A 14q+ Marker and a Late Replicating Chromosome #22 in a Brain Tumor: 
            Brief Communication

Yamada, Kiyomi; Yoshioka, Masumi; Oami, Hiroshi

doi:10.1093/jnci/59.4.1193

Cited by 28 publications

(4 citation statements)

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“…The EBV-like chimpanzee, baboon, and orangoutan viruses were studied in some detail (26)(27)(28)(29) (33). 14q+ markers were subsequently described in a variety of other lymphoreticular neoplasias (31,(34)(35)(36)(37)(38)(39) We have previously suggested (42) that BL develops in at least three steps. In African BL, the first step is the EBV-induced immortalization of some B lymphocytes upon primary infection.…”

mentioning

confidence: 99%

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Klein¹

1979

Proc. Natl. Acad. Sci. U.S.A.

261

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Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell Iymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.

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mentioning

confidence: 99%

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Klein¹

1979

Proc. Natl. Acad. Sci. U.S.A.

261

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“…The translocation has also been observed in one case each of chronic lymphocytic leukemia and lymphosarcoma (Fleischman and Prigogina, 1977 ;Zech et al, 1976). Translocations between 14q and other chromosomes have been reported in other types of malignant lymphoma (Fleischman and Prigogina, 1977;Mark et al, 1977;Yamada et al, 1977). In the present investigation, answers to the following questions were sought.…”

mentioning

confidence: 70%

“…In eight non-BL cases, including one case of plasma-cell leukemia from the literature, the translocation involved Nos. 1, 10, 11, and 14 (McCaw et al, 1975;Fleischman and Prigogina, 1977;Mark et al, 1977;Yamada et al, 1977; Liang and Rowley, 1978). Two reports give the origin of a 14q+ marker as a 14q tandem translocation (Fukuhara ef al., 1976) and as a 14q duplication (Mark, 1975); in the former study, reinterpretation suggests that only one case (case 19 in this series) of nine with a 14qf marker shows a complex 14q tandem translocation.…”

Section: Receptor Site In the 14q Translocationmentioning

confidence: 99%

Chromosome 14 translocations in non‐burkitt lymphomas

Fukuhara

Rowley

1978

Intl Journal of Cancer

150

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Chromosome studies were performed on malignant cells obtained from 27 patients with non-Burkitt lymphomas. A marker chromosome affecting the long arm of No. 14 (14q+) was the single most frequent abnormality and was noted in 17 of these patients. The frequency of the 14q+ marker varied with the type of lymphoma. For patients with malignant lymphoma, histiocytic, the frequency was 5 of 8; for mixed-cell type, 1 of 3; for poorly differentiated lymphocytic, 8 of 8; for well-differentiated lymphocytic, 0 of 3; for lymphoblastic, 0 of 1; for Hodgkin's disease, 2 of 3; and for mycosis fungoides, 1 of 1. The donor chromosome involved in the 14q translocation was identified in 12 cases; certain chromosomes appeared to be affected more frequently than others. Although the break point was band 14q32 in most cases, the exact location of the receptor site on 14q was not always consistent. The distal part of 14q24 was also involved as a receptor site in at least one translocation. These findings suggest that, in some types of lymphoid malignancy, cells with a 14q translocation have a proliferative advantage over cells with other chromosome rearrangments. The presence of the 14q translocation may be important in the future for the distinction among morphologically different, but functionally comparable, subgroups of lymphoid malignancies.

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“…In other instances the 14qf chromosome has had a varying morphology depending on the origin of the translocated segment. In a range of non-Burkitt lymphomas these have included chromosome number 1 (Yamada et al, 1977;Fukuhara and Rowley, 1978), chromosomes 4, 15 and 18 (Fukuhara and Rowley, 1978), chromosomes 10 and 11 (Mark et al, 1977) and chromosome 14 (Mark, 1975;Fukuhara et al, 1976). Chromosome number 11 was involved in a case of B-cell ALL (Cimino et al, 1978) and multiple myeloma (Liang and Rowley, 1978).…”

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confidence: 99%

A 14q+ chromosome in a B‐cell acute lymphocytic leukemia and in a leukemic non‐endemic Burkitt lymphoma

Slater

Philip

Badsberg

et al. 1979

Intl Journal of Cancer

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Une analyse des chromosomes par des techniques de coloration des bandes a BtB effectuee sur les cellules d'une leucemie lyniphocytaire aigue (ALL) d'origine B et d u type Burkitt, et d'un lymphome de Burkitt rton endtmique se presentant comme un cas d'ALL. Un marqueur 14q+ a ttB observt chez les deux patients; il etait morphologiquement identique C ceux qui ont Bt6 signales dans des cas de lymphome de Burkitt endemique ou non et dans quelques autres n6oplasmes d'origine B. Toutefois, la provenance du segment transloqu6 n'a pu &re dkterminbe dans aucun des deux cas. En outre, les deux patients possedaient un chromosome 13q+ avec une cassure dans la rtgion 13q3, mais il s'agissait d'un mat6riel different d'origine inconnue. Parmi les autres marqueurs du cas d'ALL, on a observe des rkarrangements des bras Iq et 6q. Des 6udes en strie ont montre que les cellules qui presentent, outre le chromosome 14q+, une duplication partielle du bras long du chromosome no 1 jouent un rBle important dans I'tvolution du caryotype de la population maligne. Dans ce cas, le chromosome 14q+ avait une region satellite brillante en fluorescence, ce qui indique probablement un d6veloppement monoclonal de la population de cellules leucemiques. I1 ressort de la pr6sente communication ainsi que d'autres rapports que 1'ALL de type B se caractkrise par un chromosome 14q+. Etant donne les similitudes patholobiques et cytogenktiques entre certains types d'ALL d'origine B et le lymphome de Rurkitt, i I est suggbr6 qu'il peut s'agir d e manifestations difftrentes du mEme trouble.

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A 14q+ Marker and a Late Replicating Chromosome #22 in a Brain Tumor: Brief Communication

Cited by 28 publications

References 0 publications

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Chromosome 14 translocations in non‐burkitt lymphomas

A 14q+ chromosome in a B‐cell acute lymphocytic leukemia and in a leukemic non‐endemic Burkitt lymphoma

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