139
Views
9
CrossRef citations to date
0
Altmetric
Review

Targeted molecular therapy in peripheral T-cell lymphomas

, , , , &
Pages 551-562 | Published online: 10 Jan 2014

References

  • Jaffe ES, Harris NL, Stein H, Campo E, Pileri SA, Swerdlow SH. Introduction and overview of the classification of the lymphoid neoplasms. In: WHO Classification of Tumors of Hematopoietic and Lymphoid tissues. Swerdlow S, Campo E, Harris NL et al. (Eds). International Agency for Research on Cancer, Lyon, France, 158–166 (2008).
  • WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues Swerdlow S, Campo E, Harris N et al. (Eds). International Agency for Research on Cancer, Lyon, France (2008).
  • Vose J, Armitage J, Weisenburger D. International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes. J. Clin. Oncol.26(25), 4124–4130 (2008).
  • Gallamini A, Stelitano C, Calvi R et al. Peripheral T-cell lymphoma unspecified (PTCL-U): a new prognostic model from a retrospective multicentric clinical study. Blood103(7), 2474–2479 (2004).
  • Piccaluga PP, Agostinelli C, Gazzola A et al. Prognostic markers in peripheral T-cell lymphoma. Curr. Hematol. Malig. Rep.5(4), 222–228 (2010).
  • Went P, Agostinelli C, Gallamini A et al. Marker expression in peripheral T-cell lymphoma: a proposed clinical-pathologic prognostic score. J. Clin. Oncol.24(16), 2472–2479 (2006).
  • O’Connor OA. Novel agents in development for peripheral T-cell lymphoma. Semin. Hematol.47(Suppl. 1), S11–S14 (2010).
  • Lamant L, Meggetto F, al Saati T et al. High incidence of the t(2;5)(p23;q35) translocation in anaplastic large cell lymphoma and its lack of detection in Hodgkin’s disease. Comparison of cytogenetic analysis, reverse transcriptase-polymerase chain reaction, and P-80 immunostaining. Blood87(1), 284–291 (1996).
  • Palmer RH, Vernersson E, Grabbe C, Hallberg B. Anaplastic lymphoma kinase: signalling in development and disease. Biochem. J.420(3), 345–361 (2009).
  • Piccaluga PP, Gazzola A, Mannu C et al. Pathobiology of anaplastic large cell lymphoma. Adv. Hematol.345053 (2011).
  • Barreca A, Lasorsa E, Riera L et al. Anaplastic lymphoma kinase in human cancer. J. Mol. Endocrininol.47(1), R11–R23 (2011).
  • Chiarle R, Simmons WJ, Cai H et al. Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target. Nat. Med.11(6), 623–629 (2005).
  • Piva R, Agnelli L, Pellegrino E et al. Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms. J. Clin. Oncol.28(9), 1583–1590 (2010).
  • Butrynski JE, D’Adamo DR, Hornick JL et al. Crizotinib in ALK-rearranged inflammatory myofibroblastic tumor. N. Engl. J. Med.363(18), 1727–1733 (2010).
  • Agostinelli C, Piccaluga PP, Went P et al. Peripheral T cell lymphoma, not otherwise specified: the stuff of genes, dreams and therapies. J. Clin. Pathol.61(11), 1160–1167 (2008).
  • Piccaluga PP, Agostinelli C, Califano A et al. Gene expression analysis of peripheral T cell lymphoma, unspecified, reveals distinct profiles and new potential therapeutic targets. J. Clin. Invest.117(3), 823–834 (2007).
  • Iqbal J, Weisenburger DD, Greiner TC et al. Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma. Blood115(5), 1026–1036 (2010).
  • Tsai MS, Bogart DF, Castaneda JM, Li P, Lupu R. Cyr61 promotes breast tumorigenesis and cancer progression. Oncogene21(53), 8178–8185 (2002).
  • Lin MT, Chang CC, Chen ST et al. Cyr61 expression confers resistance to apoptosis in breast cancer MCF-7 cells by a mechanism of NF-κB-dependent XIAP up-regulation. J. Biol. Chem.279(23), 24015–24023 (2004).
  • Martinez-Delgado B, Cuadros M, Honrado E et al. Differential expression of NF-κB pathway genes among peripheral T-cell lymphomas. Leukemia19(12), 2254–2263 (2005).
  • Hartmann S, Gesk S, Scholtysik R et al. High resolution SNP array genomic profiling of peripheral T cell lymphomas, not otherwise specified, identifies a subgroup with chromosomal aberrations affecting the REL locus. Br. J. Haematol.148(3), 402–412 (2009).
  • Piccaluga PP, Agostinelli C, Zinzani PL, Baccarani M, Dalla Favera R, Pileri SA. Expression of platelet-derived growth factor receptor α in peripheral T-cell lymphoma not otherwise specified. Lancet Oncol.6(6), 440 (2005).
  • Piccaluga PP, Agostinelli C, Califano A et al. Gene expression analysis of angioimmunoblastic lymphoma indicates derivation from T follicular helper cells and vascular endothelial growth factor deregulation. Cancer Res.67(22), 10703–10710 (2007).
  • Huang Y, de Reynies A, de Leval L et al. Gene expression profiling identifies emerging oncogenic pathways operating in extranodal NK/T-cell lymphoma, nasal-type. Blood115(6), 1226–1237 (2009).
  • Ri M, Iida S, Ishida T et al. Bortezomib-induced apoptosis in mature T-cell lymphoma cells partially depends on upregulation of Noxa and functional repression of Mcl-1. Cancer Sci.100(2), 341–348 (2008).
  • Heider U, Rademacher J, Lamottke B et al. Synergistic interaction of the histone deacetylase inhibitor SAHA with the proteasome inhibitor bortezomib in cutaneous T cell lymphoma. Eur. J. Haematol.82(6), 440–449 (2009).
  • Li T, Morgan MJ, Choksi S, Zhang Y, Kim YS, Liu ZG. MicroRNAs modulate the noncanonical transcription factor NF-κB pathway by regulating expression of the kinase IKKα during macrophage differentiation. Nat. Immunol.11(9), 799–805 (2010).
  • McConkey DJ, Zhu K. Mechanisms of proteasome inhibitor action and resistance in cancer. Drug Resist. Updat.11(4–5), 164–179 (2008).
  • Adams J, Kauffman M. Development of the proteasome inhibitor Velcade (bortezomib). Cancer Invest.22(2), 304–311 (2004).
  • Juvekar A, Manna S, Ramaswami S et al. Bortezomib induces nuclear translocation of IκBα resulting in gene specific suppression of NFκB-dependent transcription and induction of apoptosis in CTCL. Mol. Cancer Res.9(2), 183–194 (2011).
  • Compagno M, Lim WK, Grunn A et al. Mutations of multiple genes cause deregulation of NF-κB in diffuse large B-cell lymphoma. Nature459(7247), 717–721 (2009).
  • Izban KF, Ergin M, Qin JZ et al. Constitutive expression of NF-κB is a characteristic feature of mycosis fungoides: implications for apoptosis resistance and pathogenesis. Hum. Pathol.31(12), 1482–1490 (2000).
  • Sors A, Jean-Louis F, Pellet C et al. Down-regulating constitutive activation of the NF-κB canonical pathway overcomes the resistance of cutaneous T-cell lymphoma to apoptosis. Blood107(6), 2354–2363 (2006).
  • Zinzani PL, Musuraca G, Tani M et al. Phase II trial of proteasome inhibitor bortezomib in patients with relapsed or refractory cutaneous T-cell lymphoma. J. Clin. Oncol.25(27), 4293–4297 (2007).
  • Lee J, Suh C, Kang HJ et al. Phase I study of proteasome inhibitor bortezomib plus CHOP in patients with advanced, aggressive T-cell or NK/T-cell lymphoma. Ann. Oncol.19(12), 2079–2083 (2008).
  • Heldin CH, Westermark B. Mechanism of action and in vivo role of platelet-derived growth factor. Physiol. Rev.79(4), 1283–1316 (1999).
  • Pardanani A, Tefferi A. Imatinib targets other than bcr/abl and their clinical relevance in myeloid disorders. Blood104(7), 1931–1939 (2004).
  • Peng B, Hayes M, Resta D et al. Pharmacokinetics and pharmacodynamics of imatinib in a Phase I trial with chronic myeloid leukemia patients. J. Clin. Oncol.22(5), 935–942 (2004).
  • Falini B, Pileri S, Pizzolo G et al. CD30 (Ki-1) molecule: a new cytokine receptor of the tumor necrosis factor receptor superfamily as a tool for diagnosis and immunotherapy. Blood85(1), 1–14 (1995).
  • Matsumoto K, Terakawa M, Miura K, Fukuda S, Nakajima T, Saito H. Extremely rapid and intense induction of apoptosis in human eosinophils by anti-CD30 antibody treatment in vitro. J. Immunol.172(4), 2186–2193 (2004).
  • Durkop H, Latza U, Hummel M, Eitelbach F, Seed B, Stein H. Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin’s disease. Cell68(3), 421–427 (1992).
  • Dearden C. Alemtuzumab in peripheral T-cell malignancies. Cancer Biother. Radiopharm.19(4), 391–398 (2004).
  • Halene S, Zieske A, Berliner N. Sustained remission from angioimmunoblastic T-cell lymphoma induced by alemtuzumab. Nat. Clin. Pract. Oncol.3(3), 165–168; quiz 169 (2006).
  • Ansell SM, Horwitz SM, Engert A et al. Phase I/II study of an anti-CD30 monoclonal antibody (MDX-060) in Hodgkin’s lymphoma and anaplastic large-cell lymphoma. J. Clin. Oncol.25(19), 2764–2769 (2007).
  • Forero-Torres A, Leonard JP, Younes A et al. A Phase II study of SGN-30 (anti-CD30 mAb) in Hodgkin lymphoma or systemic anaplastic large cell lymphoma. Br. J. Haematol.146(2), 171–179 (2009).
  • Younes A, Bartlett NL, Leonard JP et al. Brentuximab vedotin (SGN-35) for relapsed CD30-positive lymphomas. N. Engl. J. Med.363(19), 1812–1821 (2010).
  • Gallamini A, Zaja F, Patti C et al. Alemtuzumab (Campath-1H) and CHOP chemotherapy as first-line treatment of peripheral T-cell lymphoma: results of a GITIL (Gruppo Italiano Terapie Innovative nei Linfomi) prospective multicenter trial. Blood110(7), 2316–2323 (2007).
  • Kluin-Nelemans HC, van Marwijk Kooy M, Lugtenburg PJ et al. Intensified alemtuzumab-CHOP therapy for peripheral T-cell lymphoma. Ann. Oncol.22(7), 1595–1600 (2011).
  • Amengual JE, Raphael BG. Sustained, durable responses with alemtuzumab in refractory angioimmunoblastic T-cell lymphoma. Leuk. Lymphoma51(7), 1347–1350 (2010).
  • Piccaluga PP, Agostinelli C, Righi S, Zinzani PL, Pileri SA. Expression of CD52 in peripheral T-cell lymphoma. Haematologica92(4), 566–567 (2007).
  • Rodig SJ, Abramson JS, Pinkus GS et al. Heterogeneous CD52 expression among hematologic neoplasms: implications for the use of alemtuzumab (CAMPATH-1H). Clin. Cancer Res.12(23), 7174–7179 (2006).
  • Chang ST, Lu CL, Chuang SS. CD52 expression in non-mycotic T- and NK/T-cell lymphomas. Leuk. Lymphoma48(1), 117–121 (2007).
  • Jiang L, Yuan CM, Hubacheck J et al. Variable CD52 expression in mature T cell and NK cell malignancies: implications for alemtuzumab therapy. Br. J. Haematol.145(2), 173–179 (2009).
  • Geissinger E, Bonzheim I, Roth S, Rosenwald A, Muller-Hermelink HK, Rudiger T. CD52 expression in peripheral T-cell lymphomas determined by combined immunophenotyping using tumor cell specific T-cell receptor antibodies. Leuk. Lymphoma50(6), 1010–1016 (2009).
  • Mohan SR, Clemente MJ, Afable M et al. Therapeutic implications of variable expression of CD52 on clonal cytotoxic T cells in CD8+ large granular lymphocyte leukemia. Haematologica94(10), 1407–1414 (2009).
  • Cortelezzi A, Pasquini MC, Gardellini A et al. Low-dose subcutaneous alemtuzumab in refractory chronic lymphocytic leukaemia (CLL): results of a prospective, single-arm multicentre study. Leukemia23(11), 2027–2033 (2009).
  • Cortelezzi A, Pasquini MC, Sarina B et al. A pilot study of low-dose subcutaneous alemtuzumab therapy for patients with hemotherapy-refractory chronic lymphocytic leukemia. Haematologica90(3), 410–412 (2005).
  • Zinzani PL, Alinari L, Tani M, Fina M, Pileri S, Baccarani M. Preliminary observations of a Phase II study of reduced-dose alemtuzumab treatment in patients with pretreated T-cell lymphoma. Haematologica90(5), 702–703 (2005).
  • Kim YH, Duvic M, Obitz E et al. Clinical efficacy of zanolimumab (HuMax-CD4): two Phase 2 studies in refractory cutaneous T-cell lymphoma. Blood109(11), 4655–4662 (2007).
  • d’Amore F, Radford J, Relander T et al. Phase II trial of zanolimumab (HuMax-CD4) in relapsed or refractory non-cutaneous peripheral T cell lymphoma. Br. J. Haematol.150(5), 565–573 (2010).
  • Gloghini A, Buglio D, Khaskhely NM et al. Expression of histone deacetylases in lymphoma: implication for the development of selective inhibitors. Br. J. Haematol.147(4), 515–525 (2009).
  • Strahl BD, Allis CD. The language of covalent histone modifications. Nature403(6765), 41–45 (2000).
  • Roth SY, Denu JM, Allis CD. Histone acetyltransferases. Ann. Rev. Biochem.70, 81–120 (2001).
  • Gray SG, Ekstrom TJ. The human histone deacetylase family. Exp. Cell Res.262(2), 75–83 (2001).
  • Blander G, Guarente L. The Sir2 family of protein deacetylases. Ann. Rev. Biochem.73, 417–435 (2004).
  • Copeland A, Buglio D, Younes A. Histone deacetylase inhibitors in lymphoma. Curr. Opin. Oncol.22(5), 431–436 (2010).
  • Lagger G, O’Carroll D, Rembold M et al. Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression. EMBO J.21(11), 2672–2681 (2002).
  • Minucci S, Pelicci PG. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nature Rev.6(1), 38–51 (2006).
  • Jeong JW, Bae MK, Ahn MY et al. Regulation and destabilization of HIF-1α by ARD1-mediated acetylation. Cell111(5), 709–720 (2002).
  • Marks PA, Richon VM, Rifkind RA. Histone deacetylase inhibitors: inducers of differentitiation or apoptosis of transformed cells. J. Natl Cancer Inst.92(15), 1210–1216 (2000).
  • Haberland M, Johnson A, Mokalled MH, Montgomery RL, Olson EN. Genetic dissection of histone deacetylase requirement in tumor cells. Proc. Natl Acad. Sci. USA106(19), 7751–7755 (2009).
  • Deroanne CF, Bonjean K, Servotte S et al. Histone deacetylases inhibitors as anti-angiogenic agents altering vascular endothelial growth factor signaling. Oncogene21(3), 427–436 (2002).
  • Rosato RR, Almenara JA, Grant S. The histone deacetylase inhibitor MS-275 promotes differentiation or apoptosis in human leukemia cells through a process regulated by generation of reactive oxygen species and induction of p21CIP1/WAF1 1. Cancer Res.63(13), 3637–3645 (2003).
  • Carew JS, Giles FJ, Nawrocki ST. Histone deacetylase inhibitors: mechanisms of cell death and promise in combination cancer therapy. Cancer Letters269(1), 7–17 (2008).
  • Whitesell L, Lindquist SL. HSP90 and the chaperoning of cancer. Nat. Rev.5(10), 761–772 (2005).
  • Lane AA, Chabner BA. Histone deacetylase inhibitors in cancer therapy. J. Clin. Oncol.27(32), 5459–5468 (2009).
  • Piekarz RL, Frye R, Turner M et al. Phase II multi-institutional trial of the histone deacetylase inhibitor romidepsin as monotherapy for patients with cutaneous T-cell lymphoma. J. Clin. Oncol.27(32), 5410–5417 (2009).
  • Piekarz RL, Robey R, Sandor V et al. Inhibitor of histone deacetylation, depsipeptide (FR901228), in the treatment of peripheral and cutaneous T-cell lymphoma: a case report. Blood98(9), 2865–2868 (2001).
  • Olsen EA, Kim YH, Kuzel TM et al. Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. J. Clin. Oncol.25(21), 3109–3115 (2007).
  • Zhang C, Richon V, Ni X, Talpur R, Duvic M. Selective induction of apoptosis by histone deacetylase inhibitor SAHA in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. J. Invest. Dermatol.125(5), 1045–1052 (2005).
  • de Leval L, Rickman DS, Thielen C et al. The gene expression profile of nodal peripheral T-cell lymphoma demonstrates a molecular link between angioimmunoblastic T-cell lymphoma (AITL) and follicular helper T (TFH) cells. Blood109(11), 4952–4963 (2007).
  • Tripodo C, Gri G, Piccaluga PP et al. Mast cells and Th17 cells contribute to the lymphoma-associated pro-inflammatory microenvironment of angioimmunoblastic T-cell lymphoma. Am. J. Pathol.177(2), 792–802 (2010).
  • Richardson PG, Schlossman RL, Weller E et al. Immunomodulatory drug CC-5013 overcomes drug resistance and is well tolerated in patients with relapsed multiple myeloma. Blood100(9), 3063–3067 (2002).
  • Mitsiades N, Mitsiades CS, Poulaki V et al. Apoptotic signaling induced by immunomodulatory thalidomide analogs in human multiple myeloma cells: therapeutic implications. Blood99(12), 4525–4530 (2002).
  • Chanan-Khan A, Miller KC, Musial L et al. Clinical efficacy of lenalidomide in patients with relapsed or refractory chronic lymphocytic leukemia: results of a Phase II study. J. Clin. Oncol.24(34), 5343–5349 (2006).
  • Weber DM, Chen C, Niesvizky R et al. Lenalidomide plus dexamethasone for relapsed multiple myeloma in North America. N. Engl. J. Med.357(21), 2133–2142 (2007).
  • List A, Dewald G, Bennett J et al. Lenalidomide in the myelodysplastic syndrome with chromosome 5q deletion. N. Engl. J. Med.355(14), 1456–1465 (2006).
  • Raza A, Reeves JA, Feldman EJ et al. Phase 2 study of lenalidomide in transfusion-dependent, low-risk, and intermediate-1 risk myelodysplastic syndromes with karyotypes other than deletion 5q. Blood111(1), 86–93 (2008).
  • Dueck G, Chua N, Prasad A et al. Interim report of a Phase 2 clinical trial of lenalidomide for T-cell non-Hodgkin lymphoma. Cancer116(19), 4541–4548 (2010).
  • Strupp C, Aivado M, Germing U, Gattermann N, Haas R. Angioimmunoblastic lymphadenopathy (AILD) may respond to thalidomide treatment: two case reports. Leuk. Lymphoma43(1), 133–137 (2002).
  • Dogan A, Ngu LS, Ng SH, Cervi PL. Pathology and clinical features of angioimmunoblastic T-cell lymphoma after successful treatment with thalidomide. Leukemia19(5), 873–875 (2005).
  • Bruns I, Fox F, Reinecke P et al. Complete remission in a patient with relapsed angioimmunoblastic T-cell lymphoma following treatment with bevacizumab. Leukemia19(11), 1993–1995 (2005).
  • Aguiar Bujanda D. Complete response of relapsed angioimmunoblastic T-cell lymphoma following therapy with bevacizumab. Ann. Oncol.19(2), 396–397 (2008).
  • Gottardi M, Danesin C, Canal F et al. Complete remission induced by thalidomide in a case of angioimmunoblastic T-cell lymphoma refractory to autologous stem cell transplantation. Leuk. Lymphoma49(9), 1836–1838 (2008).
  • Ramasamy K, Lim Z, Pagliuca A, Salisbury JR, Mufti GJ, Devereux S. Successful treatment of refractory angioimmunoblastic T-cell lymphoma with thalidomide and dexamethasone. Haematologica91(8 Suppl.), ECR44 (2006).
  • Taniguchi T, Minami Y. The IL-2/IL-2 receptor system: a current overview. Cell73(1), 5–8 (1993).
  • Wagner DK, Kiwanuka J, Edwards BK, Rubin LA, Nelson DL, Magrath IT. Soluble interleukin-2 receptor levels in patients with undifferentiated and lymphoblastic lymphomas: correlation with survival. J. Clin. Oncol.5(8), 1262–1274 (1987).
  • LeMaistre CF, Saleh MN, Kuzel TM et al. Phase I trial of a ligand fusion-protein (DAB389IL-2) in lymphomas expressing the receptor for interleukin-2. Blood91(2), 399–405 (1998).
  • Prince HM, Duvic M, Martin A et al. Phase III placebo-controlled trial of denileukin diftitox for patients with cutaneous T-cell lymphoma. J. Clin. Oncol.28(11), 1870–1877 (2010).
  • Dang NH, Pro B, Hagemeister FB et al. Phase II trial of denileukin diftitox for relapsed/refractory T-cell non-Hodgkin lymphoma. Br. J. Haematol.136(3), 439–447 (2007).
  • Altman JK, Platanias LC. Exploiting the mammalian target of rapamycin pathway in hematologic malignancies. Curr. Opin. Hematol.15(2), 88–94 (2008).
  • Johnston PB, Inwards DJ, Colgan JP et al. A Phase II trial of the oral mTOR inhibitor everolimus in relapsed Hodgkin lymphoma. Am. J. Hematol.85(5), 320–324 (2010).
  • Darwiche N, Sinjab A, Abou-Lteif G et al. Inhibition of mammalian target of rapamycin signaling by everolimus induces senescence in adult T-cell leukemia/lymphoma and apoptosis in peripheral T-cell lymphomas. Int. J. Cancer.129(4), 993–1004 (2011).
  • Johnston PB, Ansell SM, Colgan JP et al. mTOR inhibition for relapsed or refractory Hodgkin lymphoma: promising single agent activity with everolimus (RAD001). Blood (ASH Annual Meeting Abstracts)110, 2555 (2007).
  • Johnston PB, Yuan R, Cavalli F, Witzig TE. Targeted therapy in lymphoma. J. Hematol. Oncol.3, 45 (2010).
  • Sirotnak FM, DeGraw JI, Moccio DM, Samuels LL, Goutas LJ. New folate analogs of the 10-deaza-aminopterin series. Basis for structural design and biochemical and pharmacologic properties. Cancer Chemother. Pharmacol.12(1), 18–25 (1984).
  • O’Connor OA, Hamlin PA, Portlock C et al. Pralatrexate, a novel class of antifol with high affinity for the reduced folate carrier-type 1, produces marked complete and durable remissions in a diversity of chemotherapy refractory cases of T-cell lymphoma. Br. J. Haematol.139(3), 425–428 (2007).
  • O’Connor OA, Horwitz S, Hamlin P et al. Phase II–I–II study of two different doses and schedules of pralatrexate, a high-affinity substrate for the reduced folate carrier, in patients with relapsed or refractory lymphoma reveals marked activity in T-cell malignancies. J. Clin. Oncol.27(26), 4357–4364 (2009).
  • O’Connor O PB, Pinter-Brown LL. Results of the pivotal, multicenter, Phase II study of pralatrexate in patients with relapsed or refractory peripheral T-cell lymphoma (PTCL). J. Clin. Oncol.27(15 Suppl.), (2009) (Abstract 8561).
  • Malik SM, Liu K, Qiang X et al. Folotyn (pralatrexate injection) for the treatment of patients with relapsed or refractory peripheral T-cell lymphoma: U.S. Food and Drug Administration drug approval summary. Clin. Cancer Res.16(20), 4921–4927 (2010).
  • Marchi E, Paoluzzi L, Scotto L et al. Pralatrexate is synergistic with the proteasome inhibitor bortezomib in in vitro and in vivo models of T-cell lymphoid malignancies. Clin. Cancer Res.16(14), 3648–3658 (2010).
  • Horwitz S, Vose JM, O’Connor O. A Phase 1/2A open label study of pralatrexate and gemcitabine in patients with relapsed or refractory lymphoproliferative malignancies. Presented at: 51st American Society of Hematology Annual Meeting. New Orleans, LA, USA, 5–8 December 2009.
  • Piccaluga PP, Agostinelli C, Tripodo C et al. Peripheral T-cell lymphoma classification: the matter of cellular derivation. Expert Rev. Hematol.4(4), 415–425 (2011).

Websites

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.