Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets.
Aged
Aged, 80 and over
Animals
Cell Line, Tumor
Female
Fusion Proteins, bcr-abl
/ genetics
Gene Expression Profiling
/ methods
Glucocorticoids
/ genetics
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ genetics
Male
Mice
Middle Aged
Oncogenes
/ genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma
/ genetics
Proteomics
/ methods
Signal Transduction
/ genetics
Transcription, Genetic
/ genetics
Up-Regulation
/ genetics
Journal
Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
received:
27
07
2020
accepted:
25
10
2020
revised:
30
09
2020
pubmed:
11
11
2020
medline:
17
8
2021
entrez:
10
11
2020
Statut:
ppublish
Résumé
The oncogenic protein Bcr-Abl has two major isoforms, p190
Identifiants
pubmed: 33168949
doi: 10.1038/s41375-020-01082-4
pii: 10.1038/s41375-020-01082-4
pmc: PMC8257498
doi:
Substances chimiques
Glucocorticoids
0
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1964-1975Références
Pane F, Intrieri M, Quintarelli C, Izzo B, Muccioli GC, Salvatore F. BCR/ABL genes and leukemic phenotype: from molecular mechanisms to clinical correlations. Oncogene. 2002;21:8652–67.
pubmed: 12476311
Hantschel O. Structure, regulation, signaling, and targeting of Abl kinases in cancer. Genes Cancer. 2012;3:436–46.
pubmed: 23226581
pmcid: 3513796
Wong S, Witte ON. The BCR-ABL story: bench to bedside and back. Annu Rev Immunol. 2004;22:247–306.
pubmed: 15032571
Demehri S, O’Hare T, Eide CA, Smith CA, Tyner JW, Druker BJ, et al. The function of the pleckstrin homology domain in BCR–ABL-mediated leukemogenesis. Leukemia. 2010;24:226–9.
pubmed: 19759561
Roumiantsev S, de Aos IE, Varticovski L, Ilaria RL, Van, Etten RA. The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase. Blood. 2001;97:4–13.
pubmed: 11133737
Score J, Calasanz MJ, Ottman O, Pane F, Yeh RF, Sobrinho-Simões MA, et al. Analysis of genomic breakpoints in p190 and p210 BCR-ABL indicate distinct mechanisms of formation. Leukemia. 2010;24:1742–50.
pubmed: 20703256
Baccarani M, Iacobucci I, Chiaretti S, Foà’ R, Balasubramanian P, Paietta E, et al. In Ph+BCR-ABL1 P210+ acute lymphoblastic leukemia the e13a2 (B2A2) transcript is prevalent. Leukemia 2020;34:929–31.
pubmed: 31595038
Burmeister T, Schwartz S, Bartram CR, Gökbuget N, Hoelzer D, Thiel E. Patients’ age and BCR-ABL frequency in adult B-precursor ALL: a retrospective analysis from the GMALL study group. Blood. 2008;112:918–9.
pubmed: 18650471
Chereda B, Melo JV. The Biology and Pathogenesis of Chronic Myeloid Leukemia. In: Hehlmann R, editor. Chronic Myeloid Leukemia. Cham: Springer International Publishing; 2016. p. 17–39. (Hematologic Malignancies). 10.1007/978-3-319-33198-0_2
Verma D, Kantarjian HM, Jones D, Luthra R, Borthakur G, Verstovsek S, et al. Chronic myeloid leukemia (CML) with P190 BCR-ABL: analysis of characteristics, outcomes, and prognostic significance. Blood. 2009;114:2232–5.
pubmed: 19531657
pmcid: 4828071
Arun AK, Senthamizhselvi A, Mani S, Vinodhini K, Janet NB, Lakshmi KM, et al. Frequency of rare BCR-ABL1 fusion transcripts in chronic myeloid leukemia patients. Int J Lab Hematol. 2017;39:235–42.
pubmed: 28035733
Molica M, Zacheo I, Diverio D, Alimena G, Breccia M. Long-term outcome of chronic myeloid leukaemia patients with p210 and p190 co-expression at baseline. Br J Haematol. 2015;169:148–50.
pubmed: 25296902
Pardanani A, Tefferi A, Litzow MR, Zent C, Hogan WJ, McClure RF, et al. Chronic myeloid leukemia with p190BCR-ABL: prevalence, morphology, tyrosine kinase inhibitor response, and kinase domain mutation analysis. Blood. 2009;114:3502–3.
pubmed: 19833856
Hur M, Song EY, Kang S-H, Shin D-H, Kim JY, Park SS, et al. Lymphoid preponderance and the absence of basophilia and splenomegaly are frequent in m-bcr-positive chronic myelogenous leukemia. Ann Hematol. 2002;81:219–23.
pubmed: 11976825
Gong Z, Medeiros LJ, Cortes JE, Zheng L, Khoury JD, Wang W, et al. Clinical and prognostic significance of e1a2 BCR-ABL1 transcript subtype in chronic myeloid leukemia. Blood Cancer J. 2017;7:e583. 14
pubmed: 28708130
pmcid: 5549254
Järås M, Johnels P, Agerstam H, Lassen C, Rissler M, Edén P, et al. Expression of P190 and P210 BCR/ABL1 in normal human CD34(+) cells induces similar gene expression profiles and results in a STAT5-dependent expansion of the erythroid lineage. Exp Hematol. 2009;37:367–75.
pubmed: 19135771
Van Etten RA. Studying the pathogenesis of BCR-ABL+ leukemia in mice. Oncogene 2002;21(Dec):8643–51.
pubmed: 12476310
Li S, Ilaria RL, Million RP, Daley GQ, Van, Etten RA. The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity. J Exp Med. 1999;189:1399–412.
pubmed: 10224280
pmcid: 2193055
Kovacic B, Hoelbl A, Litos G, Alacakaptan M, Schuster C, Fischhuber KM, et al. Diverging fates of cells of origin in acute and chronic leukaemia. EMBO Mol Med. 2012;4:283–97.
pubmed: 22323443
pmcid: 3376859
Ilaria RL, Van, Etten RA. P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members. J Biol Chem. 1996;271:31704–10.
pubmed: 8940193
Harnois T, Constantin B, Rioux A, Grenioux E, Kitzis A, Bourmeyster N. Differential interaction and activation of Rho family GTPases by p210bcr-abl and p190bcr-abl. Oncogene. 2003;22:6445–54.
pubmed: 14508524
Goss VL, Lee KA, Moritz A, Nardone J, Spek EJ, MacNeill J, et al. A common phosphotyrosine signature for the Bcr-Abl kinase. Blood. 2006;107:4888–97.
pubmed: 16497976
pmcid: 1895816
Reckel S, Hamelin R, Georgeon S, Armand F, Jolliet Q, Chiappe D, et al. Differential signaling networks of Bcr–Abl p210 and p190 kinases in leukemia cells defined by functional proteomics. Leukemia. 2017;31:1502–12.
pubmed: 28111465
pmcid: 5508078
Cutler JA, Tahir R, Sreenivasamurthy SK, Mitchell C, Renuse S, Nirujogi RS, et al. Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis. Leukemia. 2017;31:1513–24.
pubmed: 28210003
Doma E, Mayer I, Brandstoetter T, Maurer B, Grausenburger R, Menzl I, et al. A cutting-edge approach unravels a novel role for CDK6 in leukemic progenitor cells. bioRxiv. 2020 Oct;2020.10.05.325886.
Adnan Awad S, Dufva O, Ianevski A, Ghimire B, Koski J, Maliniemi P, et al. RUNX1 mutations in blast-phase chronic myeloid leukemia associate with distinct phenotypes, transcriptional profiles, and drug responses. Leukemia. 2020; 10.1038/s41375-020-01011-5.
Pemovska T, Kontro M, Yadav B, Edgren H, Eldfors S, Szwajda A, et al. Individualized systems medicine strategy to tailor treatments for patients with chemorefractory acute myeloid leukemia. Cancer Disco. 2013;3:1416–29.
Agirre X, Román-Gómez J, Vázquez I, Jiménez-Velasco A, Larráyoz MJ, Lahortiga I, et al. Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib. Cancer Genet Cytogenet. 2005;160:22–6.
pubmed: 15949566
Junmei Z, Fengkuan Y, Yongping S, Baijun F, Yuzhang L, Lina L, et al. Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib. SpringerPlus. 2015;4:170.
pubmed: 25897414
pmcid: 4397260
Adnan Awad S, Kankainen M, Ojala T, Koskenvesa P, Eldfors S, Ghimire B, et al. Mutation accumulation in cancer genes relates to nonoptimal outcome in chronic myeloid leukemia. Blood Adv. 2020;4:546–59.
pubmed: 32045476
pmcid: 7013270
Kim T, Tyndel MS, Kim HJ, Ahn J-S, Choi SH, Park HJ, et al. Spectrum of somatic mutation dynamics in chronic myeloid leukemia following tyrosine kinase inhibitor therapy. Blood. 2017;129:38–47.
pubmed: 27733357
Hantschel O, Warsch W, Eckelhart E, Kaupe I, Grebien F, Wagner K-U, et al. BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia. Nat Chem Biol. 2012;8:285–93.
pubmed: 22286129
Liu BC, Sarhan J, Panda A, Muendlein HI, Ilyukha V, Coers J, et al. Constitutive interferon maintains GBP expression required for release of bacterial components upstream of pyroptosis and Anti-DNA responses. Cell Rep. 2018;24:155–168.e5. 03
pubmed: 29972777
pmcid: 6063733
Majoros A, Platanitis E, Kernbauer-Hölzl E, Rosebrock F, Müller M, Decker T. Canonical and non-canonical aspects of JAK-STAT signaling: lessons from interferons for cytokine responses. Front Immunol. 2017;8:29.
pubmed: 28184222
pmcid: 5266721
DeLong JH, Hall AO, Konradt C, Coppock GM, Park J, Pritchard GH, et al. Cytokine- and TCR-mediated regulation of T cell expression of Ly6C and Sca-1. J Immunol. 2018;200:1761–70.
pubmed: 29358280
Czech J, Cordua S, Weinbergerova B, Baumeister J, Crepcia A, Han L, et al. JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation. Leukemia. 2019;33:995–1010.
pubmed: 30470838
Wang W-B, Levy DE, Lee C-K. STAT3 negatively regulates type I IFN-mediated antiviral response. J Immunol Balt Md. 2011;187:2578–85. 1950
Tanabe Y, Nishibori T, Su L, Arduini RM, Baker DP, David M. Cutting edge: role of STAT1, STAT3, and STAT5 in IFN-alpha beta responses in T lymphocytes. J Immunol Balt Md. 1950;174:609–13. 2005 Jan
Landolfo S, Guarini A, Riera L, Gariglio M, Gribaudo G, Cignetti A, et al. Chronic myeloid leukemia cells resistant to interferon-alpha lack STAT1 expression. Hematol J J Eur Haematol Assoc. 2000;1:7–14.
Hu Y, Liu Y, Pelletier S, Buchdunger E, Warmuth M, Fabbro D, et al. Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia. Nat Genet. 2004;36:453–61.
pubmed: 15098032
Rix U, Hantschel O, Dürnberger G, Remsing Rix LL, Planyavsky M, Fernbach NV, et al. Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets. Blood. 2007;110:4055–63.
pubmed: 17720881
Berger A, Hoelbl-Kovacic A, Bourgeais J, Hoefling L, Warsch W, Grundschober E, et al. PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis. Leukemia. 2014;28:629–41.
pubmed: 24263804
Basak C, Pathak SK, Bhattacharyya A, Mandal D, Pathak S, Kundu M. NF-κB- and C/EBPβ-driven interleukin-1β gene expression and pak1-mediated caspase-1 activation play essential roles in interleukin-1β release from helicobacter pylori lipopolysaccharide-stimulated macrophages. J Biol Chem. 2005;280:4279–88.
pubmed: 15561713
Flis S, Bratek E, Chojnacki T, Piskorek M, Skorski T. Simultaneous Inhibition of BCR-ABL1 Tyrosine Kinase and PAK1/2 Serine/Threonine Kinase Exerts Synergistic Effect against Chronic Myeloid Leukemia Cells. Cancers (Basel). 2019;11:1544. https://doi.org/10.3390/cancers11101544 .
doi: 10.3390/cancers11101544
Cassier PA, Castets M, Belhabri A, Vey N. Targeting apoptosis in acute myeloid leukaemia. Br J Cancer. 2017;117:1089–98.
pubmed: 29017180
pmcid: 5674101
Samudio I, Konopleva M, Carter B, Andreeff M. Apoptosis in leukemias: regulation and therapeutic targeting. Cancer Treat Res. 2010;145:197–217.
pubmed: 20306253
Weisberg E, Ray A, Barrett R, Nelson E, Christie AL, Porter D, et al. Smac mimetics: implications for enhancement of targeted therapies in leukemia. Leukemia. 2010;24:2100–9.
pubmed: 20844561
pmcid: 4037865
Huang W, Liu B, Eklund EA. Investigating the role of the innate immune response in relapse or blast crisis in chronic myeloid leukemia. Leukemia. 2020;34:2364–74.
pubmed: 32080344
pmcid: 7438233
Bernardo PS, Lemos LGT, de Moraes GN, Maia RC. Unraveling survivin expression in chronic myeloid leukemia: Molecular interactions and clinical implications. Blood Rev. 2020;43:100671.
pubmed: 32107072
Luong-Gardiol N, Siddiqui I, Pizzitola I, Jeevan-Raj B, Charmoy M, Huang Y, et al. γ-catenin-dependent signals maintain BCR-ABL1+ B cell acute lymphoblastic leukemia. Cancer Cell. 2019;35:649–663.e10. 15
pubmed: 30991025
Chesi M, Mirza NN, Garbitt VM, Sharik ME, Dueck AC, Asmann YW, et al. IAP antagonists induce anti-tumor immunity in multiple myeloma. Nat Med. 2016;22:1411–20.
pubmed: 27841872
pmcid: 5515246
Arora V, Cheung HH, Plenchette S, Micali OC, Liston P, Korneluk RG. Degradation of survivin by the X-linked inhibitor of apoptosis (XIAP)-XAF1 complex. J Biol Chem. 2007;282:26202–9.
pubmed: 17613533
Voncken JW, Kaartinen V, Pattengale PK, Germeraad WT, Groffen J, Heisterkamp N. BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice. Blood 1995;86:4603–11.
pubmed: 8541551
Beider K, Darash-Yahana M, Blaier O, Koren-Michowitz M, Abraham M, Wald H, et al. Combination of imatinib with CXCR4 antagonist BKT140 overcomes the protective effect of stroma and targets CML in vitro and in vivo. Mol Cancer Ther. 2014;13:1155–69.
pubmed: 24502926
Bao J, Li X, Li Y, Huang C, Meng X, Li J. MicroRNA-141-5p acts as a tumor suppressor via targeting RAB32 in chronic myeloid leukemia. Front Pharm. 2019;10:1545.
Qadir AS, Ceppi P, Brockway S, Law C, Mu L, Khodarev NN, et al. CD95/Fas increases stemness in cancer cells by inducing a STAT1 dependent type I interferon response. Cell Rep. 2017;18:2373–86.
pubmed: 28273453
pmcid: 5474321
Dietrich PA, Yang C, Leung HHL, Lynch JR, Gonzales E, Liu B, et al. GPR84 sustains aberrant β-catenin signaling in leukemic stem cells for maintenance of MLL leukemogenesis. Blood. 2014;124:3284–94.
pubmed: 25293777