Mitochondrial inhibitors circumvent adaptive resistance to venetoclax and cytarabine combination therapy in acute myeloid leukemia

[1]  Yongjin P. Park.  Faculty Opinions recommendation of SCENIC: single-cell regulatory network inference and clustering. , 2021, Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature.

[2]  Xiwei Wu,et al.  Targeting the metabolic vulnerability of acute myeloid leukemia blasts with a combination of venetoclax and 8-chloro-adenosine , 2021, Journal of Hematology & Oncology.

[3]  D. Figarella-Branger,et al.  SCENITH: A Flow Cytometry-Based Method to Functionally Profile Energy Metabolism with Single-Cell Resolution. , 2020, Cell metabolism.

[4]  Austin E. Gillen,et al.  Fatty acid metabolism underlies venetoclax resistance in acute myeloid leukemia stem cells , 2020, Nature Cancer.

[5]  F. Bost,et al.  Autophagy regulates fatty acid availability for oxidative phosphorylation through mitochondria-endoplasmic reticulum contact sites , 2020, Nature Communications.

[6]  D. Bottomly,et al.  Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia , 2020, Nature Cancer.

[7]  J. Welch,et al.  Outcomes of relapsed or refractory acute myeloid leukemia after frontline hypomethylating agent and venetoclax regimens. , 2020, Haematologica.

[8]  G. Dupont,et al.  Dual dynamics of mitochondrial permeability transition pore opening , 2020, Scientific Reports.

[9]  M. Konopleva,et al.  Advances in the Treatment of Acute Myeloid Leukemia: New Drugs and New Challenges. , 2020, Cancer discovery.

[10]  L. Harrington,et al.  Mitochondrial Oxidative Phosphorylation Regulates the Fate Decision between Pathogenic Th17 and Regulatory T Cells , 2020, Cell reports.

[11]  Qi Zhang,et al.  Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML. , 2020, Blood.

[12]  John G Doench,et al.  Targeting Regnase-1 programs long-lived effector T cells for cancer therapy , 2019, Nature.

[13]  M. Verzi,et al.  HNF4 Regulates Fatty Acid Oxidation and is Required for Renewal of Intestinal Stem Cells in Mice. , 2019, Gastroenterology.

[14]  T. Ketela,et al.  Inhibition of mitochondrial translation overcomes venetoclax resistance in AML through activation of the integrated stress response , 2019, Science Translational Medicine.

[15]  L. Linares,et al.  Metabolic functions of the tumor suppressor p53: Implications in normal physiology, metabolic disorders, and cancer , 2019, Molecular metabolism.

[16]  C. Récher,et al.  Targeting Myeloperoxidase Disrupts Mitochondrial Redox Balance and Overcomes Cytarabine Resistance in Human Acute Myeloid Leukemia. , 2019, Cancer research.

[17]  Christopher J. Ott,et al.  Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies. , 2019, Cancer cell.

[18]  S. Asthana,et al.  Clonal selection with Ras pathway activation mediates secondary clinical resistance to selective FLT3 inhibition in acute myeloid leukemia. , 2019, Cancer discovery.

[19]  J. Sarry,et al.  Help from outside: cysteine to survive in AML. , 2019, Blood.

[20]  A. D’Alessandro,et al.  Cysteine depletion targets leukemia stem cells through inhibition of electron transport complex II. , 2019, Blood.

[21]  M. Tosolini,et al.  Single-Cell Signature Explorer for comprehensive visualization of single cell signatures across scRNA-seq datasets , 2019, bioRxiv.

[22]  Mike Tyers,et al.  Mubritinib Targets the Electron Transport Chain Complex I and Reveals the Landscape of OXPHOS Dependency in Acute Myeloid Leukemia. , 2019, Cancer cell.

[23]  J. Rathmell,et al.  Mitochondrial Homeostasis in AML and Gasping for Response in Resistance to BCL2 Blockade. , 2019, Cancer discovery.

[24]  T. Sakellaropoulos,et al.  Targeting Mitochondrial Structure Sensitizes Acute Myeloid Leukemia to Venetoclax Treatment. , 2019, Cancer discovery.

[25]  Stefano Monti,et al.  hypeR: An R Package for Geneset Enrichment Workflows , 2019, bioRxiv.

[26]  S. McWeeney,et al.  The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML Cells. , 2019, Cancer discovery.

[27]  C. McCall,et al.  Systematic Dissection of the Metabolic-Apoptotic Interface in AML Reveals Heme Biosynthesis to Be a Regulator of Drug Sensitivity. , 2019, Cell metabolism.

[28]  M. Stagi,et al.  Mitochondrial respiratory chain deficiency inhibits lysosomal hydrolysis , 2019, Autophagy.

[29]  R. Satija,et al.  Normalization and variance stabilization of single-cell RNA-seq data using regularized negative binomial regression , 2019, Genome Biology.

[30]  S. Haferkamp,et al.  Metabolic targeting synergizes with MAPK inhibition and delays drug resistance in melanoma. , 2019, Cancer letters.

[31]  G. Boucher,et al.  Genetic characterization of ABT-199 sensitivity in human AML , 2018, Leukemia.

[32]  Austin E. Gillen,et al.  Venetoclax with azacitidine disrupts energy metabolism and targets leukemia stem cells in patients with acute myeloid leukemia , 2018, Nature Medicine.

[33]  A. D’Alessandro,et al.  Inhibition of Amino Acid Metabolism Selectively Targets Human Leukemia Stem Cells. , 2018, Cancer cell.

[34]  Beth Wilmot,et al.  Functional Genomic Landscape of Acute Myeloid Leukemia , 2018, Nature.

[35]  E. Olejniczak,et al.  A Novel MCL1 Inhibitor Combined with Venetoclax Rescues Venetoclax-Resistant Acute Myelogenous Leukemia. , 2018, Cancer discovery.

[36]  B. Leber,et al.  Identification of Chemotherapy-Induced Leukemic-Regenerating Cells Reveals a Transient Vulnerability of Human AML Recurrence. , 2018, Cancer cell.

[37]  J. Chipuk,et al.  FBXW7 regulates a mitochondrial transcription program by modulating MITF , 2018, Pigment cell & melanoma research.

[38]  A. Rasola,et al.  Metabolic Plasticity of Tumor Cell Mitochondria , 2018, Front. Oncol..

[39]  K. Flaherty,et al.  Toward Minimal Residual Disease-Directed Therapy in Melanoma , 2018, Cell.

[40]  M. Protopopova,et al.  An inhibitor of oxidative phosphorylation exploits cancer vulnerability , 2018, Nature Medicine.

[41]  H. Düssmann,et al.  BCL2 and BCL(X)L selective inhibitors decrease mitochondrial ATP production in breast cancer cells and are synthetically lethal when combined with 2-deoxy-D-glucose , 2018, Oncotarget.

[42]  Bo Wang,et al.  Acquired resistance to IDH inhibition through trans or cis dimer-interface mutations , 2018, Nature.

[43]  David S. Wishart,et al.  MetaboAnalyst 4.0: towards more transparent and integrative metabolomics analysis , 2018, Nucleic Acids Res..

[44]  Paul Hoffman,et al.  Integrating single-cell transcriptomic data across different conditions, technologies, and species , 2018, Nature Biotechnology.

[45]  Marina Konopleva,et al.  Synthetic Lethality of Combined Bcl-2 Inhibition and p53 Activation in AML: Mechanisms and Superior Antileukemic Efficacy. , 2017, Cancer cell.

[46]  M. Selak,et al.  Resistance Is Futile: Targeting Mitochondrial Energetics and Metabolism to Overcome Drug Resistance in Cancer Treatment. , 2017, Cell metabolism.

[47]  P. Siegel,et al.  PGC-1α Promotes Breast Cancer Metastasis and Confers Bioenergetic Flexibility against Metabolic Drugs. , 2017, Cell metabolism.

[48]  W. Parak,et al.  Maintenance of cellular respiration indicates drug resistance in acute myeloid leukemia. , 2017, Leukemia research.

[49]  S. Fesik,et al.  MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation. , 2017, Cell metabolism.

[50]  Eyal Gottlieb,et al.  Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemic stem cells , 2017, Nature Medicine.

[51]  M. Previati,et al.  Calcium regulates cell death in cancer: Roles of the mitochondria and mitochondria-associated membranes (MAMs). , 2017, Biochimica et biophysica acta. Bioenergetics.

[52]  M. Carroll,et al.  Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism. , 2017, Cancer discovery.

[53]  Gary D Bader,et al.  Tracing the origins of relapse in acute myeloid leukaemia to stem cells , 2017, Nature.

[54]  J. Aerts,et al.  SCENIC: Single-cell regulatory network inference and clustering , 2017, Nature Methods.

[55]  E. Rego,et al.  Targeting the mitochondria in acute myeloid leukemia , 2017, Applied Cancer Research.

[56]  Joshua D. Rabinowitz,et al.  Metabolite Spectral Accuracy on Orbitraps. , 2017, Analytical chemistry.

[57]  G. Bultynck,et al.  Modulation of Ca2+ Signaling by Anti-apoptotic B-Cell Lymphoma 2 Proteins at the Endoplasmic Reticulum–Mitochondrial Interface , 2017, Front. Oncol..

[58]  M. Brand,et al.  Quantifying intracellular rates of glycolytic and oxidative ATP production and consumption using extracellular flux measurements , 2017, The Journal of Biological Chemistry.

[59]  A. Letai,et al.  Efficacy and Biological Correlates of Response in a Phase II Study of Venetoclax Monotherapy in Patients with Acute Myelogenous Leukemia. , 2016, Cancer discovery.

[60]  K. Moore,et al.  Making a Hematopoietic Stem Cell. , 2016, Trends in cell biology.

[61]  C. Récher,et al.  A robust and rapid xenograft model to assess efficacy of chemotherapeutic agents for human acute myeloid leukemia , 2015, Blood Cancer Journal.

[62]  L. Ligat,et al.  Human Monocyte Recognition of Adenosine-Based Cyclic Dinucleotides Unveils the A2a Gαs Protein-Coupled Receptor Tonic Inhibition of Mitochondrially Induced Cell Death , 2014, Molecular and Cellular Biology.

[63]  Lorenzo Galluzzi,et al.  Metabolic control of cell death , 2014, Science.

[64]  John M. Asara,et al.  Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function , 2014, Nature.

[65]  Eun Mi Kim,et al.  Nuclear and cytoplasmic p53 suppress cell invasion by inhibiting respiratory Complex-I activity via Bcl-2 family proteins , 2014, Oncotarget.

[66]  A. Letai,et al.  Selective BCL-2 inhibition by ABT-199 causes on-target cell death in acute myeloid leukemia. , 2014, Cancer discovery.

[67]  G. Gillet,et al.  Non-apoptotic roles of Bcl-2 family: the calcium connection. , 2013, Biochimica et biophysica acta.

[68]  G. Bultynck,et al.  Altered Ca(2+) signaling in cancer cells: proto-oncogenes and tumor suppressors targeting IP3 receptors. , 2013, Biochimica et biophysica acta.

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

[70]  John M. Ashton,et al.  BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. , 2013, Cell stem cell.

[71]  J. Nordenström.  The calcium connection , 2013 .

[72]  A. Letai,et al.  Relative Mitochondrial Priming of Myeloblasts and Normal HSCs Determines Chemotherapeutic Success in AML , 2012, Cell.

[73]  V. Pertegato,et al.  Assessment of mitochondrial respiratory chain enzymatic activities on tissues and cultured cells , 2012, Nature Protocols.

[74]  Kirby D. Johnson,et al.  Master regulatory GATA transcription factors: mechanistic principles and emerging links to hematologic malignancies , 2012, Nucleic acids research.

[75]  A. Letai,et al.  Pretreatment Mitochondrial Priming Correlates with Clinical Response to Cytotoxic Chemotherapy , 2011, Science.

[76]  Paolo Bernardi,et al.  Mitochondrial permeability transition in Ca(2+)-dependent apoptosis and necrosis. , 2011, Cell calcium.

[77]  Joshua D Rabinowitz,et al.  Metabolomic analysis and visualization engine for LC-MS data. , 2010, Analytical chemistry.

[78]  Rafael A. Irizarry,et al.  A framework for oligonucleotide microarray preprocessing , 2010, Bioinform..

[79]  T. Chou.  Drug combination studies and their synergy quantification using the Chou-Talalay method. , 2010, Cancer research.

[80]  K. Kaluarachchi,et al.  Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction. , 2010, The Journal of clinical investigation.

[81]  R. Denton,et al.  Regulation of mitochondrial dehydrogenases by calcium ions. , 2009, Biochimica et biophysica acta.

[82]  Guy A Rutter,et al.  Mitochondrial calcium as a key regulator of mitochondrial ATP production in mammalian cells. , 2009, Biochimica et biophysica acta.

[83]  A. Halestrap.  What is the mitochondrial permeability transition pore? , 2009, Journal of molecular and cellular cardiology.

[84]  John Calvin Reed,et al.  Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia. , 2006, Cancer cell.

[85]  Rainer Breitling,et al.  RankProd: a bioconductor package for detecting differentially expressed genes in meta-analysis , 2006, Bioinform..

[86]  K. Gunter,et al.  Mitochondrial calcium transport: mechanisms and functions. , 2000, Cell calcium.

[87]  G. Miotto,et al.  Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence. , 1999, Biophysical journal.

[88]  J C Reed,et al.  Mitochondria and apoptosis. , 1998, Science.

[89]  Austin E. Gillen,et al.  Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia , 2020 .

[90]  C. J. Noorden,et al.  The history of Z-VAD-FMK, a tool for understanding the significance of caspase inhibition. , 2001 .

[91]  C. V. van Noorden.  The history of Z-VAD-FMK, a tool for understanding the significance of caspase inhibition. , 2001, Acta histochemica.