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Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome‐wide clonal evolution
Author(s) -
Xerri Luc,
Adélaïde José,
Avenin Morgan,
Guille Arnaud,
Taix Sebastien,
Bonnet Nathalie,
Carbuccia Nadine,
Garnier Séverine,
Mescam Lenaïg,
Murati Anne,
Chaffanet Max,
Coso Diane,
Bouabdallah Reda,
Bertucci François,
Birnbaum Daniel
Publication year - 2019
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.13783
Subject(s) - lymphomatoid papulosis , anaplastic large cell lymphoma , lymphoma , nodal , biology , context (archaeology) , lymph node , clone (java method) , cancer research , pathology , cd30 , medicine , gene , immunology , genetics , paleontology
Aims This study sought to clarify the molecular pathways underlying the putative evolution from lymphomatoid papulosis (LyP) to cutaneous anaplastic large‐cell lymphoma (c‐ ALCL ) and lymph node invasion ( LNI ). Methods and results We analysed nine sequential tumours from the same patient presenting with parallel evolution of LyP ( n = 3) and c‐ ALCL ( n = 1) with LNI ( n = 1), combined with systemic diffuse large B‐cell lymphoma ( DLBCL ) ( n = 4). Clonality analysis showed a common clonal T‐cell origin in the five CD 30+ lesions, and a common clonal B‐cell origin in the four DLBCL relapses. Array‐comparative genomic hybridisation and targeted next‐generation sequencing analysis demonstrated relative genomic stability of LyP lesions as compared with clonally related anaplastic large‐cell lymphoma ( ALCL ) tumours, which showed 4q and 22q13 deletions involving the PRDM 8 and TIMP 3 tumour suppressor genes, respectively. The three analysed CD 30+ lesions showed mostly private (specific to each sample) genetic alterations, suggesting early divergence from a common precursor. In contrast, DLBCL tumours showed progressive accumulation of private alterations, indicating late divergence. Conclusions Sequential cutaneous and nodal CD 30+ tumours were clonally related. This suggests that LyP, c‐ ALCL and LNI represent a continuous spectrum of clonal evolution emerging from a common precursor of cutaneous CD 30+ lymphoproliferations. Therefore, nodal ALCL tumours in the context of LyP should be considered as a form of transformation rather than composite lymphoma.