Augmented efficacy of brentuximab vedotin combined with ruxolitinib and/or Navitoclax in a murine model of human Hodgkin's lymphoma

Proceedings of the National Academy of Sciences of the United States of America

Volumn 113, Issue 6, 2016, Pages 1624-1629

  Ju, Wei ^a   Zhang, Meili ^a,b   Wilson, Kelli M ^c   Petrus, Michael N ^a   Bamford, Richard N ^d   Zhang, Xiaohu ^c   Guha, Rajarshi ^c   Ferrer, Marc ^c   Thomas, Craig J ^c   Waldmann, Thomas A ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b FREDERICK NATIONAL LABORATORY FOR CANCER RESEARCH   (United States)

^c NATIONAL INSTITUTES OF HEALTH   (United States)

^d Transponics   (United States)

Author keywords

Brentuximab vedotin; Hodgkin's lymphoma; Navitoclax; Ruxolitinib

Indexed keywords

BRENTUXIMAB VEDOTIN; CASPASE 3; CASPASE 9; CYTOCHROME C; CYTOKINE; INTERLEUKIN 13; INTERLEUKIN 6; JANUS KINASE; NAVITOCLAX; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BCL XL; PUMA PROTEIN; RUXOLITINIB; STAT PROTEIN; ANILINE DERIVATIVE; ANTIBODY CONJUGATE; ANTINEOPLASTIC AGENT; CASPASE 7; JANUS KINASE 2; PROTEIN BCL X; PYRAZOLE DERIVATIVE; SULFONAMIDE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL LINE; CONTROLLED STUDY; DRUG EFFICACY; DRUG POTENTIATION; FEMALE; HODGKIN DISEASE; MOUSE; NONHUMAN; ONCOGENE C MYC; PRIORITY JOURNAL; PROTEIN EXPRESSION; ANIMAL; APOPTOSIS; CELL PROLIFERATION; DISEASE COURSE; DISEASE MODEL; DRUG EFFECTS; ENZYME ACTIVATION; ENZYMOLOGY; GENE DOSAGE; GENETICS; HUMAN; METABOLISM; MITOCHONDRION; PATHOLOGY; PHOSPHORYLATION; PRECLINICAL STUDY; SIGNAL TRANSDUCTION; TREATMENT OUTCOME; TUMOR CELL LINE; WESTERN BLOTTING;

ANILINE COMPOUNDS; ANIMALS; ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS; APOPTOSIS; BCL-X PROTEIN; BLOTTING, WESTERN; CASPASE 3; CASPASE 7; CELL LINE, TUMOR; CELL PROLIFERATION; DISEASE MODELS, ANIMAL; DISEASE PROGRESSION; DRUG EVALUATION, PRECLINICAL; ENZYME ACTIVATION; GENE DOSAGE; HODGKIN DISEASE; HUMANS; IMMUNOCONJUGATES; JANUS KINASE 2; MICE; MITOCHONDRIA; PHOSPHORYLATION; PYRAZOLES; SIGNAL TRANSDUCTION; STAT TRANSCRIPTION FACTORS; SULFONAMIDES; TREATMENT OUTCOME;

EID: 84957818851     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1524668113     Document Type: Article

References (35)

1. Chen X, Soma LA, Fromm JR (2013) Targeted therapy for Hodgkin lymphoma and systemic anaplastic large cell lymphoma: focus on brentuximab vedotin. Onco Targets Ther 7:45-56.
2. Kanzler H, Küppers R, Hansmann ML, Rajewsky K (1996) Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells. J Exp Med 184(4):1495-1505.
3. Batlevi CL, Younes A (2013) Novel therapy for Hodgkin lymphoma. Hematol Am Soc Hematol Educ Program 2013(1):394-399.
4. Diaz T, et al. (2011) Lestaurtinib inhibition of the Jak/STAT signaling pathway in Hodgkin lymphoma inhibits proliferation and induces apoptosis. PLoS One 6(4):e18856.
5. Baus D, Pfitzner E (2006) Specific function of STAT3, SOCS1, and SOCS3 in the regulation of proliferation and survival of classical Hodgkin lymphoma cells. Int J Cancer 118(6):1404-1413.
6. Staudt LM (2000) The molecular and cellular origins of Hodgkin's disease. J Exp Med 191(2):207-212.
7. García JF, et al.; Spanish Hodgkin Lymphoma Study Group (2003) Hodgkin and Reed- Sternberg cells harbor alterations in the major tumor suppressor pathways and cellcycle checkpoints: analyses using tissue microarrays. Blood 101(2):681-689.
8. Skinnider BF, et al. (2001) Interleukin 13 and interleukin 13 receptor are frequently expressed by Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood 97(1): 250-255.
9. Kube D, et al. (2001) STAT3 is constitutively activated in Hodgkin cell lines. Blood 98(3):762-770.
10. Hinz M, et al. (2002) Nuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activity. J Exp Med 196(5):605-617.
11. Kapp U, et al. (1999) Interleukin 13 is secreted by and stimulates the growth of Hodgkin and Reed-Sternberg cells. J Exp Med 189(12):1939-1946.
12. Joos S, et al. (2000) Genomic imbalances including amplification of the tyrosine kinase gene JAK2 in CD30+ Hodgkin cells. Cancer Res 60(3):549-552.
13. Van Roosbroeck K, et al. (2011) JAK2 rearrangements, including the novel SEC31AJAK2 fusion, are recurrent in classical Hodgkin lymphoma. Blood 117(15):4056-4064.
14. Rui L, et al. (2010) Cooperative epigenetic modulation by cancer amplicon genes. Cancer Cell 18(6):590-605.
15. Derenzini E, et al. (2011) The JAK inhibitor AZD1480 regulates proliferation and immunity in Hodgkin lymphoma. Blood Cancer J 1(12):e46.
16. Younes A, et al. (2012) Phase I study of a novel oral Janus kinase 2 inhibitor, SB1518, in patients with relapsed lymphoma: evidence of clinical and biologic activity in multiple lymphoma subtypes. J Clin Oncol 30(33):4161-4167.
17. Waibel M, et al. (2013) Combined targeting of JAK2 and Bcl-2/Bcl-xL to cure mutant JAK2-driven malignancies and overcome acquired resistance to JAK2 inhibitors. Cell Reports 5(4):1047-1059.
18. Guo J, et al. (2015) JAK2V617F drives Mcl-1 expression and sensitizes hematologic cell lines to dual inhibition of JAK2 and Bcl-xL. PLoS One 10(3):e0114363.
19. Zhang M, et al. (2015) Selective targeting of JAK/STAT signaling is potentiated by BclxL blockade in IL-2-dependent adult T-cell leukemia. Proc Natl Acad Sci USA 112(40): 12480-12485.
20. Dürkop H, et al. (1992) Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin's disease. Cell 68(3):421-427.
21. Younes A (2011) CD30-targeted antibody therapy. Curr Opin Oncol 23(6):587-593.
22. Bradley AM, Devine M, DeRemer D (2013) Brentuximab vedotin: an anti-CD30 antibody- drug conjugate. Am J Health Syst Pharm 70(7):589-597.
23. Younes A, et al. (2010) Brentuximab vedotin (SGN-35) for relapsed CD30-positive lymphomas. N Engl J Med 363(19):1812-1821.
24. Pro B, et al. (2012) Brentuximab vedotin (SGN-35) in patients with relapsed or refractory systemic anaplastic large-cell lymphoma: results of a phase II study. J Clin Oncol 30(18):2190-2196.
25. Younes A, et al. (2012) Results of a pivotal phase II study of brentuximab vedotin for patients with relapsed or refractory Hodgkin's lymphoma. J Clin Oncol 30(18):2183-2189.
26. Mottok A, Renné C, Willenbrock K, Hansmann ML, Bräuninger A (2007) Somatic hypermutation of SOCS1 in lymphocyte-predominant Hodgkin lymphoma is accompanied by high JAK2 expression and activation of STAT6. Blood 110(9):3387-3390.
27. Francisco JA, et al. (2003) cAC10-vcMMAE, an anti-CD30-monomethyl auristatin E conjugate with potent and selective antitumor activity. Blood 102(4):1458-1465.
28. Tschopp J, Thome M, Hofmann K, Meinl E (1998) The fight of viruses against apoptosis. Curr Opin Genet Dev 8(1):82-87.
29. Pan G, Humke EW, Dixit VM (1998) Activation of caspases triggered by cytochrome c in vitro. FEBS Lett 426(1):151-154.
30. Kuida K, et al. (1998) Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Cell 94(3):325-337.
31. Cochet O, Frelin C, Peyron J-F, Imbert V (2006) Constitutive activation of STAT proteins in the HDLM-2 and L540 Hodgkin lymphoma-derived cell lines supports cell survival. Cell Signal 18(4):449-455.
32. Willis SN, Adams JM (2005) Life in the balance: how BH3-only proteins induce apoptosis. Curr Opin Cell Biol 17(6):617-625.
33. Youle RJ, Strasser A (2008) The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol 9(1):47-59.
34. Green MR, et al. (2012) Constitutive AP-1 activity and EBV infection induce PD-L1 in Hodgkin lymphomas and posttransplant lymphoproliferative disorders: implications for targeted therapy. Clin Cancer Res 18(6):1611-1618.
35. Ansell SM, et al. (2015) PD-1 blockade with nivolumab in relapsed or refractory Hodgkin's lymphoma. N Engl J Med 372(4):311-319.