Clusters of chromosome 9 aberrations are associated with clinico‐pathologic subsets of non‐Hodgkin's lymphoma

Abstract

In this study we analyzed nonrandom aberrations affecting chromosome 9 in a series of 426 consecutively ascertained, karyotypically abnormal non-Hodgkin's lymphoma (NHL) tumors derived from 407 patients. Cytogenetic abnormalities were correlated with clinical, histologic, and immunologic features. Structural abnormalities of chromosome 9 were identified in 60 specimens derived from 59 patients. The recurring abnormalities among these were associated with 4 clinico-pathologic subsets. The first comprised 7 cases of t(9;14)(p13;q32), 6 of which had small lymphocytic lymphoma, plasmacytoid subtype, and an indolent clinical course. The second group included 12 cases with breaks at 9q11-13 and diffuse lymphomas with a large-cell component and a typical response to combination chemotherapy. The third group was comprised of 7 cases with 9q deletions, with a common deleted region encompassing 9q31-32. These cases were characterized by diffuse B-cell histology, young age, and poor clinical outcome. The fourth subset included 5 intermediate- to high-grade T-cell tumors with breaks at 9q34. This analysis of chromosome 9 aberrations in NHL comprises the first such effort based on a large series of tumors. We identify and report here new clinico-pathologic subsets with shared abnormalities of chromosome 9, which should facilitate new approaches to the analysis of the etiology and clinical behavior of NHL.

Secondary chromosomal abnormalities predict outcome in pediatric and adult high‐stage Burkitt lymphoma

“…56 The regions of minimal common 6q deletion vary with disease type, suggesting that different tumor suppressor genes might be affected in each of these neoplasms. [57][58][59] In BL cell lines these deletions are consistently associated with loss of heterozygosity in the 6q25-27 region. 56 Genes possibly affected by 6q abnormalities include BACH2 (encoding for B-lineage specific transcription factor, a putative tumor suppressor gene), on 6q15, 60,61 and BLIMP1 (B-lymphocyte maturation promoting), on 6q21-q22.1.…”

Role of tumor suppressor genes in the development of adult T cell leukemia/lymphoma (ATLL)

“…[285][286][287] In hematologic malignancies, deletions involving the long arm of chromosome 6 are observed primarily in lymphoid malignancies, ie ALL, [288][289][290] lymphoproliferative disorders and NHL. 288,[291][292][293][294] These results indicate that the long arm of chromosome 6 harbors a yet uncharacterized tumor suppressor gene(s) that is altered in many tumors. Cytogenetic studies showed that chromosome 6q is also often affected in acute/lymphomatous ATLL.…”

Cdk9, a member of the cdc2-like family of kinases, binds to gp130, the receptor of the IL-6 family of cytokines

“…Its expression is ubiquitous, and is greater in terminally differentiated tissues, suggesting a role for this kinase in specialized functions in the cell (Gran˜a et al, 1994). Cdk9 maps to chromosome 9q34.1 (Bullrich et al, 1995), a region involved in non-random chromosome alterations, such as T-cell non-Hodgkin's lymphomas, bladder tumors and several myeloproliferative disorders (Offit et al, 1993;Orlow et al, 1994). Cyclin partners of Cdk9 are members of the family of the T cyclins (T1, T2a and T2b) (Peng et al, 1998) and cyclin K (Fu et al, 1999).…”