Chromosomes and causation of human cancer and leukemia.XXVI. Banding studies in acute lymphoblastic leukemia (ALL)

Oshimura, Mitsuo; Freeman, Arnold I.; Sandberg, Avery A.

doi:10.1002/1097-0142(197709)40:3<1161::aid-cncr2820400327>3.0.co;2-2

Cited by 177 publications

(16 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The near identity of a gene sequence of PDGF and v-sis has added credence to this hypothesis (21). A characteristic translocation involving chromosome 4 (q21) and chromosome 11 has been observed in some cases of acute leukemia (28). However, recent phenotypic studies suggesting that the t(4; 11)-associated acute leukemia represents a proliferation of myeloid progenitor cells (29) as well as the identification of the TCGF gene on q26-28 make it difficult to implicate TCGF in the etiology of this disease.…”

mentioning

confidence: 99%

Gene for T-Cell Growth Factor: Location on Human Chromosome 4q and Feline Chromosome B1

Seigel

Harper

Wong‐Staal

et al. 1984

Science

View full text Add to dashboard Cite

T-cell growth factor (TCGF) or interleukin-2 (IL-2), an immunoregulatory lymphokine, is produced by lectin- or antigen-activated mature T lymphocytes and in a constitutive manner by certain T-cell lymphoma cell lines. By means of a molecular clone of human TCGF and DNA extracted from a panel of somatic cell hybrids (rodent cells X normal human lymphocytes), the TCGF structural gene was identified on human chromosome 4. In situ hybridization of the TCGF clone to human chromosomes resulted in significant labeling of the midportion of the long arm of chromosome 4, indicating that the TCGF gene was located at band q26-28. Genomic DNA from a panel of hybrids prepared with HUT-102 B2 cells was examined with the same molecular clone. In this clone of cells, which produces human T-cell leukemia virus, the TCGF gene was also located on chromosome 4 and was apparently not rearranged. The homologous TCGF locus in the domestic cat was assigned to chromosome B1 by using a somatic cell hybrid panel that segregates cat chromosomes. Linkage studies as well as high-resolution G-trypsin banding indicate that this feline chromosome is partially homologous to human chromosome 4.

show abstract

mentioning

confidence: 99%

Gene for T-Cell Growth Factor: Location on Human Chromosome 4q and Feline Chromosome B1

Seigel

Harper

Wong‐Staal

et al. 1984

Science

View full text Add to dashboard Cite

show abstract

“…These observations can be explained either in terms of clonal selection or on the basis of clonal evolution, whereby an underlying acquired genetic variability permits the sequential selection of progressively more malignant cell sublines (46,47). Clonal evolution has been demonstrated in other hematologic malignancies (59)(60)(61). It may be possible to study these processes in detail in future studies of the lymphomas by carrying out serial dual parameter flow cytometry studies in conjunction with cytogenetic studies in individual patients.…”

mentioning

confidence: 99%

Dual parameter flow cytometry studies in human lymphomas.

Shackney¹,

Skramstad²,

Cunningham³

et al. 1980

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Dual parameter flow cytometry studies using Coulter volume and cell DNA content were carried out in monodisperse cell suspensions of 64 samples of human lymphoma, chronic lymphocytic leukemia, hairy cell leukemia, and benign lymphoid proliferations. Differences in mean Coulter volume among the lymphomas were due 1)oth to the intrinsic differences in mean G1 cell Coulter volume and to the presence of increased fractions of larger S and G2 cells, especially among the large B cell lymphomas.However, the relative contribution of larger non-G, cells to the overall population Coulter volume distribution was a relatively minor one; the presence of cells in S did not increase mean Coulter volume by more than 10%, even in samples with high S fractions. There was a good correlation between mean GC cell Coulter volume and the log of the fraction of cells in S among the B cell lymphomas (r = 0.55). Evidence is presented that within individual samples, large cells proliferate more rapidly than small cells. This was seen in every case, both in the normal samples and in the lymphomas, and in the T cell lymphomas as well as in the B cell lymphomas. Aneuploidy was detected by flow cytometry in 11 cases; in 7 cases the aneuploid cell component could be analyzed separately from the diploid cell component on the basis of cell Coulter volume differences. Predictable relationships between cell size and proliferative behavior might be expected in the lymphomas for at least two reasons.First, cells increase both in size and in DNA content as they progress through the cell cycle. The dependence of cell size on cell position in the proliferative cycle can be demonstrated in experimental cell systems, by performing paired measurements of electronic cell volume and DNA content on individual cells by means of flow cytometry. This is illustrated in Fig. 1. Thus, the frequencies of large cells in a given lymphoma might be determined by the fractions of large S and G2 cells.Second, rapidly proliferating lymphoid cells may be intrinsically larger than slowly proliferating cells. It has been shown that large lymphocytes proliferate more rapidly than small lymphocytes in the normal lymphoid germinal center (8), and in the normal bone marrow (9-11). A relationship between proliferative rate and cell size (which is independent of relative position in the cell cycle) might be preserved in the malignant state as well.Of course, cell size differences among the lymphomas could also be due to factors that are totally unrelated to their respective proliferative rates or to the presence of different fractions of larger S and G2 cells. and DNA content were obtained in monodisperse cell suspensions of pretherapy biopsy specimens of human lymphoma by means of flow cytometry. Conventional histologic studies and immunologic surface marker studies were done in parallel on the same clinical samples. METHODSClinical samples. The collection and processing of pretherapy biopsy specimens and the techniques for determining immunologic cell surface mar...

show abstract

“…6. The break points were located between q13 and q2S (Reeves, 1973;Lawler et al, 1975;Oshimura et a/., 1977). In addition to acute lymphoblastic leukemia and the case presented, a marker 6q-has also been seen in Hodgkin's disease, non-Hodgkin's lymphomas and the effusion cells of a patient with carcinoma of the bronchus (Reeves, 1973;Ayraud, 1975).…”

Section: Discussionmentioning

confidence: 89%