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Proteomic analysis of anaplastic lymphoma cell lines: Identification of potential tumour markers
Author(s) -
Cussac Daniel,
Pichereaux Carole,
Colomba Audrey,
Capilla Florence,
Pont Frédéric,
GaitsIacovoni Frédérique,
Lamant Laurence,
Espinos Estelle,
BurletSchiltz Odile,
Monsarrat Bernard,
Delsol Georges,
Payrastre Bernard
Publication year - 2006
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200500647
Subject(s) - anaplastic large cell lymphoma , anaplastic lymphoma kinase , proteome , biology , cancer research , lymphoma , phenotype , proteomics , cell type , cell culture , cell , pathology , medicine , bioinformatics , genetics , immunology , gene , malignant pleural effusion , lung cancer
Anaplastic large‐cell lymphomas (ALCL) are high grade lymphomas of T or null phenotype often associated with the t(2;5) translocation leading to the expression of a chimeric protein consisting of the N‐terminal portion of nucleophosmin (NPM) and the intracellular domain of the anaplastic lymphoma kinase (ALK). Although ALCL are recognized as distinct clinical, biological and cytogenetic entities, heterogeneities persist in this group of tumours, which exhibit a broad spectrum of morphological features. Particularly, the common type tumour consisting in large cells contrast with the small cell variant that is sometimes associated with a leukemic phase. The ALK‐negative ALCL is often associated with a poor prognosis. Here, we investigated the proteome of these subtypes of tumours using patient‐derived cell lines. We compared the proteome of the cytosolic fraction of NPM‐ALK‐positive versus NPM‐ALK‐negative cells on one hand, and the proteome of common cell type versus small cell variant on the other hand. The identification of a set of proteins differentially expressed in the subtypes of ALCL points to new diagnosis/prognosis markers. This study also provides interesting information on the molecular mechanisms responsible for the different subtypes of ALCL.