2016 12 20; 17(12):3347-3358.
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Discovery and biological characterization of potent myeloid cell leukemia-1 inhibitors. FEBS Lett. 2017 Jan; 591(1):240-251.
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Blastic Plasmacytoid Dendritic Cell Neoplasm Is Dependent on BCL2 and Sensitive to Venetoclax. Cancer Discov. 2017 02; 7(2):156-164.
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S63845, an MCL-1 Selective BH3 Mimetic: Another Arrow in Our Quiver. Cancer Cell. 2016 Dec 12; 30(6):834-835.
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Genomic evolution and chemoresistance in germ-cell tumours. Nature. 2016 11 30; 540(7631):114-118.
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To Prime, or Not to Prime: That Is the Question. Cold Spring Harb Symp Quant Biol. 2016; 81:131-140.
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Cristae remodeling causes acidification detected by integrated graphene sensor during mitochondrial outer membrane permeabilization. Sci Rep. 2016 10 27; 6:35907.
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Directly targeting the mitochondrial pathway of apoptosis for cancer therapy using BH3 mimetics - recent successes, current challenges and future promise. FEBS J. 2016 10; 283(19):3523-3533.
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Spatial Proximity to Fibroblasts Impacts Molecular Features and Therapeutic Sensitivity of Breast Cancer Cells Influencing Clinical Outcomes. Cancer Res. 2016 11 15; 76(22):6495-6506.
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Functionally identifiable apoptosis-insensitive subpopulations determine chemoresistance in acute myeloid leukemia. J Clin Invest. 2016 10 03; 126(10):3827-3836.
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Efficacy and Biological Correlates of Response in a Phase II Study of Venetoclax Monotherapy in Patients with Acute Myelogenous Leukemia. Cancer Discov. 2016 10; 6(10):1106-1117.
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The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice. Cancer Cell. 2016 07 11; 30(1):183.
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iBH3: simple, fixable BH3 profiling to determine apoptotic priming in primary tissue by flow cytometry. Biol Chem. 2016 07 01; 397(7):671-8.
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Clonal evolution in patients with chronic lymphocytic leukaemia developing resistance to BTK inhibition. Nat Commun. 2016 05 20; 7:11589.
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BOK: Oddball of the BCL-2 Family. Trends Cell Biol. 2016 06; 26(6):389-390.
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The BCL2 selective inhibitor venetoclax induces rapid onset apoptosis of CLL cells in patients via a TP53-independent mechanism. Blood. 2016 06 23; 127(25):3215-24.
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The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice. Cancer Cell. 2016 04 11; 29(4):574-586.
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Dynamic BH3 profiling-poking cancer cells with a stick. Mol Cell Oncol. 2016 May; 3(3):e1040144.
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Defining specificity and on-target activity of BH3-mimetics using engineered B-ALL cell lines. Oncotarget. 2016 Mar 08; 7(10):11500-11.
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Mitochondria-Judges and Executioners of Cell Death Sentences. Mol Cell. 2016 Mar 03; 61(5):695-704.
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Rapid Optimization of Mcl-1 Inhibitors using Stapled Peptide Libraries Including Non-Natural Side Chains. ACS Chem Biol. 2016 05 20; 11(5):1238-44.
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MLL-Rearranged Acute Lymphoblastic Leukemias Activate BCL-2 through H3K79 Methylation and Are Sensitive to the BCL-2-Specific Antagonist ABT-199. Cell Rep. 2015 Dec 29; 13(12):2715-27.
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Cell Death and Cancer Therapy: Don't Forget to Kill the Cancer Cell! Clin Cancer Res. 2015 Nov 15; 21(22):5015-20.
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Precision medicine for cancer with next-generation functional diagnostics. Nat Rev Cancer. 2015 Dec; 15(12):747-56.
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Activity of a selective inhibitor of nuclear export, selinexor (KPT-330), against AML-initiating cells engrafted into immunosuppressed NSG mice. Leukemia. 2016 Jan; 30(1):190-9.
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Direct and immune-mediated cytotoxicity of interleukin-21 contributes to antitumor effects in mantle cell lymphoma. Blood. 2015 Sep 24; 126(13):1555-64.
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BH3 profiling identifies heterogeneous dependency on Bcl-2 family members in multiple myeloma and predicts sensitivity to BH3 mimetics. Leukemia. 2016 Mar; 30(3):761-4.
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Activity of the Type II JAK2 Inhibitor CHZ868 in B Cell Acute Lymphoblastic Leukemia. Cancer Cell. 2015 Jul 13; 28(1):29-41.
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Drug-induced death signaling strategy rapidly predicts cancer response to chemotherapy. Cell. 2015 Feb 26; 160(5):977-989.
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RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis. Sci Signal. 2014 Dec 23; 7(357):ra122.
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Potent and specific peptide inhibitors of human pro-survival protein Bcl-xL. J Mol Biol. 2015 Mar 27; 427(6 Pt B):1241-1253.
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Bcl-xL controls a switch between cell death modes during mitotic arrest. Cell Death Dis. 2014; 5:e1429.
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Designed BH3 peptides with high affinity and specificity for targeting Mcl-1 in cells. ACS Chem Biol. 2014 Sep 19; 9(9):1962-8.
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Cell and molecular determinants of in vivo efficacy of the BH3 mimetic ABT-263 against pediatric acute lymphoblastic leukemia xenografts. Clin Cancer Res. 2014 Sep 01; 20(17):4520-31.
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Maturation stage of T-cell acute lymphoblastic leukemia determines BCL-2 versus BCL-XL dependence and sensitivity to ABT-199. Cancer Discov. 2014 Sep; 4(9):1074-87.
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Bcl-xL controls a switch between cell death modes during mitotic arrest. Cell Death Dis. 2014 Jun 12; 5:e1291.
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APC(Cdc20) suppresses apoptosis through targeting Bim for ubiquitination and destruction. Dev Cell. 2014 May 27; 29(4):377-91.
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Increased mitochondrial apoptotic priming of human regulatory T cells after allogeneic hematopoietic stem cell transplantation. Haematologica. 2014 Sep; 99(9):1499-508.
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Modulation of Mcl-1 sensitizes glioblastoma to TRAIL-induced apoptosis. Apoptosis. 2014 Apr; 19(4):629-42.
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Decreased mitochondrial priming determines chemoresistance of colon cancer stem cells. Cell Death Differ. 2014 Jul; 21(7):1170-7.
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Failure to induce apoptosis via BCL-2 family proteins underlies lack of efficacy of combined MEK and PI3K inhibitors for KRAS-mutant lung cancers. Cancer Res. 2014 Jun 01; 74(11):3146-56.
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Selective BCL-2 inhibition by ABT-199 causes on-target cell death in acute myeloid leukemia. Cancer Discov. 2014 Mar; 4(3):362-75.
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BID preferentially activates BAK while BIM preferentially activates BAX, affecting chemotherapy response. Mol Cell. 2013 Sep 26; 51(6):751-65.
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Mitochondria: gatekeepers of response to chemotherapy. Trends Cell Biol. 2013 Dec; 23(12):612-9.
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High mitochondrial priming sensitizes hESCs to DNA-damage-induced apoptosis. Cell Stem Cell. 2013 Oct 03; 13(4):483-91.
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Overcoming stroma-mediated treatment resistance in chronic lymphocytic leukemia through BCL-2 inhibition. Leuk Lymphoma. 2013 Aug; 54(8):1823-5.
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p53 regulates a non-apoptotic death induced by ROS. Cell Death Differ. 2013 Nov; 20(11):1465-74.
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BH3 profiling in whole cells by fluorimeter or FACS. Methods. 2013 Jun 01; 61(2):156-64.
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BCL-2 inhibition: stemming the tide of myeloid malignancies. Cell Stem Cell. 2013 Mar 07; 12(3):269-70.
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ABT-199: taking dead aim at BCL-2. Cancer Cell. 2013 Feb 11; 23(2):139-41.
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KPT-330 inhibitor of CRM1 (XPO1)-mediated nuclear export has selective anti-leukaemic activity in preclinical models of T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia. Br J Haematol. 2013 Apr; 161(1):117-27.
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Priming BCL-2 to kill: the combination therapy of tamoxifen and ABT-199 in ER+ breast cancer. Breast Cancer Res. 2013; 15(5):317.
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Relative mitochondrial priming of myeloblasts and normal HSCs determines chemotherapeutic success in AML. Cell. 2012 Oct 12; 151(2):344-55.
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Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors. Cancer Discov. 2012 Oct; 2(10):934-47.
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Decreased mitochondrial apoptotic priming underlies stroma-mediated treatment resistance in chronic lymphocytic leukemia. Blood. 2012 Oct 25; 120(17):3501-9.
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BCL2 suppresses PARP1 function and nonapoptotic cell death. Cancer Res. 2012 Aug 15; 72(16):4193-203.
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Targeting the B-cell lymphoma/leukemia 2 family in cancer. J Clin Oncol. 2012 Sep 01; 30(25):3127-35.
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BH3-only proteins are part of a regulatory network that control the sustained signalling of the unfolded protein response sensor IRE1a. EMBO J. 2012 May 16; 31(10):2322-35.
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BH3 profiling--measuring integrated function of the mitochondrial apoptotic pathway to predict cell fate decisions. Cancer Lett. 2013 May 28; 332(2):202-5.
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Who put the "A" in Atg12: autophagy or apoptosis? Mol Cell. 2011 Dec 23; 44(6):844-5.
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P-selectin glycoprotein ligand regulates the interaction of multiple myeloma cells with the bone marrow microenvironment. Blood. 2012 Feb 09; 119(6):1468-78.
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Pretreatment mitochondrial priming correlates with clinical response to cytotoxic chemotherapy. Science. 2011 Nov 25; 334(6059):1129-33.
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Targeting Bcl-2 in CLL: cui bono? Blood. 2011 Sep 29; 118(13):3453-4.
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The Bcl-2 repertoire of mesothelioma spheroids underlies acquired apoptotic multicellular resistance. Cell Death Dis. 2011 Jun 23; 2:e174.
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A new face of BCL-2 inhibition in CLL. Blood. 2011 Mar 10; 117(10):2750-1.
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Heightened mitochondrial priming is the basis for apoptotic hypersensitivity of CD4+ CD8+ thymocytes. Proc Natl Acad Sci U S A. 2010 Jul 20; 107(29):12895-900.
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Displacement of Bim by Bmf and Puma rather than increase in Bim level mediates paclitaxel-induced apoptosis in breast cancer cells. Cell Death Differ. 2010 Oct; 17(10):1624-35.
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Acquired resistance to ABT-737 in lymphoma cells that up-regulate MCL-1 and BFL-1. Blood. 2010 Apr 22; 115(16):3304-13.
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The landscape of somatic copy-number alteration across human cancers. Nature. 2010 Feb 18; 463(7283):899-905.
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BH3-only proteins and their effects on cancer. Adv Exp Med Biol. 2010; 687:49-63.
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MCL-1-dependent leukemia cells are more sensitive to chemotherapy than BCL-2-dependent counterparts. J Cell Biol. 2009 Nov 02; 187(3):429-42.
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Parkin selectively alters the intrinsic threshold for mitochondrial cytochrome c release. Hum Mol Genet. 2009 Nov 15; 18(22):4317-28.
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Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression. Blood. 2009 Sep 24; 114(13):2699-708.
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Hiding from ABT-737 in lymph nodes. Blood. 2009 Apr 30; 113(18):4132-3.
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Puma strikes Bax. J Cell Biol. 2009 Apr 20; 185(2):189-91.
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Control of mitochondrial apoptosis by the Bcl-2 family. J Cell Sci. 2009 Feb 15; 122(Pt 4):437-41.
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Mimicking the BH3 domain to kill cancer cells. Oncogene. 2008 Dec; 27 Suppl 1:S149-57.
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Alteration of the mitochondrial apoptotic pathway is key to acquired paclitaxel resistance and can be reversed by ABT-737. Cancer Res. 2008 Oct 01; 68(19):7985-94.
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BIM and other BCL-2 family proteins exhibit cross-species conservation of function between zebrafish and mammals. Cell Death Differ. 2008 Jun; 15(6):1063-72.
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Regulation of Bcl-2 family proteins by posttranslational modifications. Curr Mol Med. 2008 Mar; 8(2):102-18.
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Diagnosing and exploiting cancer's addiction to blocks in apoptosis. Nat Rev Cancer. 2008 Feb; 8(2):121-32.
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Rational design of therapeutics targeting the BCL-2 famil: Are some cancer cells primed for death but waiting for a final push?. Programmed Cell Death in Cancer Progression and Therapy. 2008; 159-176.

Rational design of therapeutics targeting the BCL-2 family: are some cancer cells primed for death but waiting for a final push? Adv Exp Med Biol. 2008; 615:159-75.
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Apoptosis Dysregulation in CLL. Chronic Lymphocytic Leukemia. 2008.

Proapoptotic BH3-only BCL-2 family protein BIM connects death signaling from epidermal growth factor receptor inhibition to the mitochondrion. Cancer Res. 2007 Dec 15; 67(24):11867-75.
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BH3 domains define selective inhibitory interactions with BHRF-1 and KSHV BCL-2. Cell Death Differ. 2008 Mar; 15(3):580-8.
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BCL-2 dependence and ABT-737 sensitivity in acute lymphoblastic leukemia. Blood. 2008 Feb 15; 111(4):2300-9.
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BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional chemotherapeutic agents. Cancer Cell. 2007 Aug; 12(2):171-85.
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Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. J Clin Invest. 2007 Jan; 117(1):112-21.
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Restoring cancer's death sentence. Cancer Cell. 2006 Nov; 10(5):343-5.
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Laying the foundations of programmed cell death. Cell Death Differ. 2006 Aug; 13(8):1245-7.
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Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members. Cancer Cell. 2006 May; 9(5):351-65.
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BH3 peptidomimetics potently activate apoptosis and demonstrate single agent efficacy in neuroblastoma. Oncogene. 2006 Aug 03; 25(33):4525-33.
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Growth factor withdrawal and apoptosis: the middle game. Mol Cell. 2006 Mar 17; 21(6):728-30.
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A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib. Cancer Cell. 2005 Nov; 8(5):407-19.
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Pharmacological manipulation of Bcl-2 family members to control cell death. J Clin Invest. 2005 Oct; 115(10):2648-55.
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BCL-2: found bound and drugged! Trends Mol Med. 2005 Oct; 11(10):442-4.
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An inhibitor of Bcl-2 family proteins induces regression of solid tumours. Nature. 2005 Jun 02; 435(7042):677-81.
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Lymphoid Neoplasms. Molecular Hematology. 2005; 105-114.

Antiapoptotic BCL-2 is required for maintenance of a model leukemia. Cancer Cell. 2004 Sep; 6(3):241-9.
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Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1. Nature. 2003 Dec 11; 426(6967):671-6.
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Smallpox and smallpox vaccination. N Engl J Med. 2003 May 08; 348(19):1920-5; author reply 1920-5.
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BH3 domains as BCL-2 inhibitors: prototype cancer therapeutics. Expert Opin Biol Ther. 2003 Apr; 3(2):293-304.
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Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. Cancer Cell. 2002 Sep; 2(3):183-92.
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