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Biomedical subjects

N B Atkin

Publications and source records attributed to N B Atkin.

At least 73 records · Page 4Linked to original sources

Cytogenetic study of ten carcinomas of the bladder: involvement of chromosomes 1 and 11.

In direct preparations of ten untreated transitional cell carcinomas of the bladder, chromosomes #1 and #11 were most frequently involved in structural changes (in at least seven tumors each). Three tumors had one or two 11p- chromosomes, and, in other tumors, chromosome #11 had taken part in translocations or isochromosome formation, which, except in one tumor, resulted in a loss of short arm material. Also, there was a tendency for the presence of fewer than expected normal chromosomes #11. Chromosome #1 anomalies are common in most types of tumor; however, chromosome #11 abnormalities, particularly the loss of short arm material, are not common and may thus characterize carcinoma of the bladder, a finding that is of interest in view of the location of an oncogene, c-Ha-ras1, on 11p. Translocations probably involved chromosome #17 in four tumors. Structurally changed chromosomes #3 were seen in four tumors, including one or two 3q- chromosomes in two or possibly three tumors.

Adult↗

Chromosome study of five cancers of the prostate.

Nonrandom chromosome changes were sought in direct preparations of tumour material from the primary site of four carcinomas and one leiomyosarcoma of the prostate. Two of the carcinomas had previously received oestrogen therapy. A deleted chromosome 10, del(10)(q24), was found in all four carcinomas and may represent a specific marker in prostatic carcinoma. Three of the carcinomas also had a deleted chromosome 7, del(7)(q22), while the fourth had a 7p+. Deleted chromosomes 7 and 10 were not identified among the markers present in the leiomyosarcoma. All five tumours contained one or more abnormal chromosomes derived from chromosome 1. A Y chromosome was present in the leiomyosarcoma but in none of the carcinomas.

Adenocarcinoma↗

Chromosome analysis of three seminomas.

Each of three seminomas revealed chromosome #1 and #12 structural changes in direct preparations and short-term cultures. The #1 changes involved duplication of 1q and loss of 1p; in two, the breakpoint was in the heterochromatic region. The anomaly in #12 was a short arm isochromosome, usually present in duplicate. In one tumor, these were the only structural changes; in the other two, there was also involvement of #7, with extra copies of 7p. In one of these two tumors, a heterochromatic minute was identified after C-banding, and in the other, aside from two different markers containing part of #7, there was a dicentric derived from two chromosomes #15; this tumor proved to be prognostically unfavorable. Three normal chromosomes #1 and XXY sex chromosomes were present in each tumor. Chromosomes #11 and #13 were generally underrepresented, and #12 and #19-22 were over-represented.

Adult↗

Chromosome 1 heterochromatin variants and cancer: a reassessment.

Evidence for a relationship between chromosome #1 heterochromatin polymorphisms and cancer has been reviewed. Eighty-four of 135 (62%) patients with epithelial malignancies were heteromorphic for C-band size compared with 38 of 107 (36%) controls (significant at the 0.1% level). However, only 33 of 67 (49%) patients with nonepithelial malignancies were heteromorphic (not significantly different from controls). Similarly, the incidence of partial inversions of the C-band region in one or both homologs was significantly greater than controls [28 of 107 (26%)] for patients with epithelial [66 of 135 (49%)] but not nonepithelial [25 of 67 (37%)] malignancies. However, when the presence of either or both size heteromorphism and inversions were assessed, the incidence was significantly higher in patients with nonepithelial [46 of 67 (69%), including 11 of 11 patients with leukemia or myeloproliferative disorders] as well as epithelial [112 of 135 (83%)] malignancies compared with controls [52 of 107 (49%)]. Forty-seven of the patients did not differ significantly from controls with respect to the incidence of chromosome #1 heteromorphism as revealed by the Giemsa-11 technique. However, 26 patients assessed for their chromosome #1 lateral asymmetry pattern differed significantly from controls, having a higher incidence of compound asymmetry with a large proximal and small distal block and a lower incidence of simple asymmetry.

Chromatin↗

Nonrandom chromosome changes in carcinoma of the cervix uteri. II. Ten tumors in the triploid-tetraploid range.

Nonrandom chromosome changes in direct preparations of 10 cervical carcinomas with modal numbers in the range of 60-82 were similar to those found in a previous study on near-diploid tumors: Chromosomes 1 (seven tumors) and 11 (five tumors) were most often involved in structural rearrangements and a small metacentric, often present in duplicate, was seen in six tumors. The appearances of the small metacentric again suggested an origin from a chromosome #4 or #5: either a long arm deletion or a short arm isochromosome; in one tumor, Giemsa-11 banding was more compatible with a #4 than a #5. Chromosome #17 anomalies were probably present in four tumors, and two tumors had markers, probably derived from chromosome #2, containing homogeneously staining regions.

Chromosome Aberrations↗

i(12p): specific chromosomal marker in seminoma and malignant teratoma of the testis?

A similar small marker chromosome, frequently present in duplicate, was seen in direct preparations and short-term cultures of each of ten seminomas, one combined seminoma and teratoma, and one malignant teratoma of the testis. In the four most favorable tumors (seminomas) this chromosome was identified as an i(12p). The findings may point to a chromosomal change that is specific for malignant testicular tumors.

Chromosome Aberrations↗

Chromosome 1 C-band heteromorphisms in patients with carcinoma in situ and invasive carcinoma of the cervix uteri.

A significantly higher incidence of heteromorphism for the size of the C-band regions of the chromosome 1 homologues was found in the lymphocytes of patients with carcinoma in situ and invasive carcinoma of the cervix uteri than in controls (15 out of 19 and 12 out of 18 patients, respectively, as compared with 13 out of 38 controls). There was also a higher incidence of partial inversions of this region in patients with carcinoma in situ and invasive carcinoma although the differences from that found in the controls were not statistically significant. C-band variants of chromosome 1 may play a part in the cytogenetic events that determine the early stages of some forms of malignancy.

Adenocarcinoma↗

Nonrandom chromosome changes in carcinoma of the cervix uteri. I. Nine near-diploid tumors.

Chromosome analysis of G- and C-banded preparations of tumor material, processed by a direct method, from nine primary carcinomas of the cervix with modal chromosome numbers in the range 41-49 showed the nonrandom involvement of certain chromosomes in structural and numerical changes. Besides chromosome No. 1 (six tumors), structural changes involved chromosomes No. 11 (five tumors with variable breakpoints and translocation partners), No. 3 (three tumors) No. 6 (three tumors), and No. 17 (17p+ in two tumors). A small metacentric (present in duplicate in most metaphases of one tumor), which may have been a 5q- (?) (with an interstitial long arm deletion), was seen in five tumors. Additional normal chromosomes included chromosomes No. 1 (one tumor without structural changes in this chromosome showing trisomy 1) and No. 3 (four tumors showing trisomy in the absence of structural changes involving this chromosome). Losses commonly affected the B, D, and G groups, particularly chromosomes No. 13 (three tumors) and No. 21 (six tumors), as well as chromosome No. 18 (four tumors). Two X chromosomes were present in all tumors except the two with the lowest modal numbers, both of which lacked an X chromosome.

Aneuploidy↗

Break points in chromosome #1 abnormalities of 218 human neoplasms.

A survey of 343 break points that lead to chromosome #1 abnormalities in 218 human neoplasms showed that 49.9% were located in or immediately adjacent to the centromeric heterochromatin. Amongst rearrangements with breaks in bands p 12-q21 were 27 isochromosomes, 22 translocations of the long arm, and four translocations of the short arm to the heterochromatic regions of other chromosomes, and 35 deletions resulting in chromosomes consisting mainly or solely of one arm. Deletions following breakage at various sites in the short arm of chromosome #1 are frequent in malignancies and are quite often found in cells that are trisomic for the long arm. It is suggested that fragility of chromosomes generated as a result of early events in carcinogenesis may be one source of chromosome rearrangements, including those of chromosome #1, on which selection can operate and give rise to progressively more malignant clones.

Chromosome Aberrations↗

Three or four copies of a dicentric 17q isochromosome in an acute myeloproliferative disorder.

The majority of metaphases in the bone marrow of a male patient aged 72 with a rapidly evolving aleukemic erythremic myelosis had 48 chromosomes with three copies, or 49 chromosomes with four copies, of an i(17q), which was seen to be dicentric in C-banded and Giemsa-11-banded preparations. There was also loss of a chromosome No. 5 and the addition of a chromosome resembling a No. 22. The presence of multiple copies of the isochromosome is postulated to be related to the acuteness of the condition.

Acute Disease↗