Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology | Zendy

Rina Kansal | Zendy; Sheila N.J. Sait | Zendy; AnneMarie W. Block | Zendy; Pamela Ward | Zendy; Felicity L R Kelly | Zendy; Richard T. Cheney | Zendy; Myron S. Czuczman | Zendy; Martin L. Brecher | Zendy; Maurice Barcos | Zendy

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Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology

Author(s) -

Rina Kansal,

Sheila N.J. Sait,

AnneMarie W. Block,

Pamela Ward,

Felicity L R Kelly,

Richard T. Cheney,

Myron S. Czuczman,

Martin L. Brecher,

Maurice Barcos

Publication year - 2004

Publication title -

modern pathology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.596

H-Index - 153

eISSN - 1530-0285

pISSN - 0893-3952

DOI - 10.1038/modpathol.3800299

Subject(s) - anaplastic lymphoma kinase , anaplastic large cell lymphoma , cd30 , lymphoma , pathology , large cell lymphoma , fluorescence in situ hybridization , biology , immunophenotyping , trisomy , gene rearrangement , large cell , cancer research , medicine , chromosome , gene , immunology , genetics , cancer , adenocarcinoma , flow cytometry , malignant pleural effusion , lung cancer

The purpose of this study was to evaluate fluorescence in situ hybridization abnormalities of the 2p23 anaplastic lymphoma kinase (ALK) gene loci in lymphomas with anaplastic morphology. We studied 24 anaplastic large cell lymphomas (ALCL) classified by World Health Organization criteria [17 primary nodal/systemic (10 ALK+, 7 ALK-), seven primary cutaneous], and 17 additional non-Hodgkin's lymphomas [one ALK+ B-lineage lymphoma, 14 ALK- diffuse large B-cell lymphomas (seven anaplastic variants, five nonanaplastic, two secondary CD30+), two follicular lymphomas]. ALK- lymphomas with anaplastic morphology showed extra nonrearranged anaplastic lymphoma kinase gene loci (P=0.004) due to trisomy 2 irrespective of the following factors: B or T/null phenotype (P=0.315), diagnostic categories of systemic or cutaneous ALCL or the above-mentioned B-cell lymphomas (P=0.131), and CD30 positivity by immunohistochemistry (P=1.000). Trisomy 2 was absent in all ALK+ lymphomas (P=0.009), which showed rearranged ALK gene loci (P<0.001). Whether trisomy 2 is a primary or secondary event that leads to ALK- lymphomas cannot be determined from this study. Its presence in secondary B-cell lymphomas suggests that trisomy 2 may be a secondary cytogenetic aberration in lymphomas in general. Further investigation of this finding is necessary to further our understanding of the heterogeneous group of ALK- lymphomas.

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