Am Potter

Abnormalities of chromosomes 3 and 8 in posterior uveal melanoma correlate with prognosis

Posterior uveal melanomas have nonrandom alterations affecting chromosomes 3, 6, and 8. Loss of chromosome 3 in uveal melanoma has been shown to act as a predictor of disease‐free and overall survival. To confirm the significance of chromosome 3 loss and to extend the observations to include those of the associated alterations of chromosome 8, we have conducted a cytogenetic analysis on a series of 42 tumours from patients with primary uveal melanoma who were followed up for a median of 31 months (range = 8‐96 months). Abnormalities of chromosomes 3 and 8 were the commonest changes and were confirmed in 10 tumours using flourescence in situ hybridization. Monosomy of chromosome 3 was found in 21 (50%) of the tumours, and 23 (54%) tumours had additional copies of 8q. Alterations of chromosomes 3 and 8 were found occurring together in 19 (45%) of the tumours and were significantly associated with a ciliary body component (P < 0.0001). Prognostic indicators and changes of chromosomes 3 and 8 were analysed for correlation with patient survival. Of the chosen parameters, only ciliary body involvement (P = 0.003), monosomy of chromosome 3 (P = 0.0007), and additional copies of 8q (P = 0.003) correlated with reducted survival. Evaluation of the dosage effect of additional copies of chromosome arm 8q showed a significant association with reduced survival (P = 0.0001), which was also predictive of a decreased disease‐free interval (P = 0.01). Thus, the cytogenetic analysis of uveal melanoma may provide a valuable predictor of prognosis. Genes Chromosom. Cancer 19:22–28, 1997.

Cytogenetic analysis of a United Kingdom series of non-Hodgkins lymphomas

We describe cytogenetic analyses of cells derived from 40 non-Hodgkins lymphoma (NHL) node biopsies, 23 of which were from patients who had not been treated before biopsy. We noted that the chromosomes most frequently gained were X (32%), 12 (27%), and 3 (24%). Monosomies were much less common; loss of chromosome 13 (13.5%) was most frequent. Structural abnormalities primarily involved chromosomes 14 (70%), 1 (40.5%), 18 (38%), 6 (35%), and 17 (22%). Low-and high-grade disease showed similar patterns of structural changes; however, a markedly greater number of chromosome gains were associated with low-grade disease. Biopsy samples from patients who had previously been treated showed an increased frequency of structural abnormalities, as well as a significantly larger number of chromosome gains. The importance of these observations, particularly with regard to possible oncogene involvement in lymphoma evolution, is discussed.

Chromosome studies in eleven colorectal tumors

Cytogenetic analysis is presented on seven freshly derived colorectal tumors and four established cell lines (SW 742, SW 480, SW 948, and HT 29). No chromosome change was common to all tumors, although previous nonrandom findings were confirmed. Single chromosome abnormalities were identified in two cases, 47,XX,+i(7p) and 46,XX,-17,+der(17),t(17;?)(p;?), and their relevance to tumor origin and development is discussed. The association of i(8q) with tumors of the rectosigmoidal region is confirmed, and it is suggested that other rearrangements involving loss of 8p may have the same association. Abnormalities resulting in loss of 20p and duplication of 20q, not previously reported as a nonrandom change, were seen in seven out of 11 cases.

Trisomy 15 associated with loss of the Y chromosome in bone marrow: a possible new aging effect.

Trisomy 15 as a single autosomal abnormality is a rare finding in hematological disorders and has not as yet been associated with any specific disease type. We report 20 cases of trisomy 15 observed in the bone marrow of patients referred for a suspected hematological malignancy. Most patients were elderly, and a marked male predominance was evident. Aneuploidy for the Y chromosome was observed in addition to +15 in 11 out of 15 male patients. A myelodysplastic disorder (MDS) was confirmed in six cases, and acute myeloid leukemia (AML) in one. There was no evidence of malignant hematological diseases in the remaining 13 patients. We propose that there may be an association between loss of the Y chromosome and trisomy 15 and that trisomy 15, like missing Y, may not always be a marker of malignancy, but may reflect an underlying age effect. The possibility that its presence may herald the development of a malignant condition cannot, however, be excluded.

Nonendemic Burkitt's lymphoma with complex chromosome abnormalities involving chromosomes 2 and 8

A long surviving patient with nonendemic Burkitts lymphoma and complex cytogenetic findings is presented. Chromosome abnormalities were seen as a minor clone in peripheral blood and were considered consistent with the t(2;8)(p12;q24) variant. The karyotype was 47,XY, -2, -8, + der2(8qter-8q24::2p12-2qter), + der8(8pter-8q23::2p12-2pter) + der8(8qter-8cen::1q21-1qter). This case illustrates the value of extensive chromosome analysis in hematologic disorders and, at the time of writing, is the first example in Britain of the t(2;8) variant in Burkitts lymphoma.

Cytogenetic findings on six posterior uveal melanomas. Involvement of chromosomes. 3, 6 and 8.

Six posterior uveal melanomas were karyotyped after short-term culture. One had a normal chromosome complement; the remaining five had limited chromosome changes. Involvement of chromosomes 1 and 6 was noted in two and four cases, respectively, and three ciliary body tumours demonstrated both monosomy 3 and i(8q).

15 or trisomy 15 (as sole autosomal abnormality)

Review on +15 or trisomy 15 (as sole autosomal abnormality), with data on clinics, and the genes involved.

Subpopulations of colon cancer cells survive freezing

Dear Editor: Tumor cell lines are usually preserved in liquid or vapor phase nitrogen under conditions which allow 8 0 9 0 % recovery of viable ceils: the assumption is made that the freezing process does not distort the spectrum of subpopulations of cells. We have tested this assumption using cells from an in vitro established mucinous colorectal tumor cell line NYT27 for which cytogenetic studies were carried out at passage levels 0, 5 and 10, (P0, P5 and P10) and on cells reconstituted from liquid nitrogen after in vitro passage level 4, 9 and 19 (FP5, FPIO and FP20). In particular, the influence of storage on new structural rearrangements was recorded. The methods of ceil culture and chromosome analysis of the NYT27 cells from the original tumor (PO) have been described (Yaseen et al., 1990). The distribution of chromosome numbers for 119 cells at passage five (P5) indicated significant differences from that of 100 FP5 cells. The numbers of chromosome in P5 ceils varied from 69-78 , with a regular distribution frequency between these extremes and a modal number of 74-75; in contrast, for FP5 cells, the chromosome number varied from 6 6 8 4 with a wide distribution frequency and a modal number of 74-78 . For P5 ceils, the karyotype of clone A was identified at P0, and its chromosome composition suggested that it was the stem clone from which other clones present at P5, were derived. Thirty-two P5 ceils were karyotyped; eight subclones were recognized, and the percentage distribution of each clone shown in Figure 1. Although subclones A, E, G, B and J identified at P0 were not present at P5, the major sublines D, E and F were present in a proportion similar to that seen at P0. The karyotype distribution of 22, FP5 cells is also shown in Figure 1. In this instance, although the cell karyotypes appeared to have been derived from B, showing trisomy #5, #11, #12, #21, no cells were identified with the t(17 ;21) seen in C which characterizes the karyotype evolution of both PO and P5; no two cells had the same chromosome complement, and all demonstrated a new evolution pattern from B. Thus, in both chromosome numbers, and in detailed karyotype characteristics, P5 and FP5 cells showed marked differences. After 10 in vitro passages of cell line NYT27 (P 10), the distribution of chromosome numbers for 100 cells varied from 69 to 82 without a regular distribution curve or model number; however, more cells with a higher number of chromosomes were identified than at P5. In contrast, similar analysis for 100 cells frozen at passage nine and reconstituted (FP10) showed chromosome numbers varying from 67 to 84 with a model number of 78 to 79. In comparison with P10 cells, FP10 contained more cells with a higher number of chromosomes. Thirty-six P10 ceils and 28 FP10 cells karyotyped: the results were not significantly different from that of P5 and FP5 cells; however, P10 cells showed increased diversity in chromosome number when compared to P5 cells, whilst