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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The karyotype and the banding pattern of chromosomes through different techniques following Giemsa staining have been worked out in an Ehrlich mouse ascites tumour cell line. The stemline cells show a mode at 74-76. A metacentric chromosome is present in almost all the cells. Some cells show a long telocentric chromosome with a possible secondary constriction. C-bands are restricted at the telomeric regions of the chromosomes excepting in the metacentric one. From the banding pattern it seems that the nucleolar organizers are located at the telomeric region. No band is associated with the second constriction of the long telocentric chromosome. It is suggested that the long metacentric chromosome has arisen out of a Robertsonian translocation involving end to end centromeric fusion of two non-homologue chromosomes.
Z Krebsforsch Klin Onkol Cancer Res Clin Oncol 1976 Feb 25
PMID:Chromosomal banding and karyotype analysis in an Ehrlich mouse ascites tumor cell line. 13 Jul 47

The chromosomal localization of satellite DNA in two tissue culture lines derived -rom malignant mouse CNS tumors was investigated by in situ hybridization of 3H single-stranded satellite DNA purified by isopynic centrifugation in alkaline CSC1. Both tumors were glioblastomas originally induced by a methylcholanthrene implantation into the cerebrum of C3H mice; both displayed aneuploid chromosomal constitutions. One of these glioblastomas (TC 541) revealed labelling only of centromeric portions of the chromosomes even in cells containing greater than 200 chromosomes and thus it had a pattern of satellite distribution comparable to that of normal cells. The other glioblastoma (TC 509), that produced C-type particles and had a decrease in satellite DNA, displayed interstitial and telomeric label in some chromosomes in addition to labelling of the centromeres. "Hoechst 33258" fluorescence showed some interstitial and telomeric bright bands as well as centromeric bright regions, though to be consistent with in situ studies. The localization of satellite DNA to the chromosome arms and its possible relation to C-type virus is discussed.
Int J Cancer 1976 May 15
PMID:Localization of mouse satellite DNA on chromosomes of experimentally induced glioblastomas; non-centromeric lable in one glioblastoma producing C-type particles. 17 13

Small DNA-containing particles called double minutes (dm) were observed in metaphases during a survey of human tumor cell lines. Detection of dm in uncultured malignant effusions, in a series of 14 breast carcinoma cell lines, and in a cervical carcinoma cell line, and a literature survey indicated that dm may be more common among human malignant cells than previously suspected. Some of the human breast carcinoma cell lines showed a high incidence of dm, which permitted a series of cytochemical studies. The dm stained identically with euchromatic regions of human chromosomes. Unlike typical chromsomes, dm contained neither C-bands nor Cd bands indicative of paracentromeric heterochromatin and centromeres, respectively. The dm were observed to cluster at the ends of chromosomes, and individual dm adhered to chromosomes. This clustering behavior allows dm to pass through cell division in the absence of centromeric regions. These results should alert tumor cytogeneticists to the possibility that their material may contain a low incidence of undetected dm.
J Natl Cancer Inst 1979 Feb
PMID:Double minutes in human carcinoma cell lines, with special reference to breast tumors. 28 61

Cytogenetic studies on 26 carcinomas of the cervix showed that chromosome 1 was consistently involved in the changes: either one or more structurally abnormal chromosomes or a relative excess of normal chromosomes were present. Several types of structural change were repeatedly seen: short arm deletions (1p-, in seven tumors); long arm isochromosomes (i(1q), in six tumors); and translocations of unidentified chromosomal material onto one of the arms (possibly in eleven tumors; in four of these, there was an additional C-band on the long arm). In one tumor, there was a short arm isochromosome (i(1p)). The most consistent feature of the aneuploid complements of these tumors appeared to be the presence in excess of the centromeric region and at least part of the adjacent heterochromatin of chromosome 1.
Cancer 1979 Aug
PMID:Chromosome 1 in 26 carcinomas of the cervix uteri: structural and numerical changes. 28 31

Detailed karyotypic analysis with G- and C-banding has been performed on cells of four malignant melanomas. The modal number in two cases was in the hypodiploid range, the chromosome numbers varying from 39 to 43. These two tumors had 5 to 13 marker chromosomes. The other two tumors were in the polyploid range, with modal numbers of 63 to 157 chromosomes. The cells had a minimum of 11 and a maximum of 40 marker chromosomes. Chromosome no. 1 was more frequently involved in aberrations than any other chromosome. The most common breakpoints on this chromosome were 1q21, 1q25 and 1q32. Frequent breakpoints were also noticed in the centromeric region in various chromosomes. In chromosome no. 1, however, the centromeric area does not seem to be involved. The more common breakpoints on the various chromosomes were 1q21, 1q25, 1q32, 5p13, 9q13, 11q23, 12q13. No common markers were noticed among these four cases of melanoma, but are noticed in unrelated tumors.
Cancer 1977 Sep
PMID:Chromosomes and causation of human cancer and leukemia. XXII. Karyotypic changes in malignant melanoma. 90 36

Forty-two Ph1-positive cases of chronic myelocytic leukemia (CML) were examined with chromosomal banding techniques. Thirty-seven of these cases had the "standard" type of Ph1 translocation between chromosomes No. 9 and No. 22 [t(9;22)(q34;q11)] in the Ph1-positive marrow cells; 5 cases had unusual types of Ph1 translocation. Of the 37 cases, 21 had additional numerical and/or structural chromosomal changes, 2 had a missing Y chromosome, and 1 had an extra Ph1 in the Ph1-positive cells. In the 5 cases with unusual types of Ph1 translocation, chromosomes No. 2, No. 9 No. 10, and No. 13 were involved. The clinical picture in these 5 patients did not differ materially from that of the other Ph1-positive patients with CML, probably indicating that the recipient chromosome, with which the translocation from No. 22 takes place, does not play a crucial role in the course of the CML. In the 21 cases with abnormal karyotypes, nonrandom chromosomal changes were observed. Most of the changes were related to events occurring at the centromeric region. The prognosis of cases with only an extra No. 8 or Ph1 appears to be better than that for cases with an iso-17q [I(17a)] chromosome or other extra chromosomes. The presence of the Ph1 (delected No. 22) in every case points to the essentiality of this karyotypic findings in the diagnosis of CML and possibly in the genesis of the disease.
Cancer 1975 Oct
PMID:Chromosomes and causation of human cancer and leukemia. XVI. Banding studies of chronic myelocytic leukemia, including five unusual Ph11 translocations. 105 43

The chromosomes of 12 adult patients with acute leukemia were analyzed by conventional means and by Giemsa and centromeric banding techniques. Acute myeloblastic leukemia was diagnosed in 7, acute myelomonocytic leukemia in 2, and acute undifferentiated leukemia in 3. Bone marrow was aspirated from patients when in relapse or remission, and both euploid and aneuploid cells were examined. All patients showed trisomy no. 9 and many showed additional numerical or structural changes in some or all their cells. These changes included monosomy no. 21 and/or monosomy no. 8. The proportion of trisomy no. 9 cells was 30-50% in patients in full remission and up to 100% in patients in relapse; thus trisomy no. 9 might be an important marker of leukemic cells. A mechanism was proposed to explain the induction and selection of the trisomy no. 9 karotype.
J Natl Cancer Inst 1975 Oct
PMID:Cytogenetic basis of acute myeloid leukemia. 105 86

A murine anaplastic sarcoma and an in vitro cell line established from it were studied by the TG banding technique. The neoplasm originated in a BALB/c mouse inoculated with human tumor cells. Microchromatin bodies were found in 100% of the karyotypes in the original tumor and in the 120 in vitro passages. A long marker chromosome, also observed in all metaphases, was interpreted as a translocation in tandem of a No. 16 chromosome into a No. 1; this involved loss of the centromeric part of chromosome No. 1.
J Natl Cancer Inst 1975 Sep
PMID:Minute chromatin bodies in a murine in vitro cell line. 115 49

The bone marrow cells of BALB/c mice with T2 murine leukemia were analyzed cytogenetically. Of 98 leukemia metaphases, 16.3% were hypodiploid, 4.1% hyperdiploid, and 79.5% diploid. The distribution of G bands in diploid metaphases indicated that almost half of them were pseudodiploid, with chromosome abnormalities such as trisomies, monosomies, nullisomies, unidentified chromosomes, translocations, deletions, or duplications. Since all mouse chromosomes are acrocentric and can be identified only tentatively most of the anomalies detected with G-banding procedures would have passed unnoticed with conventional cytogenetic techniques. The C-banding pattern of leukemia cells did not differ from that of normal controls. However, a considerable number of leukemia cell metaphases had bridges connecting the centromeric C bands of two or more chromosomes. This phenomenon probably indicates an increased stickiness of the heterochromatin, which may produce mitotic nondisjunction and the appearance of monosomies and trisomies.
J Natl Cancer Inst 1975 Oct
PMID:G- and C-banding patterns in the T2 murine leukemia. 118 98

A t(3;5)(q25.1;q34) reciprocal translocation identifies a subset of cases of myelodysplastic syndrome or acute myeloid leukemia (AML) that are characterized by increased numbers of megakaryocytes and severe trilineage dysplasia. As a first step in characterizing the t(3;5) breakpoints, we asked whether the translocation involves the CSFIR/PDGFRB locus at 5q33-q35. Pulsed-field gel electrophoretic analysis of a region extending 580 kb 5' to the PDGFRB gene and 120 kb 3' to the CSFIR gene did not reveal aberrant restriction fragments in leukemic cell DNA, confirming that the breakpoint does not occur in the vicinity of these genes. To sublocalize the breakpoint, we performed Southern blot hybridizations using DNA from human x hamster somatic cell hybrids containing the normal 3, the normal 5, the derivative 3, or the derivative 5 human chromosome. Using a series of polymorphic DNA probes from the long arm of chromosome 5, which have been linked by genetic recombination, we bracketed the breakpoint to within a region that spans approximately 13 centimorgans (sex average) and is flanked by the q34-qter markers cKK5.19 and L1200 (D5S62). This analysis places the chromosome 5 breakpoint of the t(3;5) considerably telomeric to the CSFIR/PDGFRB locus, confirming our studies with pulsed-field electrophoresis. Future efforts to identify the genes affected by the t(3;5) should focus on the 5q segment described in this study.
Genes Chromosomes Cancer 1992 Nov
PMID:Sublocalization of the chromosome 5 breakpoint of the 3;5 translocation in myelodysplastic syndromes and acute myeloid leukemia. 128 27


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