Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

Abstract

SummaryCytogenetic correlations among most types of peripheral T-cell lymphoma (PTCL) have not been very informative to date. This study aimed to identify recurrent chromosomal abnormalities in angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALK-ALCL) and peripheral T-cell lymphoma, unspecified (PTCL-US), and to evaluate their prognostic value. We reviewed the cytogenetic findings of 90 previously-diagnosed cases of PTCL and correlated the cytogenetic findings with the specific histological subtype. The most common abnormalities for AITL were 5q (55%), 21 (41%) and 3q (36%) gains, concurrent trisomies of 5 and 21 (41%), and loss of 6q (23%). In ALK(-) ALCL, gains of 1q (50%) and 3p (30%), and losses of 16pter (50%), 6q13q21 (30%), 15 (30%), 16qter (30%) and 17p13 (30%) were frequent findings. In PTCL-US, frequent gains involved 7q22q31 (33%), 1q (24%), 3p (20%), 5p (20%), and 8q24qter (22%), and losses of 6q22q24 (26%) and 10p13pter (26%). We did not observe any association between specific chromosomal abnormalities and overall survival (OS). However, cases with complex karyotypes, most frequently observed in ALK(-) ALCL and PTCL-US, had a significantly shorter OS. Although, genetic differences were noted in these subtypes, further studies are needed to determine the key pathogenetic events in PTCL.

Genetic alterations in systemic nodal and extranodal non‐cutaneous lymphomas derived from mature T cells and natural killer cells

“…(8)(9)(10)(11)(12)(13)(14)(15)(16) Most frequent gains occur on chromosomal regions 1q32-qter, 2p (2p15-p16), 7q22-ter, 8q (8q24), 9q33-qter, 11q (11q13), and 17q (17cen-q21). Recurrent losses mainly affect 6q (6q21), 9p21, 10 (10cen-p12, 10q23-q24), 13q (13q21), 14q (14q12-q21), 16q (16q11-q21), and 17p (17p13).…”

Integrative clinicopathological and molecular analyses of angioimmunoblastic T-cell lymphoma and other nodal lymphomas of follicular helper T-cell origin

“…Maria Pamela Dobay, 1 Francois Lemonnier, 2,3 Edoardo Missiaglia, 1,4 Christian Bastard, 5 David Vallois,4 Jean-Philippe Jais, 6 Laurianne Scourzic, 7 Aurélie Dupuy, 2,3 Virginie Fataccioli, 2,3,14 Anais Pujals, 2,3,14 Marie Parrens, 8 Fabien Le Bras, 9 Thérèse Rousset, 10 Jean-Michel Picquenot, 11 Nadine Martin, 2,3 Corinne Haioun, 2,3,9 Richard Delarue, 12 Olivier A. Bernard, 7 Mauro Delorenzi, 1,13 …”

Aspects moléculaires des lymphomes T périphériques (1)

“…Enfin, les déséquilibres observés en CGH (comparative genomic hybridization) diffèrent de ceux retrouvés dans les LAIT ou les LAGC. Il s'agit de gains récurrents des 1q, 3p, 5p, 7q, 8q, 17q et 22q et de pertes des 6q, 10p et 13q [19,51,52].…”

“…Les lymphoproliférations T de présentation essentiellement leucémique (leucémie à cellules natural killer, leucémies à grands lymphocytes à grains, leucémie prolymphocytaire T), les lymphomes T primitifs cutanés (syndrome de Sézary, mycosis fungoïde) et les entités de lymphomes T périphériques dont la prévalence est inférieure à 5 % (lymphome T hépatosplénique, lymphome T sous-cutané de type panniculite) ne seront pas traités ici. < Anomalies cytogénétiques Des aberrations chromosomiques clonales sont observées dans plus de 90 % des cas, principalement des trisomies touchant les chromosomes 5 ou 21, un gain du 3q, du 5q et une perte du 6q [19]. Des translocations impliquant le locus du TCR (récepteur à l'antigène des lymphocytes T) sont retrouvées chez 15 % des patients [20].…”