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BMC Cancer
Published in: BMC Cancer 1/2011

Open Access 01-12-2011 | Research article

Tyrosine kinase chromosomal translocations mediate distinct and overlapping gene regulation events

Authors: Hani Kim, Lisa C Gillis, Jordan D Jarvis, Stuart Yang, Kai Huang, Sandy Der, Dwayne L Barber

Published in: BMC Cancer | Issue 1/2011

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Abstract

Background

Leukemia is a heterogeneous disease commonly associated with recurrent chromosomal translocations that involve tyrosine kinases including BCR-ABL, TEL-PDGFRB and TEL-JAK2. Most studies on the activated tyrosine kinases have focused on proximal signaling events, but little is known about gene transcription regulated by these fusions.

Methods

Oligonucleotide microarray was performed to compare mRNA changes attributable to BCR-ABL, TEL-PDGFRB and TEL-JAK2 after 1 week of activation of each fusion in Ba/F3 cell lines. Imatinib was used to control the activation of BCR-ABL and TEL-PDGFRB, and TEL-JAK2-mediated gene expression was examined 1 week after Ba/F3-TEL-JAK2 cells were switched to factor-independent conditions.

Results

Microarray analysis revealed between 800 to 2000 genes induced or suppressed by two-fold or greater by each tyrosine kinase, with a subset of these genes commonly induced or suppressed among the three fusions. Validation by Quantitative PCR confirmed that eight genes (Dok2, Mrvi1, Isg20, Id1, gp49b, Cxcl10, Scinderin, and collagen Vα1(Col5a1)) displayed an overlapping regulation among the three tested fusion proteins. Stat1 and Gbp1 were induced uniquely by TEL-PDGFRB.

Conclusions

Our results suggest that BCR-ABL, TEL-PDGFRB and TEL-JAK2 regulate distinct and overlapping gene transcription profiles. Many of the genes identified are known to be involved in processes associated with leukemogenesis, including cell migration, proliferation and differentiation. This study offers the basis for further work that could lead to an understanding of the specificity of diseases caused by these three chromosomal translocations.
Appendix
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Literature
1.
Konopka J, Watanabe S, Witte O: An alteration of the human c-abl protein in K562 leukemia cells unmasks associated tyrosine kinase activity. Cell. 37: 1035-1042.
2.
Golub TR, Barker GF, Lovett M, Gilliland DG: Fusion of PDGF receptor b to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation. Cell. 1994, 77: 307-316. 10.1016/0092-8674(94)90322-0.CrossRefPubMed
3.
Lacronique V, Boureux A, Valle VD, Poirel H, Quang CT, Mauchauffe M, Berthou C, Lessard M, Berger R, Ghysdael J, et al: A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia. Sci. 1997, 278 (5341): 1309-1312. 10.1126/science.278.5341.1309.CrossRef
4.
Peeters P, Raynaud SD, Cools J, Wlodarska I, Grosgeorge J, Philip P, Monpoux F, Van Rompaey L, Baens M, Van den Berghe H, et al: Fusion of TEL, the ETS-variant gene 6 (ETV6), to the receptor-associated kinase JAK2 as a result of t(9;12) in a lymphoid and t(9;15;12) in a myeloid leukemia. Blood. 1997, 90 (7): 2535-2540.PubMed
5.
Carlesso N, Frank DA, Griffin JD: Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996, 183 (3): 811-820. 10.1084/jem.183.3.811.CrossRefPubMed
6.
Frank DA, Varticovski L: BCR/abl leads to the constitutive activation of Stat proteins, and shares an epitope with tyrosine phosphorylated Stats. Leukemia. 1996, 10 (11): 1724-1730.PubMed
7.
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 (49): 31704-31710. 10.1074/jbc.271.49.31704.CrossRefPubMed
8.
Chai S, Nichols G, Rothman P: Constitutive activation of JAKs and STATs in BCR-Abl-expressing cell lines and peripheral blood cells derived from leukemic patients. J Immunol. 1997, 159 (10): 4720-4728.PubMed
9.
Shuai K, Halpern J, Hoeve Jt, Rao X, Sawyers CL: Constitutive activation of STAT5 by the BCR-ABL oncogene in chronic myelogenous leukemia. Oncogene. 1996, 13: 247-254.PubMed
10.
Ho JM, Beattie BK, Squire JA, Frank DA, Barber DL: Fusion of the ets transcription factor TEL to Jak2 results in constitutive Jak-Stat signaling. Blood. 1999, 93 (12): 4354-4364.PubMed
11.
Wilbanks A, Mahajan S, Frank D, Druker B, Gilliland D, Carroll M: TEL/PDGFbetaR fusion protein activates STAT1 and STAT5: a common mechanism for transformation by tyrosine kinase fusion proteins. Exp Hematol. 2000, 28: 584-593. 10.1016/S0301-472X(00)00138-7.CrossRefPubMed
12.
Sternberg DW, Tomasson MH, Carroll M, Curley DP, Barker G, Caprio M, Wilbanks A, Kazlauskas A, Gilliland DG: The TEL/PDGFbeta R fusion in chronic myelomonocytic leukemia signals through STAT5-dependent and STAT5-independent pathways. Blood. 2001, 98 (12): 3390-3397. 10.1182/blood.V98.12.3390.CrossRefPubMed
13.
Nelson EA, Walker SR, Weisberg E, Bar-Natan M, Barrett R, Gashin LB, Terrell S, Klitgaard JL, Santo L, Addorio MR, et al: The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors. Blood. 2011, 117 (12): 3421-3429. 10.1182/blood-2009-11-255232.CrossRefPubMedPubMedCentral
14.
Mahlmann S, McLaughlin J, Afar DE, Mohr R, Kay RJ, Witte ON: Dissection of signaling pathways and cloning of new signal transducers in tyrosine kinase-induced pathways by genetic selection. Leukemia. 1998, 12 (12): 1858-1865. 10.1038/sj.leu.2401231.CrossRefPubMed
15.
Sattler M, Mohi MG, Pride YB, Quinnan LR, Malouf NA, Podar K, Gesbert F, Iwasaki H, Li S, Van Etten RA, et al: Critical role for Gab2 in transformation by BCR/ABL. Cancer Cell. 2002, 1 (5): 479-492. 10.1016/S1535-6108(02)00074-0.CrossRefPubMed
16.
Ho JM, Nguyen MH, Dierov JK, Badger KM, Beattie BK, Tartaro P, Haq R, Zanke BW, Carroll MP, Barber DL: TEL-JAK2 constitutively activates the extracellular signal-regulated kinase (ERK), stress-activated protein/Jun kinase (SAPK/JNK), and p38 signaling pathways. Blood. 2002, 100 (4): 1438-1448.PubMed
17.
Atfi A, Prunier C, Mazars A, Defachelles AS, Cayre Y, Gespach C, Bourgeade MF: The oncogenic TEL/PDGFR beta fusion protein induces cell death through JNK/SAPK pathway. Oncogene. 1999, 18 (26): 3878-3885. 10.1038/sj.onc.1202734.CrossRefPubMed
18.
Wheadon H, Welham MJ: The coupling of TEL/PDGF{beta}R to distinct functional responses is modulated by the presence of cytokine: involvement of mitogen-activated protein kinases. Blood. 2003, 102 (4): 1480-1489. 10.1182/blood-2002-09-2974.CrossRefPubMed
19.
Skorski T, Bellacosa A, Nieborowska-Skorska M, Majewski M, Martinez R, Choi JK, Trotta R, Wlodarski P, Perrotti D, Chan TO, et al: Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3 k/Akt-dependent pathway. Embo J. 1997, 16 (20): 6151-6161. 10.1093/emboj/16.20.6151.CrossRefPubMedPubMedCentral
20.
Nguyen MH, Ho JM, Beattie BK, Barber DL: TEL-JAK2 mediates constitutive activation of the phosphatidylinositol 3'-kinase/protein kinase B signaling pathway. J Biol Chem. 2001, 276 (35): 32704-32713. 10.1074/jbc.M103100200.CrossRefPubMed
21.
Dierov J, Xu Q, Dierova R, Carroll M: TEL/platelet-derived growth factor receptor beta activates phosphatidylinositol 3 (PI3) kinase and requires PI3 kinase to regulate the cell cycle. Blood. 2002, 99 (5): 1758-1765. 10.1182/blood.V99.5.1758.CrossRefPubMed
22.
Naughton R, Quiney C, Turner SD, Cotter TG: Bcr-Abl-mediated redox regulation of the PI3K/AKT pathway. Leukemia. 2009, 23 (8): 1432-1440. 10.1038/leu.2009.49.CrossRefPubMed
23.
Ren R: Mechanism of Bcr-Abl in the pathogenesis of chronic myelogenous leukaemia. Nat Rev Cancer. 2005, 5: 172-183. 10.1038/nrc1567.CrossRefPubMed
24.
Chalandon Y, Schwaller J: Targeting mutated protein tyrosine kinases and their signaling pathways in hematologic malignancies. Haematologica. 2005, 90: 949-968.PubMed
25.
Chalandon Y, Schwaller J: Targeting mutated protein tyrosine kinases and their signaling pathwyas in hematologic malignancies. Haematologica. 2005, 90: 949-968.PubMed
26.
Van Etten R, Shannon K: Focus on myeloproliferative diseases and myelodysplastic syndromes. Cancer Cell. 2004, 6: 547-552. 10.1016/j.ccr.2004.12.004.CrossRefPubMed
27.
Steer E, Cross N: Myeloproliferative disorders with translocations of chromosome 5q31-35: role of the platelet-derived growth factor receptor Beta. Acta Haematol. 2002, 107: 113-122. 10.1159/000046641.CrossRefPubMed
28.
Eisen MB, Spellman PT, Brown PO, Botstein D: Cluster analysis and display of genome-wide expression patterns. PNAS. 1998, 95 (25): 14863-14868. 10.1073/pnas.95.25.14863.CrossRefPubMedPubMedCentral
29.
Deininger M, Buchdunger E, Druker BJ: The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood. 2005, 105 (7): 2640-2653. 10.1182/blood-2004-08-3097.CrossRefPubMed
30.
Druker BJ: Translation of the Philadelphia chromosome into therapy for CML. Blood. 2008, 112 (13): 4808-4817. 10.1182/blood-2008-07-077958.CrossRefPubMed
31.
Salgia R, Brunkhorst B, Pisick E, Li J, Lo S, Chen L, Griffin J: Increased tyrosine phosphorylation of focal adhesion proteins in myeloid cell lines expressing p210BCR/ABL. Oncogene. 1995, 11: 1149-1144.PubMed
32.
Nowicki M, Pawlowski P, Fischer T, Hess G, Pawlowski T, Skorski T: Chronic myelogenous leukemia molecular signature. Oncogene. 2003, 22: 3952-3963. 10.1038/sj.onc.1206620.CrossRefPubMed
33.
Der SD, Zhou A, Williams BRG, Silverman RH: Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays. PNAS. 1998, 95 (26): 15623-15628. 10.1073/pnas.95.26.15623.CrossRefPubMedPubMedCentral
34.
Ohmine K, Ota J, Ueda M, Ueno S, Yoshida K, Yamashita Y, Kirito K, Imagawa S, Nakamura Y, Saito K, et al: Characterization of stage progression in chronic myeloid leukemia by DNA microarray with purified hematopoietic stem cells. Oncogene. 2001, 20: 8249-8257. 10.1038/sj.onc.1205029.CrossRefPubMed
35.
Kronenwett R, Butterweck U, Steidl U, Kliszewski S, Neumann F, Bork S, Blanco E, Roes N, Graf T, Brors B, et al: Distinct molecular phenotype of malignant CD34(+) hematopoietic stem and progenitor cells in chronic myelogenous leukemia. Oncogene. 2005, 24: 5313-5324. 10.1038/sj.onc.1208596.CrossRefPubMed
36.
Advani A, Dressman H, Quiroz M, Taylor G, Pendergast A: Elevated expression of a subset of interferon inducible genes in primary bone marrow cells expressing p185 Bcr-Abl versus p210 Bcr-Abl by DNA microarray analysis. Leuk Res. 2004, 28: 285-294. 10.1016/S0145-2126(03)00264-9.CrossRefPubMed
37.
Yong ASM, Szydlo RM, Goldman JM, Apperley JF, Melo JV: Molecular profiling of CD34+ cells identifies low expression of CD7, along with high expression of proteinase 3 or elastase, as predictors of longer survival in patients with CML. Blood. 2006, 107 (1): 205-212. 10.1182/blood-2005-05-2155.CrossRefPubMed
38.
Bruns I, Czibere A, Fischer JC, Roels F, Cadeddu RP, Buest S, Bruennert D, Huenerlituerkoglu AN, Stoecklein NH, Singh R, et al: The hematopoietic stem cell in chronic phase CML is characterized by a transcriptional profile resembling normal myeloid progenitor cells and reflecting loss of quiescence. Leukemia. 2009, 23 (5): 892-899. 10.1038/leu.2008.392.CrossRefPubMed
39.
Vianello F, Villanova F, Tisato V, Lymperi S, Ho KK, Gomes AR, Marin D, Bonnet D, Apperley J, Lam EW, et al: Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis. Haematologica. 2010, 95 (7): 1081-1089. 10.3324/haematol.2009.017178.CrossRefPubMedPubMedCentral
40.
Nardi V, Naveiras O, Azam M, Daley GQ: ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines. Blood. 2009, 113 (16): 3813-3820. 10.1182/blood-2008-07-167189.CrossRefPubMedPubMedCentral
41.
Eaves C, Cashman J, Wolpe S, Eaves A: Unresponsiveness of primitive chronic myeloid leukemia cells to macrophage inflammatory protein 1 alpha, an inhibitor of primitive normal hematopoietic cells. PNAS. 1993, 90: 12015-12019. 10.1073/pnas.90.24.12015.CrossRefPubMedPubMedCentral
42.
Wark G, Heyworth C, Spooncer E, Czaplewski L, Francis J, Dexter T, Whetton A: Abl protein kinase abrogates the response of multipotent haemopoietic cells to the growth inhibitor macrophage inflammatory protein-1 alpha. Oncogene. 1998, 16: 1319-1324. 10.1038/sj.onc.1201914.CrossRefPubMed
43.
Salgia R, Quackenbush E, Lin J, Souchkova N, Sattler M, Ewaniuk DS, Klucher KM, Daley GQ, Kraeft SK, Sackstein R, et al: The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alpha. Blood. 1999, 94 (12): 4233-4246.PubMed
44.
Chen YY, Malik M, Tomkowicz BE, Collman RG, Ptasznik A: BCR-ABL1 alters SDF-1alpha-mediated adhesive responses through the beta2 integrin LFA-1 in leukemia cells. Blood. 2008, 111 (10): 5182-5186. 10.1182/blood-2007-10-117705.CrossRefPubMedPubMedCentral
45.
Ptasznik A, Urbanowska E, Chinta S, Costa MA, Katz BA, Stanislaus MA, Demir G, Linnekin D, Pan ZK, Gewirtz AM: Crosstalk Between BCR/ABL Oncoprotein and CXCR4 Signaling through a Src Family Kinase in Human Leukemia Cells. J Exp Med. 2002, 196 (5): 667-678. 10.1084/jem.20020519.CrossRefPubMedPubMedCentral
46.
Arm J, Gurish M, Reynolds D, Scott H, Gartner C, Austen K, Katz H: Molecular cloning of gp49, a cell-surface antigen that is preferentially expressed by mouse mast cell progenitors and is a new member of the immunoglobulin superfamily. J Biol Chem. 1991, 266 (24): 15966-15973.PubMed
47.
Daheshia M, Friend DS, Grusby MJ, Austen KF, Katz HR: Increased Severity of Local and Systemic Anaphylactic Reactions in gp49B1-deficient Mice. J Exp Med. 2001, 194 (2): 227-234. 10.1084/jem.194.2.227.CrossRefPubMedPubMedCentral
48.
Katz HR, Vivier E, Castells MC, McCormick MJ, Chambers JM, Austen KF: Mouse mast cell gp49B1 contains two immunoreceptor tyrosine-based inhibition motifs and suppresses mast cell activation when coligated with the high-affinity Fc receptor for†IgE. PNAS. 1996, 93 (20): 10809-10814. 10.1073/pnas.93.20.10809.CrossRefPubMedPubMedCentral
49.
Iida S, Kohro T, Kodama T, Nagata S, Fukunaga R: Identification of CCR2, flotillin, and gp49B genes as new G-CSF targets during neutrophilic differentiation. J Leukoc Biol. 2005, 78 (2): 481-490. 10.1189/jlb.0904515.CrossRefPubMed
50.
Heino J: The collagen receptor integrins have distinct ligand recognition and signaling functions. Matrix Biol. 2000, 19: 319-323. 10.1016/S0945-053X(00)00076-7.CrossRefPubMed
51.
Gordon M, Dowding C, Riley G, Goldman J, Greaves M: Altered adhesive interactions with marrow stroma of haematopoietic progenitor cells in chronic myeloid leukaemia. Nature. 1987, 328: 342-344. 10.1038/328342a0.CrossRefPubMed
52.
Bhatia R, Wayner E, McGlave P, Verfaillie C: Interferon-alpha restores normal adhesion of chronic myelogenous leukemia hematopoietic progenitors to bone marrow stroma by correcting impaired beta 1 integrin receptor function. J Clin Invest. 1994, 94: 384-391. 10.1172/JCI117333.CrossRefPubMedPubMedCentral
53.
Bhatia R, Verfaillie CM: Inhibition of BCR-ABL expression with antisense oligodeoxynucleotides restores beta 1 integrin-mediated adhesion and proliferation inhibition in chronic myelogenous leukemia hematopoietic progenitors. Blood. 1998, 91 (9): 3414-3422.PubMed
54.
Verfaillie C, McCarthy J, McGlave P: Mechanisms underlying abnormal trafficking of malignant progenitors in chronic myelogenous leukemia. Decreased adhesion to stroma and fibronectin but increased adhesion to the basement membrane components laminin and collagen type IV. J Clin Invest. 1992, 90: 1232-1241. 10.1172/JCI115985.CrossRefPubMedPubMedCentral
55.
Verfaillie C, Hurley R, Lundell B, Zhao C, Bhatia R: Integrin-mediated regulation of hematopoiesis: do BCR/ABL-induced defects in integrin function underlie the abnormal circulation and proliferation of CML progenitors?. Acta Haematol. 1997, 97: 40-52. 10.1159/000203658.CrossRefPubMed
56.
Chan J, Watt S: Adhesion receptors on haematopoietic progenitor cells. Brit J Haematol. 2001, 112: 541-557. 10.1046/j.1365-2141.2001.02439.x.CrossRef
57.
Evens AM, Sehn LH, Farinha P, Nelson BP, Raji A, Lu Y, Brakman A, Parimi V, Winter JN, Schumacker PT, et al: Hypoxia-inducible factor-1 {alpha} expression predicts superior survival in patients with diffuse large B-cell lymphoma treated with R-CHOP. J Clin Oncol. 2010, 28 (6): 1017-1024. 10.1200/JCO.2009.24.1893.CrossRefPubMedPubMedCentral
58.
Wisniewski D, Strife A, Swendeman S, Erdjument-Bromage H, Geromanos S, Kavanaugh WM, Tempst P, Clarkson B: A novel SH2-containing phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase (SHIP2) is constitutively tyrosine phosphorylated and associated with src homologous and collagen gene (SHC) in chronic myelogenous leukemia progenitor cells. Blood. 1999, 93 (8): 2707-2720.PubMed
59.
Liang X, Hajivandi M, Veach D, Wisniewski D, Clarkson B, Resh MD, Pope RM: Quantification of change in phosphorylation of BCR-ABL kinase and its substrates in response to Imatinib treatment in human chronic myelogenous leukemia cells. Proteomics. 2006, 6 (16): 4554-4564. 10.1002/pmic.200600109.CrossRefPubMed
60.
Master Z, Tran J, Bishnoi A, Chen SH, Ebos JM, Van Slyke P, Kerbel RS, Dumont DJ: Dok-R binds c-Abl and regulates Abl kinase activity and mediates cytoskeletal reorganization. J Biol Chem. 2003, 278 (32): 30170-30179. 10.1074/jbc.M301339200.CrossRefPubMed
61.
Yasuda T, Shirakata M, Iwama A, Ishii A, Ebihara Y, Osawa M, Honda K, Shinohara H, Sudo K, Tsuji K, et al: Role of Dok-1 and Dok-2 in Myeloid Homeostasis and Suppression of Leukemia. J Exp Med. 2004, 200 (12): 1681-1687. 10.1084/jem.20041247.CrossRefPubMedPubMedCentral
62.
Yasuda M, Theodorakis P, Subramanian T, Chinnadurai G: Adenovirus E1B-19 K/BCL-2 Interacting Protein BNIP3 Contains a BH3 Domain and a Mitochondrial Targeting Sequence 10.1074/jbc.273.20.12415. J Biol Chem. 1998, 273 (20): 12415-12421. 10.1074/jbc.273.20.12415.CrossRefPubMed
63.
Rodriguez del Castillo A, Vitale M, Tchakarov L, Trifaró J: Human platelets contain scinderin, a Ca2+-dependent actin filament-severing protein. Thromb Haemost. 1991, 67: 248-251.
64.
Unwin RD, Sternberg DW, Lu Y, Pierce A, Gilliland DG, Whetton AD: Global effects of BCR/ABL and TEL/PDGFR-beta expression on the proteome and phosphoproteome: identification of the rho pathway as a target of BCR/ABL. J BiolChem. 2005, 280 (8): 6316-6326.
65.
Zunino R, Li Q, Rose SD, Romero-Benitez MMI, Lejen T, Brandan NC, Trifaro J-M: Expression of scinderin in megakaryoblastic leukemia cells induces differentiation, maturation, and apoptosis with release of plateletlike particles and inhibits proliferation and tumorigenesis. Blood. 2001, 98 (7): 2210-2219. 10.1182/blood.V98.7.2210.CrossRefPubMed
66.
Tam WF, Gu TL, Chen J, Lee BH, Bullinger L, Frohling S, Wang A, Monti S, Golub TR, Gilliland DG: Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells. Blood. 2008, 112 (5): 1981-1992. 10.1182/blood-2007-07-103010.CrossRefPubMedPubMedCentral
67.
Perk J, Iavarone A, Benezra R: Id family of helix-loop-helix proteins in cancer. Nat Rev Cancer. 2005, 5: 603-614. 10.1038/nrc1673.CrossRefPubMed
68.
Xu M, Nie L, Kim S, Sun X: STAT5-induced Id-1 transcription involves recruitment of HDAC1 and deacetylation of C/EBPbeta. EMBO J. 2003, 22: 893-904. 10.1093/emboj/cdg094.CrossRefPubMedPubMedCentral
69.
Cain JA, Xiang Z, O'Neal J, Kreisel F, Colson A, Luo H, Hennighausen L, Tomasson MH: Myeloproliferative disease induced by TEL-PDGFRB displays dynamic range sensitivity to Stat5 gene dosage. Blood. 2007, 109 (9): 3906-3914. 10.1182/blood-2006-07-036335.CrossRefPubMedPubMedCentral
Metadata
Title
Tyrosine kinase chromosomal translocations mediate distinct and overlapping gene regulation events
Authors
Hani Kim
Lisa C Gillis
Jordan D Jarvis
Stuart Yang
Kai Huang
Sandy Der
Dwayne L Barber
Publication date
01-12-2011
Publisher
BioMed Central
Published in
BMC Cancer / Issue 1/2011
Electronic ISSN: 1471-2407
DOI
https://doi.org/10.1186/1471-2407-11-528

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