Cytogenetics of lymphomas: A brief review of its theoretical and practical significance

doi:10.1016/S0165-4608(96)00213-0

Cancer Genetics and Cytogenetics

Volume 94, Issue 1, March 1997, Pages 20-26

https://doi.org/10.1016/S0165-4608(96)00213-0 Get rights and content

Abstract

The following specific or characteristic chromosomal abnormalities are known: t(11;18)(q21;q21) in a subset of marginal zone lymphoma, t(14;18)(q32.3;q21.3) in centroblastic-centrocytic lymphoma, t(11;14)(q13;q32) in mantle cell lymphoma, rearrangement 3q27 in centroblastic lymphoma, t(8;14)(q24;q32) in Burkitt's lymphoma, t(2;5)(p23;q35) in large cell anaplastic lymphoma of T-type and O-type, i(7)(q10) in hepatosplenic γδ T-cell lymphoma, and t(8;13)(p11;q11–12) in T-cell lymphoblastic lymphoma with eosinophilia and myeloid malignancy.

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The current World Health Organization (WHO) classification of hematolymphoid malignancies is based on a multidisciplinary approach that integrates morphologic, molecular, immunophenotypic and cytogenetic findings, among which the morphology is considered as the ‘gold standard’ in making a diagnosis of malignant NHL. Numerous recurrent and clonal cytogenetic abnormalities described in non-Hodgkin lymphoma (NHL) subsets provide the characteristic information for diagnosing specific entities, such as the t(14;18) which is highly associated with follicular lymphoma and t(11;14) with mantle cell lymphoma (Ong and Le Beau, 1998; Donner, 1997; Chaganti et al., 2000). However, does it make sense that there is clonal chromosome abnormality in reactive lymphoid hyperplasia?
Pathological analysis is the cornerstone for diagnosing malignant lymphoma. Status of cytogenetic abnormalities is frequently left unexamined if no evidence of malignancy is found in pathological analysis. In this study, we presented 3 cases in which clonal cytogenetic abnormalities were detected but morphological alterations of the same tissue did not support malignant non Hodgkin lymphoma at the first lymph node biopsy. Case 1 is a 55-year-old female with lymphadenopathy neoplastic process confirmed by flow cytometry and polymerase chain reaction (PCR). Chromosome analysis revealed 47,XX,t(3;22)(q27;q11),+del(9)(p12)[16]/46,XX[4]. The pathological analysis of subsequent lymph node biopsy indicated diffuse large B-cell lymphoma (DLBCL). Case 2, a 74-year-old female, for whom the pathological analysis, molecular studies and flow cytometric analysis of the first lymph node biopsy found no evidence of clonal cell. Cytogenetic analysis demonstrated a terminal deletion of chromosome 7 and 1, and the patient received a second lymph node biopsy and splenectomy. A pathological diagnosis of splenic marginal zone lymphoma (SMZL) was made. In Case 3 who was a 66-year-old female with right cervical and axillary lymph node enlargement. Cytogenetic analysis showed clonal karyotypic abnormalities: 48,XX, t(14;18)(q32;q21) [13]/46, XY [7]. The diagnosis of follicular lymphoma was rendered by the second biopsy of axillary lymph node according to the analysis of morphology and immunohistochemistry. We propose that clonal cytogenetic abnormalities may be a high potential risk for developing non-Hodgkin lymphomas. Follow-up and rebiopsy must be performed in patients who are cytogenetically abnormal but morphologically benign.
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The translocation results in the juxtaposition of the BCL2 locus on chromosome 18 with the IgH locus on chromosome14. The increased expression of BCL2 protein in B cells carrying this translocation prolongs their survival by delaying apoptosis [1,5]. However, additional oncogenic hits are required to induce neoplastic change in the translocation-carrying cells.
We describe a novel t(16;18)(p13;q21.3) in a male patient with follicular lymphoma. This unique chromosomal rearrangement has never been described in patients with follicular lymphoma. The breakpoint of 16p13 has several hematopoietic neoplasm-related genes such as MHC2TA, a master regulatory gene for HLA-D, and BCMA, tumor necrosis factor receptor super-family. The majority of follicular lymphomas have a rearrangement of the BCL2 gene, which is a pathogenetic factor in their development. The diagnostic and prognostic significance of this new translocation is yet to be determined.
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