Evidence from cytogenetic (karyotype) and cytometric studies in cutaneous T-cell lymphomas reported in the medical literature is reviewed. Such studies are still very scarce because of the technical difficulties which arise in culturing the cells. Automatic analysis of chromatin dispersion (flow cytometry) is currently the most promising technique.

The results of a cytogenetic study on 240 acute nonlymphocytic leukemia patients (187 adults and 53 children) were classified in NN (normal), AN (abnormal and normal) and AA (abnormal). Pronostic value of the classification was presented. A higher proportion of complete remission failures was observed in chromosomally abnormal patients (AN and AA). Survival of patients with complete remission was significantly shorter in AN and AA patients than in NN patients. An excess of constitutional chromosome abnormalities was observed in children.

Normal and abnormal results of chromosome studies performed on 101 acute nonlymphoblastic leukemia (ANLL) patients were compared according to the bone marrow and/or blood cell culture times. A higher proportion of abnormal karyotypes was observed after culture than on direct preparations in acute promyelocytic leukemia and in acute myeloblastic leukemia with t(8-21) translocation; in some cases the chromosome abnormality seen after culture was not detected with the direct technique. No clear-cut differences in chromosome studies resulted when the differing techniques were applied to other forms of ANLL. In contrast the classification of individual patients into AA and AN categories differed in some cases when determined by direct or culture techniques. These results have to be taken into consideration in the study of relationships between chromosome anomalies and prognosis.

The distribution of the phenotypes and the gene frequency of the 3rd fraction of complement (C3), the specific group (Gc), haptoglobin (Hp) and transferrin were studied in 133 patients with transitional cell cancer of the bladder (papillary cancer). Statistical analysis of these results, in comparison with the frequency of these genes in the general population, was unable to demonstrate a correlation between the distribution of these phenotypes and papillary cancer.

This editorial gives introduction to the cell and viral oncogenes, their inter-relation and normal and tumorigenic functions, and to the anti-oncogenes in the case of hereditary neoplasias.

The Birt-Hogg-Dubé syndrome is characterized: a) clinically, by an asymptomatic eruption of dome-shaped papules involving the head, neck, chest, back and arms frequently associated with acrochordons; b) histologically, by multiple follicular tumors, namely fibrofolliculomas and trichodiscomas, representing benign proliferations of mesodermal and ectodermal components of the pilar apparatus; c) by the apparent autosomal dominant mode of inheritance. This study is concerned with two families whose various members belonging to two and three generations have the clinical and histological lesions of this syndrome. In several biopsies performed, the main finding was the fibrofolliculoma isolated or associated with perifollicular fibromas; in five biopsies, was noted a typical trichodiscoma associated, in two of them, with a perifollicular fibroma. Clinically, the fibrofolliculomas were indistinguishable from trichodiscomas. We believe that the Birt-Hogg-Dubé syndrome is an autonomous well individualized skin disease. Its existence supports the view of the close interaction between the epithelial and mesodermal components of the pilar complex.

Cytogenetic analysis of resected bladder tumors was performed in 32 patients. None of these patients had previous irradiation or chemotherapy. Direct chromosome preparations were made. Of the 32 preparations, 22 had chromosome abnormalities. We have observed a good correlation between the chromosome abnormalities and the Stage/Grade of the tumors. Patients were followed from 6 to 33 months. During this period, 82% of the patients with noninvasive or submucosal invasive bladder tumors and chromosome abnormalities have had recurrences. The existence of a good correlation between chromosomal abnormalities and the capacity of the neoplasm to recur was confirmed.

The authors report five cases of cavernous hemangioma belonging to two families. In the first family, an 8 year old child was operated on in 1970 for a left frontal location. His mother, aged 39, was operated on in december, 1981, with stereotaxic approach, for two locations: one was frontal location, the other one was in the pineal region. Among the second family, a 21 year old woman was operated on in december 1976, for a cerebellar cavernous hemangioma. Her sister, aged 18, presented with subarachnoid hemorrhage in january 1980. C.T. scan showed a right temporal high attenuation area. This patient was not operated on. The aunt to those two sisters was operated on in october, 1981, for a left temporal cavernous hemangioma. Those five cases represent about half of the intracranial cavernous hemangiomas operated on in the Lille Neurosurgery Department since 1967. Even, unusual, the familial occurrence of this affection must be admitted. It shows a nosological interest, but also allows prevention by searching and surveying the asymptomatic cases, or genetic evaluation of disease risk.

Skin fibroblasts from normal children and two children with a 13q14 deletion retinoblastoma (Rb) were submitted to fractionated doses of gamma radiations. Irradiation reduced the population doublings in normal fibroblasts and the decline was inversely related to the dose. An increase in population doublings was obtained with one of the Rb cell lines. Foci appeared in the irradiated culture of the other Rb donor. It is suggested that fibroblasts from patients with Rb are able to express some phenotypical properties of transformed cells, perhaps related to factors rendering them more susceptible to carcinogens.

The chromosomal analysis of four fresh Ewing tumours shows a translocation of the band q12 of the chromosome 22 in all the clones observed. This translocation seems to preferentially involve the band q24 of the chromosome 11. These results are in favour of a consistent translocation in Ewing's sarcoma, and are to be compared with the results obtained in other malignancies. A relation between this translocation and the location of the human oncogene c-sis on the chromosome 22 should be considered.

Chromosome studies were performed on 5 Ewing sarcoma cell lines. An identical reciprocal translocation t(11; 22) (q24; q12) was found in 4 cell lines established from 3 different tumors. These results, associated with those obtained at the same time and independently from fresh tumor cells, suggest that the translocation t(11; 22)(q24; q12) may be a chromosomal marker characteristic of Ewing sarcoma cells. This translocation involves the chromosome 22 on which the H-c-sis oncogene has been located; it could be used as a new tool for exploring the role of genetic transposition in the malignant cell transformation.