Page 30 - Haematologica August 2018

1266
M. de Charette et al.
Death Pathway. Mol Cell Biol. 1998;18(11):
6387-6398.
65. Muris JJF, Meijer CJLM, Cillessen SAGM, et
al. Prognostic significance of activated cyto- toxic T-lymphocytes in primary nodal dif- fuse large B-cell lymphomas. Leukemia. 2004;18(3):589-596.
66. van Eijk M, Defrance T, Hennino A, de Groot C. Death-receptor contribution to the germinal-center reaction. Trends Immunol. 2001;22(12):677-682.
67. Afshar-Sterle S, Zotos D, Bernard NJ, et al. Fas ligand–mediated immune surveillance by T cells is essential for the control of spon- taneous B cell lymphomas. Nat Med. 2014;20(3):283-290.
68. Kondo E, Yoshino T, Yamadori I, et al. Expression of Bcl-2 protein and Fas antigen in non-Hodgkin’s lymphomas. Am J Pathol. 1994;145(2):330.
69. Chatzitolios A, Venizelos I, Tripsiannis G, Anastassopoulos G, Papadopoulos N. Prognostic significance of CD95, P53, and BCL2 expression in extranodal non- Hodgkin’s lymphoma. Ann Hematol. 2010;89(9):889-896.
70. Zoi-Toli O, Meijer CJ, Oudejans JJ, de Vries E, van Beek P, Willemze R. Expression of Fas and Fas ligand in cutaneous B-cell lym- phomas. J Pathol. 1999;189(4):533-538.
71. Eser B, Sari I, Canoz O, et al. Prognostic sig- nificance of Fas (CD95/APO-1) positivity in patients with primary nodal diffuse large B- cell lymphoma. Am J Hematol. 2006;81(5): 307-314.
72. Markovic O, Marisavljevic D, Cemerikic V, et al. Clinical and prognostic significance of apoptotic profile in patients with newly diagnosed nodal diffuse large B-cell lym- phoma (DLBCL): Apoptosis in nodal diffuse large B-cell lymphoma. Eur J Haematol. 2011;86(3):246-255.
73. Poppema S. Immunobiology and patho- physiology of Hodgkin lymphomas. Hematology Am Soc Hematol Educ Program. 2005;2005:231-238.
74. Müschen M, Rajewsky K, Krönke M, Küppers R. The origin of CD95-gene muta- tions in B-cell lymphoma. Trends Immunol. 2002;23(2):75-80.
75. Grønbaek K, Straten PT, Ralfkiaer E, et al. Somatic Fas mutations in non-Hodgkin’s lymphoma: association with extranodal dis- ease and autoimmunity. Blood. 1998;92(9): 3018-3024.
76. Niitsu N, Sasaki K, Umeda M. A high serum soluble Fas/APO-1 level is associated with a poor outcome of aggressive non-Hodgkin’s lymphoma. Leukemia. 1999;13(9):1434- 1440.
77. Hara T, Tsurumi H, Takemura M, et al. Serum-soluble fas level determines clinical symptoms and outcome of patients with aggressive non-Hodgkin’s lymphoma. Am J Hematol. 2000;64(4):257-261.
78. Hara T, Tsurumi H, Goto N, et al. Serum sol- uble Fas level determines clinical outcome of patients with diffuse large B-cell lymphoma treated with CHOP and R-CHOP. J Cancer Res Clin Oncol. 2009;135(10):1421-1428.
79. Heredia-Galvez B, Ruiz-Cosano J, Torres- Moreno D, et al. Association of polymor- phisms in TRAIL1 and TRAILR1 genes with susceptibility to lymphomas. Ann Hematol. 2014;93(2):243-247.
80. Zerafa N, Westwood JA, Cretney E, et al. Cutting edge: TRAIL deficiency accelerates hematological malignancies. J Immunol. 2005;175(9):5586-5590.
81. Lee SH, Shin MS, Kim HS, et al. Somatic mutations of TRAIL-receptor 1 and TRAIL-
receptor 2 genes in non-Hodgkin’s lym-
phoma. Oncogene. 2001;20(3):399.
82. Young KH, Weisenburger DD, Dave BJ, et al. Mutations in the DNA-binding codons of TP53, which are associated with decreased expression of TRAILreceptor-2, predict for poor survival in diffuse large B-cell lym-
phoma. Blood. 2007;110(13):4396-4405.
83. Rubio-Moscardo F, Climent J, Siebert R, et al. Mantle-cell lymphoma genotypes identi- fied with CGH to BAC microarrays define a leukemic subgroup of disease and predict patient outcome. Blood. 2005;105(11):4445-
4454.
84. Singh K, Briggs JM. Functional Implications
of the spectrum of BCL2 mutations in Lymphoma. Mutat Res Mutat Res. 2016;769:1-18.
85. Morin RD, Mendez-Lago M, Mungall AJ, et al. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011;476(7360):298.
86. Schuetz JM, Johnson NA, Morin RD, et al. BCL2 mutations in diffuse large B-cell lym- phoma. Leukemia. 2012;26(6):1383.
87. Huet S, Szafer-Glusman E, Tesson B, et al. BCL2 mutations do not confer adverse prog- nosis in follicular lymphoma patients treated with rituximab. Am J Hematol. 2017;92(6): 515-519.
88. Iqbal J, Sanger WG, Horsman DE, et al. BCL2 translocation defines a unique tumor subset within the germinal center B-cell-like diffuse large B-cell lymphoma. Am J Pathol. 2004;165(1):159-166.
89. Mounier N, Briere J, Gisselbrecht C, et al. Rituximab plus CHOP (R-CHOP) over- comes bcl-2-associated resistance to chemotherapy in elderly patients with dif- fuse large B-cell lymphoma (DLBCL). Blood. 2003;101(11):4279-4284.
90. Akyurek N, Uner A, Benekli M, Barista I. Prognostic significance of MYC , BCL2 , and BCL6 rearrangements in patients with dif- fuse large B-cell lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab: MYC, BCL2, BCL6 Rearrangements in DLBCL. Cancer. 2012;118(17):4173-4183.
91. Grange F, Petrella T, Beylot-Barry M, et al. Bcl-2 protein expression is the strongest independent prognostic factor of survival in primary cutaneous large B-cell lymphomas. Blood. 2004;103(10):3662-3668.
92. Correia C, Schneider PA, Dai H, et al. BCL2 mutations are associated with increased risk of transformation and shortened survival in follicular lymphoma. Blood. 2015;125(4): 658-667.
93. Kiyasu J, Miyoshi H, Hirata A, et al. Expression of programmed cell death ligand 1 is associated with poor overall survival in patients with diffuse large B-cell lymphoma. Blood. 2015;126(19):2193-2201.
94. Bledsoe JR, Redd RA, Hasserjian RP, et al. The immunophenotypic spectrum of pri- mary mediastinal large B-cell lymphoma reveals prognostic biomarkers associated with outcome: Immunophenotypic Prognostic Markers in PMBL. Am J Hematol. 2016;91(10):E436-E441.
95. Berghoff AS, Ricken G, Widhalm G, et al. PD1 (CD279) and PD-L1 (CD274, B7H1) expression in primary central nervous sys- tem lymphomas (PCNSL). Clin Neuropathol. 2014;33(1):42-49.
96. Green MR, Monti S, Rodig SJ, et al. Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expres- sion, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and
primary mediastinal large B-cell lymphoma.
Blood. 2010;116(17):3268-3277.
97. Twa DDW, Chan FC, Ben-Neriah S, et al.
Genomic rearrangements involving pro- grammed death ligands are recurrent in pri- mary mediastinal large B-cell lymphoma. Blood. 2014;123(13):2062-2065.
98. Chapuy B, Roemer MG, Stewart C, et al. Targetable genetic features of primary testic- ular and primary central nervous system lymphomas. Blood. 2016;127(7):869-881.
99. Georgiou K, Chen L, Berglund M, et al. Genetic basis of PD-L1 overexpression in diffuse large B-cell lymphomas. Blood. 2016;127(24):3026-3034.
100.Kataoka K, Shiraishi Y, Takeda Y, et al. Aberrant PD-L1 expression through 3 -UTR disruption in multiple cancers. Nature. 2016;534(7607):402-406.
101.Green MR, Rodig S, Juszczynski P, et al. Constitutive AP-1 activity and EBV infection induce PD-L1 in Hodgkin lymphomas and posttransplant lymphoproliferative disor- ders: implications for targeted therapy. Clin Cancer Res Off J Am Assoc Cancer Res. 2012;18(6):1611-1618.
102.
103.
Rossille D, Gressier M, Damotte D, et al. High level of soluble programmed cell death ligand 1 in blood impacts overall survival in aggressive diffuse large B-Cell lymphoma: results from a French multicenter clinical trial. Leukemia. 2014;28(12):2367-2375. Rossille D, Azzaoui I, Feldman AL, et al. Soluble programmed death-ligand 1 as a prognostic biomarker for overall survival in patients with diffuse large B-cell lymphoma: a replication study and combined analysis of 508 patients. Leukemia. 2017;31(4):988.
104. Carosella ED, Rouas-Freiss N, Roux DT-L, Moreau P, LeMaoult J. HLA-G. In: Arun K Shukla, eds. Advances in Immunology. Elsevier; 2015; p.33-144.
105. Jesionek-Kupnicka D, Bojo M, Prochorec- Sobieszek M, et al. HLA-G and MHC Class II Protein Expression in Diffuse Large B-Cell Lymphoma. Arch Immunol Ther Exp (Warsz). 2016;64(3):225-240.
106. Caocci G, Greco M, Fanni D, et al. HLA-G expression and role in advanced-stage classi- cal Hodgkin lymphoma. Eur J Histochem. 2016;60(2):2606.
107. Diepstra A, Poppema S, Boot M, et al. HLA- G protein expression as a potential immune escape mechanism in classical Hodgkin’s lymphoma. Tissue Antigens. 2008;71(3): 219-226.
108. Sebti Y, Le Maux A, Gros F, et al. Expression of functional soluble human leucocyte anti- gen-G molecules in lymphoproliferative dis- orders. Br J Haematol. 2007;138(2):202–212.
109.SebtiY,LeFriecG,PangaultC,etal.Soluble HLA-G molecules are increased in lympho- proliferative disorders. Hum Immunol. 2003;64(11):1093-1101.
110. Yong P, Kim SJ, Lee SJ, Kim BS. Serum level of soluble human leukocyte antigen-G mol- ecules in non-Hodgkin lymphoma: Does it have a prognostic value? Leuk Lymphoma. 2008;49(8):1623-1626.
111. Barclay AN, van den Berg TK. The Interaction Between Signal Regulatory Protein Alpha (SIRP-a) and CD47: Structure, Function, and Therapeutic Target. Annu Rev Immunol. 2014;32(1):25-50.
112. Chao MP, Alizadeh AA, Tang C, et al. Anti- CD47 Antibody Synergizes with Rituximab to Promote Phagocytosis and Eradicate Non- Hodgkin Lymphoma. Cell. 2010;142(5):699- 713.
113.Chao MP, Tang C, Pachynski RK, Chin R, Majeti R, Weissman IL. Extranodal dissemi-
haematologica | 2018; 103(8)