[Chromosome analysis of renal cell carcinoma].
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Carcinoma, Renal Cell↗
Biomedical subjects
M A Yoshida
Publications and source records attributed to M A Yoshida.
[Chromosome analysis of adenomatosis coli and colon carcinoma].
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Adenoma↗
Rearrangements of chromosome 3 in nonfamilial renal cell carcinomas from Japanese patients.
Cytogenetic studies were successfully carried out in 5 tumor tissues from Japanese patients with nonfamilial renal cell carcinoma, histologically diagnosed as clear cell subtype. Mitotic cells were obtained by a combined method of enzymatic disaggregation and short-term culture (6-12 days). The modal chromosome numbers were found to be diploid or near-diploid in all the cases examined. Every case showed characteristic structural and numerical abnormalities. Rearrangements in the short arm of chromosome 3 were observed as clonal abnormalities in all the cases, including a translocation t(3;6) resulting in a partial loss of 3p (3 cases), a terminal deletion of 3p (one case) and 2 different translocations involving 3p and 8p (one case). The other clonal abnormalities were a whole or partial trisomy of chromosome 7 and a loss of Y chromosome. The overall results in the present study were consistent with those of our previous data in American patients, and suggest that the rearrangements of chromosome 3 leading to a partial loss of its short arm may play primary and significant role(s) in the development of renal cell carcinoma.
Aged↗
Four cases with complex Philadelphia translocations, including one with appearance de novo of a "masked" Ph.
Four cases of chronic myelogenous leukemia (CML) with complex Philadelphia (Ph) translocations are described. The first case was that of a 50-year-old woman in the chronic phase of CML. Her leukemic cells showed a complex Ph translocation involving chromosomes #9, #11, and #22 [i.e., t(9;9;22;11)(11qter----11q11::9q11----9q34:: 9p11----9pter;22qter----22q11::9q34?;11 pter----11q11::22q11----22qter)]. In addition to the complex Ph translocation, the leukemic cells contained del(10)(p13). The second case was that of a 21-year-old man whose leukemic cells contained a translocation involving chromosomes #5, #9, and #22 [i.e., t(5;22;9)(q31;q11;q34)], resulting in a "masked" Ph chromosome. The third case was that of a 37-year-old man whose leukemic cells had a complex Ph translocation involving chromosomes #8, #9, and #22 [i.e., t(8;9;22)(q13;q34;q11)]. The fourth patient was a 41-year-old woman diagnosed as having CML in myeloid blastic phase, at which time the first specimen was examined by us. This blood sample showed a karyotype of 45,XX, -9, -17, -22, +mar1, +mar2,9q+. No Ph chromosome was present. A standard Ph translocation was detected in the cells obtained from the spleen, when the patient underwent splenectomy for treatment of the blastic crisis. Subsequent specimens obtained from the blood and bone marrow showed that the leukemic cells contained three clones: 45,XX, -9, -17, -22, +mar1, +mar2,9q+/46,XX, -17, +mar1,t(9;22)(q34;q11)/46,XX,t(9;22)(q34;q11). Cells with the "masked" Ph chromosome were thought to have been derived from the clone with the standard Ph translocation. We postulate that some variant Ph translocations, including those with a "masked" Ph chromosome, may be generated by a stepwise process following the genesis of a standard Ph translocation.
Adult↗
Establishment of a parathyroid hormone-like factor-producing esophageal carcinoma cell line (EC-GI).
A new cell line, designated EC-GI, was established from a 65-year-old patient with esophageal carcinoma who developed humoral hypercalcemia. The original tumor as well as the cell line caused marked hypercalcemia in tumor-bearing nude mice, in which a marked increase in osteoclastic bone resorption was demonstrated. The conditioned medium of EC-GI cells contained potent bone resorbing activity which stimulated cyclic AMP production in parathyroid hormone (PTH)-responsive osteoblast-like cells (ROS 17/2.8). EC-GI cells will be useful for characterization and purification of the PTH-like factor responsible for humoral hypercalcemia of malignancy.
Biological Assay↗
Cytogenetic changes at 11q11, 11q23, and 17q11 in myelodysplastic syndrome.
Cytogenetic studies were performed on two patients with myelodysplastic syndromes. One patient was a 68 year old Japanese male in whose bone marrow cells two translocations were established, i.e., t(4;11)(q13;q23) and t(11;17)(q11?;q11), as well as other karyotypic changes (-6,-18,15p+). The other patient was a 74 year old white male whose bone marrow cells showed six marker chromosomes, i.e., der(5),t(5;17)(q12;q11), der(6),t(6;5)(q27;q22), der(8),t(8;11;?)(q11;q11----q23;?), der(11),t(11;?)(q11;?), an isochromosome of the long arm of chromosome #8, and a small G-group sized marker chromosome of unknown origin. Though the translocation patterns in the abnormal cells in these two cases were different, the breakpoints of the marker chromosomes were almost the same, i.e., 11q11, 11q23, and 17q11. Also, changes of chromosome #6 were observed; the first case showed monosomy 6 and the second a 6q+ marker chromosome. In these two cases of myelodysplastic syndromes, common sites of chromosome breakage and reunion of 11q23 and 17q11 were close to recently established sites of human cellular oncogene homologs, c-ets (11q23) and c-erbA (17q21----24). These associations draw attention to a possible relationship between chromosome changes in myelodysplastic syndromes and oncogene (or other gene) activation and/or dysfunction.
Aged↗
Recurrent endometrial adenocarcinoma with rearrangement of chromosomes 1 and 11.
A chromosome study was performed in a recurrent endometrial cancer. The cytogenetic analysis performed with a quinacrine-Hoechst banding technique revealed rearrangements of chromosomes #1 and #11 [i.e.: der(11),t(1;11)(q21;q23)], which was found in all metaphases. In addition, a deletion of chromosome 6(q21), trisomy of chromosomes #7 and #10, monosomy X, and -4 as the clonal changes. Partial trisomy for a long arm of chromosome #1 also was observed in almost all analyzed metaphases (11 of 12 cells). These data showed the association of rearrangement of 1q in endometrial cancer and/or redevelopment of tumor, and also suggest the possible participation of chromosome #11 on which the human proto-oncogene c-ets was mapped.
Adenocarcinoma↗
Rearrangement of chromosome 3 in renal cell carcinoma.
Rearrangements involving chromosome #3 were detected in 8 of 12 nonfamilial renal cell carcinomas. These results suggest that rearrangement of chromosome #3 is associated with the genesis and progression of a subclass of human renal cell carcinoma.
Adult↗
14q+ in Ph-positive chronic myelogenous leukemia.
Two cases of chronic myelogenous leukemia with a Ph translocation and an additional chromosome change of the long arm of a chromosome #14 (14q+) are reported. The breakpoints on chromosome #14 were identified as 14q24 and 14q32, respectively. One of the patients did not show any evidence of blastic transformation; the other patient developed a myeloid blastic crisis when the abnormal 14q+ was seen in the bone marrow cells.
Adult↗
Chromosome anomalies suggestive of malignant transformation in bilateral renal oncocytoma.
A patient with bilateral renal oncocytoma is presented, and the clinical, radiological and pathological characteristics of this uncommon, clinically benign renal tumor are discussed briefly. Chromosomal analysis studies revealed the following clonal abnormalities: trisomy of chromosome 7, and monosomy of chromosomes 3 and 14, and the X chromosome. A possible clonal abnormality of chromosome 10 and 3 nonclonal anomalies also were identified. The same anomalies were present in both tumors. These karyotypic anomalies are compatible with malignant transformation of the cells of these tumors and, since benign tumors rarely are associated with demonstrable cytogenetic changes, they suggest that oncocytoma, although clinically benign, may have malignant potential.
Adenoma↗
Cytogenetic studies of tumor tissue from patients with nonfamilial renal cell carcinoma.
A method combining an enzymatic technique and short term culture was applied to 27 tumor tissues from 22 patients with nonfamilial renal cell carcinoma in order to establish the chromosome changes in these tumors. Chromosome analyses were successfully carried out in quinacrine mustard-Hoechst 33258 and G-banded preparations of 14 tumors from 12 patients, including 2 cases in which established cell lines were obtained after 43 and 64 days in culture and maintained for 25 and 30 passages in an in vitro system, respectively. The modal chromosome numbers ranged from 38-46 in 11 samples, involving chromosomes in structural and numerical changes and 72 chromosomes in one case, with the remaining 2 samples showing a variety of chromosome numbers. Banding analysis revealed 45 clonal aberrations in 11 tumor samples from 10 patients and nonclonal aberrations in the remaining 3 samples from 2 of the patients. Rearrangements of chromosome 3 were observed in 12 tumors, with the breakpoints on this chromosome almost totally clustered from p11 to p21. In one case both primary and metastatic tumors were studied, and an isochromosome for the long arm of chromosome 1 was observed as clonal in origin in the metastatic tissue. Two cases showed nonclonal changes. The remaining case had one clonal abnormality, i.e., deletion of 6q. Of the remaining 33 clones, chromosomes 1, 2, 6, 11, and 17 were frequently involved. These results suggest that renal cell carcinoma may be cytogenetically classified into 3 categories: (a) tumors with changes of chromosome 3: (b) tumors with other clonal aberrations; and (c) tumors without clonal changes. Rearrangements of chromosome 3 may be possibly associated with the genesis and/or progression of renal cell carcinoma.
Adult↗
Involvement of chromosomes 4, 11, and 17 in a case of myelodysplastic syndrome.
A case of myelodysplastic syndrome in a 68-year-old male in whose marrow cells two translocations were established, i.e., t(4;11)(q13;q23) and t(11;17)(p?:q11), as well as other karyotypic changes (-6,-18,15p+), is described. The relation and identity of the bands involved in the translocations affecting chromosomes #11 and #17 in leukemias in which these chromosomes are specifically affected, i.e., t(4;11) in acute myelomonocytic leukemia and t(15;17) in acute promyelocytic leukemia, are discussed in relation to the case described.
Aged↗
Two 14q+ chromosomes in malignant lymphoma: crucial cytogenetic changes on 14q.
We encountered a 36-year-old white male patient with poorly differentiated lymphocytic lymphoma, whose lymph node cells showed a clonal cytogenetic change involving chromosome #14, i.e., 47,XY, + 2,der(14),t(14;14)(14pter----14q32;14q24----14q32++ +). In addition to this change, cells with a translocation between chromosomes #2 and another #14 [t(2;14)(q21;q24)], as well as a missing chromosome #8 were found. We have reviewed the literature dealing with two or more changes affecting chromosome #14 and discussed the importance of the cytogenetic change at band 14q32 in malignant lymphoma.
Adult↗
Chromosome changes in mycosis fungoides in an XYY male.
A 32-year-old white male was diagnosed as having mycosis fungoides in 1976; bone marrow biopsy and aspiration in August 1984 revealed infiltration with neoplastic cells. Cytogenetic analysis of the cells from the bone marrow specimen showed that 48 of 50 metaphases contained an extra Y chromosome (i.e., 47,XYY). The remaining two cells were hypotetraploid and hyperpentaploid, respectively, with a common marker derived from chromosome #2. The metaphases obtained by PHA stimulation of peripheral blood cells showed a 47,XYY pattern. An interleukin 2 (IL-2) dependent T-cell line was established from the patient's blood mononuclear cells; all metaphases of this line had an extra Y chromosome. Thus, this case is one of a mycosis fungoides developing in an XYY male.
Adult↗
Mouse cell clones for improved quantitation of carcinogen-induced altered differentiation.
Two new mouse epidermal cell lines have been isolated and characterized as target cells for three chemical carcinogens. The ability to grow these cells at low density (approximately 5 clonogenic cells/cm2) has permitted more precise quantitation of chemical carcinogen-induced changes in epidermal differentiation. The cell lines, designated 291 and 271c, retain the property previously observed in primary cultures of mouse epidermal cells, that is the regulation of terminal differentiation by extracellular Ca2+ ion. Altered response to extracellular Ca2+ after carcinogen treatment of these cells is the basis of the assay endpoint. Other normal properties demonstrated by these cells are keratin immunofluorescence patterns, ability to form cornified envelopes in response to Ca2+ and a lack of tumorigenicity. Both of the lines have high cloning efficiencies (up to 20%) and characteristic epidermal morphology. Their chromosome number, however, is near tetraploid. Dose response studies indicated an increase in colonies with altered response to Ca2+ proportional to the dose of three chemical carcinogens: DMBA 0.001-0.5 microgram/ml X 24 h, MCA 0.01-5 micrograms/ml X 24 h and MNNG 0.01-0.2 micrograms/ml X 1 h. The optimized assay protocol has provided a reproducible means of quantitating carcinogen-altered epidermal cells relative to carcinogen dose, and of isolating cell clones for studies of altered differentiation in carcinogenesis and chemotherapy.
Animals↗
Isolation of mouse T-cell lymphoma lines from different long-term interleukin 2-dependent cultures.
A number of different biological properties have been ascribed to the hormone-like protein interleukin 2 (IL-2). However, the most salient feature of this lymphokine is its ability to sustain the long-term proliferation of T-cells from humans and mice. Reported herein are the results of studies demonstrating the isolation of growth factor-independent cell lines from the long-term IL-2-dependent murine T-cell line CTLL-2 that is used frequently as the source of target cells in IL-2 bioassays. Sustained log-phase growth of these T-cells in vitro has been achieved using Petri dishes of polymethylpentene; growth could not be sustained in similar dishes of glass, untreated polystyrene, polystyrene that had been treated for cell culture, or polycarbonate. The IL-2-independent line grew as a T-cell lymphoma when injected i.p. into pristane-treated, but not untreated, syngeneic C57BL/6 mice. In contrast, cells from the IL-2 parental line CTLL-2 did not grow in vivo. Characterization of the IL-2-independent lines propagated in vitro (denoted as line CEC) or in vivo (denoted as line CEP) demonstrated that they retained their dependency for 2-mercaptoethanol and expressed phenotypic profiles of their parental line CTLL-2 (Thy 1.2+, Lyt-1-; Lyt-2-). Isolation of an IL-2-independent T-cell lymphoma from a CTLL-2 line obtained from another investigator using a protocol that has proven reproducible under carefully controlled laboratory conditions and defined phenotypic traits of the syngeneic T-cell isolates provided evidence that the tumors were not a cross-culture contaminant arising as a result of a laboratory accident. Moreover, karyotypic analysis using a quinacrine:Hoechst banding technique revealed similar marker chromosomes in the IL-2-dependent and -independent lines. IL-2-independent lines have also been established from the IL-2-dependent murine T-cell line CT-6. Accordingly, the results of these studies suggest that, during prolonged cultivation that has included exposure to crude IL-2 preparations known to contain phorbol ester, possibly viruses, and other contaminants, the IL-2-dependent lines have developed subpopulations that are thought to have undergone malignant transformation of unknown etiology to generate IL-2-independent murine T-cell lymphomas that can be passaged repetitively either in vitro or in vivo.
Animals↗
Reversal of X-inactivation in female mouse somatic cells hybridized with murine teratocarcinoma stem cells in vitro.
A series of near-diploid embryonal carcinoma-like hybrid cells were obtained from polyethylene glycol mediated cell fusion between murine embryonal carcinoma cells (PSA-6TG1 or OTF9-63) having one X chromosome and thymocytes or bone marrow cells from female mice carrying Cattanach's or Searle's translocation. Prior to fusion with EC cells the somatic cells are presumed to contain only one active X chromosome. Following hybrid formation, the chronology of X chromosome replication and the expression of X-linked gene Pgk-1 indicated that all X chromosomes contributed by both parents were active in these hybrids. Experiments were performed to rule out the possibility that the hybrids were formed by fusion of EC cells with rare somatic cells in which both X chromosomes were active. Taken together the data indicate that within four days of fusion there is reactivation of the entire inactive X chromosome.
Alleles↗
Karyotypic kinship between the blue fox (Alopex lagopus Linn.) and the silver fox (Vulpes fulva Desm.).
A karyotypic comparison between the blue fox and the silver fox revealed conservation of the chromosome arm as a unit, except for large heterochromatic blocks in 10 pairs of blue fox chromosomes and the complete absence of a common metacentric autosomal pair. This finding seems to indicate that their karyotypes evolved from a common ancestral karyotype, characterized by 70-76 acrocentric autosomes, mainly through a series of independent centric fusions.
Animals↗