Translocation (2;3) in hematologic malignancies.

Cytogenetic studies have revealed nonrandom involvement of some chromosomes in specific structural abnormalities in human neoplasias. In this report we present three patients with t(2;3) associated with hematologic malignancies, and review the pertinent literature. These findings lead us to regard the region between 3q26 and 3q29 as implicated in chromosomal changes in these disorders, whereas, no vulnerable point has been observed in chromosome #2. We suggest that these translocations may activate genes on chromosome #3 related to these neoplasias.

Cytogenetic and immunologic phenotype findings in Hodgkin's disease.

There are very few chromosome studies using banding techniques of lymph nodes in Hodgkin's disease (HD), and determinations of immunologic phenotypes are scarce. We have performed both cytogenetic and immunologic studies in 12 of 22 lymph node biopsies of different histologic types obtained from 20 HD patients (no mitotic cells were found in the remaining ten lymph nodes). A near-diploid modal number was obtained in 80% of the cases, and 20% showed a bimodal distribution. Clones were observed in 50% of HD lymph nodes, with chromosome markers in 60% of them. Markers 15q+, 5p-, and der(X) and a trisomy of chromosome #21 were observed in our cases. Seventy-one percent of the lymph nodes studied showed a predominance of T lymphocytes. Within the lymph nodes, where the karyotype was determined, 4/12 lymph nodes presented a predominance of B lymphocytes, and they were all included in the group with structural chromosome abnormalities.

Sister chromatid exchange in malignant lymphomas.

Sister chromatid exchange (SCE) was evaluated in peripheral lymphocytes from 20 untreated patients with malignant lymphomas: 6 with Hodgkin's disease (HD), 14 with non-Hodgkin lymphoma (NHL), and 5 with lymphadenitis. The mean SCE frequency (+/- SE) was: 11.2 +/- 0.6, 11.0 +/- 0.6, and 7.2 +/- 0.3 for HD, NHL, and lymphadenitis patients, respectively, and 8.7 +/- 0.2 for the control group. No differences in SCE score were observed in HD and NHL. These results allowed us to consider both groups (HD and NHL) as a single neoplastic population (mean +/- SE, 11.0 +/- 0.4). No significant differences were found between the lymphadenitis and control groups. On the other hand, significantly higher SCE scores were seen in neoplastic populations than in the control and lymphadenitis groups (p less than 0.001 and p less than 0.01, respectively). When SCE was compared by chromosome number and group between neoplastic patients and controls, a higher SCE frequency was observed in chromosomes #1, #2, #3, and B, C + X, E, F chromosome groups than in controls. SCE levels were significantly higher in lymphoma patients in all chromosome numbers and groups mentioned than in patients with lymphadenitis. It is suggested that the high SCE rate in the malignant lymphoma population is possibly related to an increased chromosomal instability.

Coincidence of cytogenetic markers in four murine cell lines.

Foreign body tumorigenesis was induced by the subcutaneous implantation of a plastic or glass cylinder in BALB/c mice; the inoculation of human neoplastic cells significantly increased the incidence of these anaplastic sarcomas. Of 15 tumors studied, four presented the same markers: one induced with and three without human neoplastic cell inoculation within the foreign body. The markers observed were double minutes (DM), a long acrocentric marker (MLA), and a metacentric marker (MM). The DM are a number of small often tiny chromosomal structures appearing in pairs together with chromosomes of ordinary size. MLA is a long acrocentric derived from a translocation in tandem between chromosomes #1 and #16. MM is due to centric fusion of two chromosomes #10. Numerical anomalies consisted of gains of the same chromosomes types. It is postulated that these coincident findings are related to the foreign-body tumorigenesis.