MLL-Rearranged Acute Lymphoblastic Leukemias Activate BCL-2 through H3K79 Methylation and Are Sensitive to the BCL-2-Specific Antagonist ABT-199
暂无分享,去创建一个
K. Coombes | A. Letai | Nianxiang Zhang | I. Jeremias | M. Konopleva | M. Andreeff | H. Kantarjian | L. Golfman | S. Kornblau | K. Kojima | S. O'brien | J. Leverson | Y. Qiu | P. Zhou | Laura J. Godfrey | T. Milne | H. Geng | M. Wunderlich | J. Mulloy | P. North | M. Müschen | P. Zweidler-McKay | Helen Ma | I. Marzo | R. Jacamo | J. Kerry | E. Park | K. Harutyunyan | E. O'Brien | E. Ballabio | J. Benito | T. Chonghaile | L. Hogdal | D. Thomas | Lakiesha Debose | Óscar Gonzalo | Karine G. Harutyunyan
[1] N. Zeleznik-Le,et al. Degree of recruitment of DOT1L to MLL-AF9 defines level of H3K79 Di- and tri-methylation on target genes and transformation potential. , 2015, Cell reports.
[2] S. Molica. Highlights in the treatment of chronic lymphocytic leukemia from the 2014 meeting of the American Society of Hematology , 2015, Expert review of hematology.
[3] T. Chambers,et al. BH3 Inhibitor Sensitivity and Bcl-2 Dependence in Primary Acute Lymphoblastic Leukemia Cells. , 2015, Cancer research.
[4] Dolores Diaz,et al. Exploiting selective BCL-2 family inhibitors to dissect cell survival dependencies and define improved strategies for cancer therapy , 2015, Science Translational Medicine.
[5] John G Doench,et al. DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia , 2015, Nature Medicine.
[6] Cheng Cheng,et al. The landscape of somatic mutations in Infant MLL rearranged acute lymphoblastic leukemias , 2015, Nature Genetics.
[7] F. Behm,et al. Intensified chemotherapy without SCT in infant ALL: Results from COG P9407 (Cohort 3) , 2015, Pediatric blood & cancer.
[8] A. Letai,et al. Cell and Molecular Determinants of In Vivo Efficacy of the BH3 Mimetic ABT-263 against Pediatric Acute Lymphoblastic Leukemia Xenografts , 2014, Clinical Cancer Research.
[9] M. Loh,et al. Maturation stage of T-cell acute lymphoblastic leukemia determines BCL-2 versus BCL-XL dependence and sensitivity to ABT-199. , 2014, Cancer discovery.
[10] J. Cayuela,et al. Oncogenetics and minimal residual disease are independent outcome predictors in adult patients with acute lymphoblastic leukemia. , 2014, Blood.
[11] A. Letai,et al. Selective BCL-2 inhibition by ABT-199 causes on-target cell death in acute myeloid leukemia. , 2014, Cancer discovery.
[12] Matthew E. Ritchie,et al. Targeting BCL-2 with the BH3 mimetic ABT-199 in estrogen receptor-positive breast cancer. , 2013, Cancer cell.
[13] N. Heerema,et al. Potent obatoclax cytotoxicity and activation of triple death mode killing across infant acute lymphoblastic leukemia. , 2013, Blood.
[14] S. Cory,et al. ABT-199, a new Bcl-2-specific BH3 mimetic, has in vivo efficacy against aggressive Myc-driven mouse lymphomas without provoking thrombocytopenia. , 2013, Blood.
[15] Thomas A. Milne,et al. RUNX1 Is a Key Target in t(4;11) Leukemias that Contributes to Gene Activation through an AF4-MLL Complex Interaction , 2013, Cell reports.
[16] T. Cierpicki,et al. Leukemia fusion target AF9 is an intrinsically disordered transcriptional regulator that recruits multiple partners via coupled folding and binding. , 2013, Structure.
[17] L. Lam,et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets , 2013, Nature Medicine.
[18] J. Naval,et al. Direct Interaction of Bax and Bak Proteins with Bcl-2 Homology Domain 3 (BH3)-only Proteins in Living Cells Revealed by Fluorescence Complementation* , 2013, The Journal of Biological Chemistry.
[19] I. Jeremias,et al. In Vivo Imaging Enables High Resolution Preclinical Trials on Patients’ Leukemia Cells Growing in Mice , 2012, PloS one.
[20] Michael C. Rusch,et al. Abstract 4869: Whole genome sequence analysis of MLL rearranged infant acute lymphoblastic leukemias reveals remarkably few somatic mutations: A Report From the St Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project , 2012 .
[21] R. Lock,et al. Pharmacokinetic Modeling of an Induction Regimen for In Vivo Combined Testing of Novel Drugs against Pediatric Acute Lymphoblastic Leukemia Xenografts , 2012, PloS one.
[22] F. Peale,et al. Navitoclax (ABT-263) Reduces Bcl-xL–Mediated Chemoresistance in Ovarian Cancer Models , 2012, Molecular Cancer Therapeutics.
[23] J. Hess,et al. MLL-ENL inhibits polycomb repressive complex 1 to achieve efficient transformation of hematopoietic cells. , 2011, Cell reports.
[24] Steven M Kornblau,et al. Abnormal expression of FLI1 protein is an adverse prognostic factor in acute myeloid leukemia. , 2011, Blood.
[25] S. Robson,et al. Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia , 2011, Nature.
[26] H. Maecker,et al. The Bcl-2/Bcl-XL/Bcl-w Inhibitor, Navitoclax, Enhances the Activity of Chemotherapeutic Agents In Vitro and In Vivo , 2011, Molecular Cancer Therapeutics.
[27] C. Allis,et al. Function of leukemogenic mixed lineage leukemia 1 (MLL) fusion proteins through distinct partner protein complexes , 2011, Proceedings of the National Academy of Sciences.
[28] Adam R. Johnson,et al. Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7 , 2011, Nature.
[29] Sebastian Herzog,et al. BCL6 enables Ph+ acute lymphoblastic leukemia cells to survive BCR-ABL1 kinase inhibition , 2011, Nature.
[30] J. Zha,et al. Navitoclax Enhances the Efficacy of Taxanes in Non–Small Cell Lung Cancer Models , 2011, Clinical Cancer Research.
[31] T. Dingermann,et al. The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4. , 2010, Blood.
[32] A. Shilatifard,et al. Linking H3K79 trimethylation to Wnt signaling through a novel Dot1-containing complex (DotCom). , 2010, Genes & development.
[33] A. Roberts,et al. The Bcl-2 Homology Domain 3 Mimetic ABT-737 Targets the Apoptotic Machinery in Acute Lymphoblastic Leukemia Resulting in Synergistic in Vitro and in Vivo Interactions with Established Drugs , 2010, Molecular Pharmacology.
[34] M. Cleary,et al. A higher-order complex containing AF4 and ENL family proteins with P-TEFb facilitates oncogenic and physiologic MLL-dependent transcription. , 2010, Cancer cell.
[35] A. Shilatifard,et al. AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia. , 2010, Molecular cell.
[36] J. Testa,et al. FAS-Associated Factor 1 (FAF1): Diverse functions and implications for oncogenesis , 2009, Cell cycle.
[37] T. Volkert,et al. Aberrant chromatin at genes encoding stem cell regulators in human mixed-lineage leukemia. , 2008, Genes & development.
[38] Xiaobo Xia,et al. H3K79 methylation profiles define murine and human MLL-AF4 leukemias. , 2008, Cancer cell.
[39] C. Felix,et al. Abundant anti‐apoptotic BCL‐2 is a molecular target in leukaemias with t(4;11) translocation , 2008, British journal of haematology.
[40] S. Armstrong,et al. BCL-2 dependence and ABT-737 sensitivity in acute lymphoblastic leukemia. , 2008, Blood.
[41] A. Chinnaiyan,et al. A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification. , 2007, Blood.
[42] R. Lock,et al. Activity of vincristine, L-ASP, and dexamethasone against acute lymphoblastic leukemia is enhanced by the BH3-mimetic ABT-737 in vitro and in vivo. , 2007, Blood.
[43] R. Pieters,et al. A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial , 2007, The Lancet.
[44] S. Armstrong,et al. Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members. , 2006, Cancer cell.
[45] P. Hadwiger,et al. Targeting MLL-AF4 with short interfering RNAs inhibits clonogenicity and engraftment of t(4;11)-positive human leukemic cells. , 2005, Blood.
[46] L. Lam,et al. Souers AJ, Leverson JD, Boghaert ER et al.ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med 19:202-208 , 2013 .
[47] K. Zhao,et al. Chromatin immunoprecipitation (ChIP) for analysis of histone modifications and chromatin-associated proteins. , 2009, Methods in molecular biology.