Chromosomes of lymphosarcoma and cancer cells in bone marrow

Sandberg, Avery A.; Ishihara, Tsuyoshi; Kikuchi, Yasumoto; Crosswhite, Lois H.

doi:10.1002/1097-0142(196406)17:6<738::aid-cncr2820170609>3.0.co;2-m

Cited by 40 publications

(17 citation statements)

References 11 publications

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“…1) A trisomic condition of one of the group 17,18 chromosomes has been reported in 3 cases of lymphosarcoma (Sandberg et al, 1964), a mixed lymphoblast-reticulum cell lymphoma (Millard, 1968), and 4 cases of reticulum cell sarcoma (Lawler, Pentycross and Reeves, 1968;Miles, 1967). This anomaly has also been described in 6 out of 16 cases of primary macroglobulinaemia (Tanzer et al, 1966), and in a case of chronic granulocytic leukaemia after metamorphosis (Spiers and Baikie, 1968b).…”

Section: Experimental Evidencementioning

confidence: 99%

“…On the other hand, we will not attempt to regularly differentiate the chromosome pairs 17 and 18 from one another. While such differentiation is frequently possible in preparations of optimal quality, the morphology of chromosomes prepared from tumour tissue is often of a much lower standard (Ishihara, Kikuchi and Sandberg, 1963;Sandberg et al, 1962;Nowell and Hungerford, 1964).…”

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confidence: 99%

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A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Spiers¹,

Baikie²

1970

Br J Cancer

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The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph 1 anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph 1 in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes. Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines.

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Section: Experimental Evidencementioning

confidence: 99%

mentioning

confidence: 99%

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Spiers¹,

Baikie²

1970

Br J Cancer

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“…Considering together isolated cases and relatively small series, 19 cases of lymphoblastic lymphosarcoma, 7 of lymphocytic lymphosarcoma, 24 of reticulum cell sarcoma, 9 of follicular lymphoma and 10 of Burkitt's tumour have so far been reported (Tjio et al, 1963;Jacobs et al, 1963;Sandberg et al, 1964;Baker aiid Atkin, 1965;Fitzgerald and Adams, 1965;Sasaki et al, 1965;Stewart et al, 1965;Atkin et al, 1966;Miles et al, 1966;Miles, 1967;Kajii et al, 1968;Lawler et al, 1968;AEllard, 1968;Spiers and Baikie, 1968;Clarkson et al, 1969). In a review of Hodgkin's disease by Seif and Spriggs (1967), they collected 22 observations including 8 of their own.…”

Section: Discussionmentioning

confidence: 99%

“…

ALTHOUGH chromosome abnormalities have previously been reported in malignant lymphomas (Tjio et al, 1963;Sandberg et al, 1964;Sasaki et al, 1965; Baker and Atkin, 1965; Seif and Spriggs, 1967; Miles et al, 1966; Miles, 1967; Spiers and Baikie, 1968; Millard, 1968), the available data is scarce in comparison with the large number of cytogenetic studies in leukaemia and the similar incidence of both diseases. Approximately 80% of cases showed chromosome abnormalities which were represented by abnormal clones, with a modal number of chromosomes in the diploid range in lymphocytic lymphomas and reticulum cell sarcomas, and in the triploid-tetraploid range in Hodgkin's disease.

…”

mentioning

confidence: 99%

Cytogenetic Studies in Malignant Lymphomas: A Study of 28 Cases

Coutinho¹,

Bottura²,

Falcão³

1971

Br J Cancer

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ALTHOUGH chromosome abnormalities have previously been reported in malignant lymphomas (Tjio et al., 1963;Sandberg et al., 1964;Sasaki et al., 1965; Baker and Atkin, 1965; Seif and Spriggs, 1967; Miles et al., 1966; Miles, 1967; Spiers and Baikie, 1968; Millard, 1968), the available data is scarce in comparison with the large number of cytogenetic studies in leukaemia and the similar incidence of both diseases. Approximately 80% of cases showed chromosome abnormalities which were represented by abnormal clones, with a modal number of chromosomes in the diploid range in lymphocytic lymphomas and reticulum cell sarcomas, and in the triploid-tetraploid range in Hodgkin's disease. The present report describes chromosome analyses, by a direct method, in 28 patients with malignant lymphomas.

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“…Ishihara, Kikuchi and Sandberg (1963) observed marker chromosomes in 16 of the 20 malignant effusions studied whilst Makino et al (1964) found 1 or more present in 16 of 32 cases they analysed in detail. However, in 75 patients with acute leukaemia, Sandberg et al (1964) reported only 9 to have marker chromosomes. They were identified in 6 of the 19 solid tumours from children, a considerably higher incidence than in acute leukaemia, but somewhat lower than is encountered in adult solid tumours and effusions.…”

Section: Discussionmentioning

confidence: 99%