Novel covalent CDK7 inhibitor potently induces apoptosis in acute myeloid leukemia and synergizes with Venetoclax

[1]  A. Wei,et al.  Contemporary Approach to Acute Myeloid Leukemia Therapy in 2022. , 2022, American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting.

[2]  A. Letai,et al.  Activation of RAS/MAPK pathway confers MCL-1 mediated acquired resistance to BCL-2 inhibitor venetoclax in acute myeloid leukemia , 2022, Signal Transduction and Targeted Therapy.

[3]  L. Newell,et al.  Advances in acute myeloid leukemia , 2021, BMJ.

[4]  M. Tallman,et al.  Harnessing the benefits of available targeted therapies in acute myeloid leukaemia. , 2021, The Lancet. Haematology.

[5]  J. McGowan-Jordan,et al.  Re: International System for Human Cytogenetic or Cytogenomic Nomenclature (ISCN): Some Thoughts, by T. Liehr , 2021, Cytogenetic and Genome Research.

[6]  A. Roberts,et al.  BCL2 inhibitors and MCL1 inhibitors for hematological malignancies. , 2021, Blood.

[7]  Tuersunayi Abudureheman,et al.  CDK7 Inhibitor THZ1 Induces the Cell Apoptosis of B-Cell Acute Lymphocytic Leukemia by Perturbing Cellular Metabolism , 2021, Frontiers in Oncology.

[8]  G. Chatterjee,et al.  Clinical impact of panel-based error-corrected next generation sequencing versus flow cytometry to detect measurable residual disease (MRD) in acute myeloid leukemia (AML) , 2021, Leukemia.

[9]  M. Konopleva,et al.  Acute myeloid leukemia: current progress and future directions , 2021, Blood Cancer Journal.

[10]  Ki Yun Kim,et al.  G1 Cell Cycle Arrest and Extrinsic Apoptotic Mechanisms Underlying the Anti-Leukemic Activity of CDK7 Inhibitor BS-181 , 2020, Cancers.

[11]  Zachary L. Maas,et al.  Selective inhibition of CDK7 reveals high-confidence targets and new models for TFIIH function in transcription , 2020, Genes & development.

[12]  P. Vyas,et al.  New directions for emerging therapies in acute myeloid leukemia: the next chapter , 2020, Blood Cancer Journal.

[13]  Yue Jiang,et al.  Pharmacological inhibition of CDK7 by THZ1 impairs tumor growth in p53-mutated HNSCC. , 2020, Oral diseases.

[14]  Dayanne M. Castro,et al.  CDK7 Inhibition Potentiates Genome Instability Triggering Anti-tumor Immunity in Small Cell Lung Cancer. , 2019, Cancer cell.

[15]  R. Damoiseaux,et al.  A high-throughput screen identifies that CDK7 activates glucose consumption in lung cancer cells , 2019, Nature Communications.

[16]  David A. Orlando,et al.  Discovery and characterization of SY-1365, a selective, covalent inhibitor of CDK7. , 2019, Cancer research.

[17]  Charles Y. Lin,et al.  Development of a Selective CDK7 Covalent Inhibitor Reveals Predominant Cell-Cycle Phenotype. , 2019, Cell chemical biology.

[18]  P. Cramer,et al.  MYC Recruits SPT5 to RNA Polymerase II to Promote Processive Transcription Elongation , 2019, Molecular cell.

[19]  Z. Estrov,et al.  MYC protein expression is an important prognostic factor in acute myeloid leukemia , 2019, Leukemia & lymphoma.

[20]  Charles Y. Lin,et al.  Targeting MYC dependency in ovarian cancer through inhibition of CDK7 and CDK12/13 , 2018, eLife.

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

[22]  Y. Ben-Neriah,et al.  Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models , 2018, Cell.

[23]  Simak Ali,et al.  ICEC0942, an Orally Bioavailable Selective Inhibitor of CDK7 for Cancer Treatment , 2018, Molecular Cancer Therapeutics.

[24]  M. Levis,et al.  Advances in targeted therapy for acute myeloid leukaemia , 2018, British journal of haematology.

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

[26]  Qi Liu,et al.  The CDK7 inhibitor THZ1 alters RNA polymerase dynamics at the 5′ and 3′ ends of genes , 2017, Nucleic acids research.

[27]  R. Mesa,et al.  Combined venetoclax and alvocidib in acute myeloid leukemia , 2017, Oncotarget.

[28]  Zhenfeng Zhang,et al.  Preclinical Efficacy and Molecular Mechanism of Targeting CDK7-Dependent Transcriptional Addiction in Ovarian Cancer , 2017, Molecular Cancer Therapeutics.

[29]  G. O'Neill,et al.  Cyclin-dependent kinase 7 is a therapeutic target in high-grade glioma , 2017, Oncogenesis.

[30]  A. Letai,et al.  Discovery and biological characterization of potent myeloid cell leukemia‐1 inhibitors , 2017, FEBS letters.

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

[32]  M. Andreeff,et al.  Pharmacological activation of wild-type p53 in the therapy of leukemia. , 2016, Experimental hematology.

[33]  C. Tse,et al.  Potent and selective small-molecule MCL-1 inhibitors demonstrate on-target cancer cell killing activity as single agents and in combination with ABT-263 (navitoclax) , 2015, Cell Death and Disease.

[34]  D. MacPherson,et al.  Treating transcriptional addiction in small cell lung cancer. , 2014, Cancer cell.

[35]  Bandana Sharma,et al.  CDK7 Inhibition Suppresses Super-Enhancer-Linked Oncogenic Transcription in MYCN-Driven Cancer , 2014, Cell.

[36]  T. Albert,et al.  Cyclin-Dependent Kinase 7 Controls mRNA Synthesis by Affecting Stability of Preinitiation Complexes, Leading to Altered Gene Expression, Cell Cycle Progression, and Survival of Tumor Cells , 2014, Molecular and Cellular Biology.

[37]  Neville E. Sanjana,et al.  Improved vectors and genome-wide libraries for CRISPR screening , 2014, Nature Methods.

[38]  Sridhar Ramaswamy,et al.  Targeting transcription regulation in cancer with a covalent CDK7 inhibitor , 2014, Nature.

[39]  M. Barbacid,et al.  Genetic inactivation of Cdk7 leads to cell cycle arrest and induces premature aging due to adult stem cell exhaustion , 2012, The EMBO journal.

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

[41]  M. Cole,et al.  The Myc Transactivation Domain Promotes Global Phosphorylation of the RNA Polymerase II Carboxy-Terminal Domain Independently of Direct DNA Binding , 2007, Molecular and Cellular Biology.

[42]  M. Cole,et al.  The Proto-oncogene c-myc Acts through the Cyclin-dependent Kinase (Cdk) Inhibitor p27Kip1to Facilitate the Activation of Cdk4/6 and Early G1Phase Progression* , 2002, The Journal of Biological Chemistry.

[43]  M. Mathews,et al.  Three RNA Polymerase II Carboxyl-terminal Domain Kinases Display Distinct Substrate Preferences* , 2001, The Journal of Biological Chemistry.

[44]  X. Chen,et al.  p53 is phosphorylated by CDK7-cyclin H in a p36MAT1-dependent manner , 1997, Molecular and cellular biology.

[45]  Hilde van der Togt,et al.  Publisher's Note , 2003, J. Netw. Comput. Appl..

[46]  H. Kantarjian,et al.  Acute myeloid leukemia , 2018, Methods in Molecular Biology.