CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo

[1]  Darjus F. Tschaharganeh,et al.  CDK9-mediated transcription elongation is required for MYC addiction in hepatocellular carcinoma , 2014, Genes & development.

[2]  T. Cedena,et al.  Prognostic value of deep sequencing method for minimal residual disease detection in multiple myeloma. , 2014, Blood.

[3]  N. Puig,et al.  Critical evaluation of ASO RQ-PCR for minimal residual disease evaluation in multiple myeloma. A comparative analysis with flow cytometry , 2014, Leukemia.

[4]  Erinna F. Lee,et al.  Targeting of MCL-1 kills MYC-driven mouse and human lymphomas even when they bear mutations in p53 , 2014, Genes & development.

[5]  W. Choi,et al.  MYC/BCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Program. , 2013, Blood.

[6]  L. Lam,et al.  ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets , 2013, Nature Medicine.

[7]  A. Oriol,et al.  Superiority of bortezomib, thalidomide, and dexamethasone (VTD) as induction pretransplantation therapy in multiple myeloma: a randomized phase 3 PETHEMA/GEM study. , 2012, Blood.

[8]  J. Carpten,et al.  Clonal competition with alternating dominance in multiple myeloma. , 2012, Blood.

[9]  S. Beà,et al.  SNP-based mapping arrays reveal high genomic complexity in monoclonal gammopathies, from MGUS to myeloma status , 2012, Leukemia.

[10]  E. Lees,et al.  Dinaciclib (SCH 727965), a Novel and Potent Cyclin-Dependent Kinase Inhibitor , 2010, Molecular Cancer Therapeutics.

[11]  R. Gascoyne,et al.  MYC gene rearrangements are associated with a poor prognosis in diffuse large B-cell lymphoma patients treated with R-CHOP chemotherapy. , 2009, Blood.

[12]  R. Wäsch,et al.  ‘Light-chain escape-multiple myeloma’—an escape phenomenon from plateau phase: report of the largest patient series using LC-monitoring , 2009, Journal of Cancer Research and Clinical Oncology.

[13]  C. Scott,et al.  In vivo efficacy of the Bcl-2 antagonist ABT-737 against aggressive Myc-driven lymphomas , 2008, Proceedings of the National Academy of Sciences.

[14]  S. Amente,et al.  P-TEFb is a Crucial Co-Factor for Myc Transactivation , 2007, Cell cycle.

[15]  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.

[16]  Hiroshi Yasui,et al.  Seliciclib (CYC202 or R-roscovitine), a small-molecule cyclin-dependent kinase inhibitor, mediates activity via down-regulation of Mcl-1 in multiple myeloma. , 2005, Blood.

[17]  F. Cavalli,et al.  In vitro activity of cyclin-dependent kinase inhibitor CYC202 (Seliciclib, R-roscovitine) in mantle cell lymphomas. , 2005, Annals of oncology : official journal of the European Society for Medical Oncology.

[18]  S. Korsmeyer,et al.  An inhibitor of Bcl-2 family proteins induces regression of solid tumours , 2005, Nature.

[19]  M Hummel,et al.  Design and standardization of PCR primers and protocols for detection of clonal immunoglobulin and T-cell receptor gene recombinations in suspect lymphoproliferations: Report of the BIOMED-2 Concerted Action BMH4-CT98-3936 , 2003, Leukemia.

[20]  Takashi Okamoto,et al.  c-Myc recruits P-TEFb for transcription, cellular proliferation and apoptosis , 2003, Oncogene.

[21]  M. Fiegl,et al.  Patterns of somatic mutations in VH genes reveal pathways of clonal transformation from MGUS to multiple myeloma. , 2003, Blood.

[22]  D. Price,et al.  Control of RNA Polymerase II Elongation Potential by a Novel Carboxyl-terminal Domain Kinase* , 1996, The Journal of Biological Chemistry.

[23]  K. Langlands,et al.  Clonal selection in acute lymphoblastic leukaemia demonstrated by polymerase chain reaction analysis of immunoglobulin heavy chain and T-cell receptor delta chain rearrangements. , 1993, Leukemia.

[24]  A. Morley,et al.  Advancement of multiple myeloma from diagnosis through plateau phase to progression does not involve a new B-cell clone: evidence from the Ig heavy chain gene. , 1993, Blood.

[25]  C. Heirman,et al.  Evidence that multiple myeloma Ig heavy chain VDJ genes contain somatic mutations but show no intraclonal variation. , 1992, Blood.

[26]  A. Hagemeijer,et al.  Multiple rearranged immunoglobulin genes in childhood acute lymphoblastic leukemia of precursor B-cell origin. , 1991, Leukemia.

[27]  R. Palmiter,et al.  The c-myc oncogene driven by immunoglobulin enhancers induces lymphoid malignancy in transgenic mice , 1985, Nature.

[28]  P. Nowell.  The clonal evolution of tumor cell populations. , 1976, Science.

[29]  These authors contributed equally to this work. , 2007 .

[30]  Marcos González,et al.  Minimal residual disease monitoring in multiple myeloma: a comparison between allelic-specific oligonucleotide real-time quantitative polymerase chain reaction and flow cytometry. , 2005, Haematologica.

[31]  P. L. Bergsagel,et al.  Multiple myeloma: increasing evidence for a multistep transformation process. , 1998, Blood.