Karyotypic abnormalities and immunoglobulin gene rearrangements in Hodgkin's disease

Banks, Rosamonde E.; Gledhill, Sarah; Ross, Fiona; Krajewski, A. S.; Dewar, A E; Weir-Thompson, E M

doi:10.1016/0165-4608(91)90015-m

Cited by 11 publications

(4 citation statements)

References 33 publications

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“…Published cytogenetic studies of H D contain fewer than 50 complete karyotypes of clonally abnormal cases, including the reports reviewed by Sandberg (1990) and Thangavelu and Le Beau (1989), as well as other recent reports (Dennis et al, 1989;Banks et al, 1991). Progress in this field has been hampered by the poor yield of abnormal metaphases in chromosome preparations of HD, +10,+1 I,+12,+16,+16,+19,+21,+21,+21 which has been attributed to the low proportion of neoplastic cells in the involved lymph nodes and to their low mitotic rate.…”

Section: Discussionmentioning

confidence: 99%

Clonal cytogenetic abnormalities in Hodgkin's disease

Ladanyi

Parsa

Offit

et al. 1991

Genes Chromosomes & Cancer

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Cytogenetic studies of Hodgkin's disease (HD), in contrast to those of non-Hodgkin's lymphoma (NHL), have been limited to small numbers of cases with infrequently recurring aberrations, underscoring the need for additional studies in establishing a coherent cytogenetic picture of HD. Over a 6 1/2-year period, we received 95 specimens of HD for cytogenetic analysis. Analyzable chromosome preparations were obtained in 70 cases, of which 57 (81%) showed only normal metaphases. In the remaining 13 cases (19%), karyotypic abnormalities were observed that were nonclonal in 3 and clonal in 10. The latter 10 cases included 6 of the nodular sclerosis subtype, 3 mixed cellularity, and 1 lymphocyte-depleted; 8 of the specimens were obtained pretreatment and 2 posttreatment. Two of the cases had a clonal numerical aberration, monosomy 17 in one and trisomy 13 in the other, as their sole abnormality. The remaining 8 cases showed complex karyotypes with multiple structural rearrangements; in 3 of these, the abnormal clone was near-tetraploid. Bands involved more than once included 1p36, 1q21, and 4q35, each in 2 cases. Arms involved more than once included 6q (6q13,6q23), 9p (9p13,9p21), and 5q (5q15,5q35). Three patients had loss of part or all of 6q (del(6)(q13),del(6)(q23),i(6p). Bands 14q32 and 18q21 were not involved in any case, contrary to some previous reports. Our results confirm the frequent occurrence of 1p, 1q, and 6q abnormalities in HD. In addition, we have identified a 5q35 breakpoint, which has recently been shown to be highly specific for Ki-1-positive NHL in a case of typical nodular sclerosis HD. Its presence in HD may represent a cytogenetic link between the two entities, which are immunophenotypically related but clinically and histologically distinct.

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Section: Discussionmentioning

confidence: 99%

Clonal cytogenetic abnormalities in Hodgkin's disease

Ladanyi

Parsa

Offit

et al. 1991

Genes Chromosomes & Cancer

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“…ASA rearrangements together comprise by far the most numerous breakpoints reported in HD, [33][34][35][36][37][38][39][40][41][42][43][44] in particular those anaLeukemia lyzed before treatment, 40 implying a spontaneous origin rather than via therapeutic induction. Ectopic rDNA has been noted previously in the L-540 HD cell line 61 which, as reported in this study (Table 2), may be a more general feature of HD cell lines.…”

Section: Possible Roles For Rdna Changesmentioning

confidence: 99%

“…In contrast to ASA (p11-p13) breakpoints, there is no excess of centromeric (p10/q10) rearrangements in HD [33][34][35][36][37][38][39][40][41][42][43][44] to indicate targeting any of the several families of resident DNA repeats, notably ␣-sat. DNA.…”

Section: Possible Roles For Rdna Changesmentioning

confidence: 99%

Karyotypic dissection of Hodgkin's disease cell lines reveals ectopic subtelomeres and ribosomal DNA at sites of multiple jumping translocations and genomic amplification

MacLeod

Spitzer

Bar‐Am³

et al. 2000

Leukemia

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Although the neoplastic significance of the chromosome changes widespread in Hodgkin's disease (HD) remains obscure, a distinct cytogenetic picture has emerged combining aneuploidy with structural rearrangements clustered at certain breakpoints. Notably absent are the recurrent chromosome translocations which distinguish other hematopoietic neoplasms and serve as clues to underlying oncogene alterations. The paucity of neoplastic cells in HD biopsies hinders detailed chromosome analysis. As an alternative, we investigated a panel of well characterized cell lines by classical and molecular cytogenetics, using single-gene and subtelomeric probes, including three autologous HD examples (HDLM-1/2/3) analyzed by 'spectral karyotyping' -the first complete HD karyotype to be documented. Although complex, most rearrangements in HDLM cells arose in vivo and included few rare but many typical HD breakpoints, notably at the r(ibosomal)DNA regions. Two types of genomic rearrangement involving DNA repeats were conspicuous: insertion and genomic amplification/coamplification of rDNA -the first genomic rDNA rearrangements to be reported in a tumor cell, and the first example of multiple 'jumping translocations' (JT). Of four subtelomeric microsatellite repeats tested in HDLM cells, three exhibited interstitial sites at JT, of which two (at 5qter and 9pter) were respectively associated with deletion of the 5q31-32 myeloid region, and coamplification of a recently described HD-recurrent amplicon at 9p2 together with transcriptionally silent rDNA. Altogether, three out of four HD cell lines carried interstitial 9p subtelomeres and rDNA rearrangements. Taken together, these data suggest tumorigenic rearrangements may be facilitated by 'hitchhiking' along with mobile DNA repeat sequences which may target gene rearrangement at 9p in HD. Southern analysis of parallel rearrangements within rDNA intergenic spacers in HDLM cells highlighted several at, or near, retroposons. As well as validating HD cell lines as cytogenetic models, and resources for identifying genes rearranged in HD, our findings warrant further investigation of the roles of DNA repeat sequences, notably subtelomeric microsatellites, rDNA spacer sequences and retroposons as facilitators and markers of tumor-gene rearrangement.

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“…Acute lymphoblastic leukemia (B-ALL in 5 cases, ALL not otherwise specified (NOS) in the 3 remaining cases) (Ahmad et al, 2008;Arana-Trejo et al, 1993;Guillaume et al, 2001;Heerema et al, 1985;Silva et al, 2002;Testa et al, 1985;Tsang et al, 2001;Yamada and Furusawa, 1976), acute myeloid leukemia (one M2-AML, one AML-NOS) (Hda et al, 1996;Li et al, 1983), myelodysplastic syndromes (one case of refractory anemia (RA) and 2 cases of refractory anemia with excess of blasts (RAEB)) (Horiike et al, 1988;Guillaume et al, 2001), myeloproliferative syndromes (idiopathic myelofibrosis, one case) (Whang-Peng et al, 1978), chronic lymphocytic leukemia (2 cases, Ohtaki et al, 1986;Sadamori et al, 1984) and Hodgkin disease (2 cases, Banks et al, 1991;Kristoffersson et al, 1987).…”

Section: Phenotype/cell Stem Originmentioning

confidence: 99%