Two types of human fibroblasts have been isolated from a patient with a colon cancer with metastasis, one type was derived from a healthy part of the colon, and the other one isolated from a metastasized lymph node close to the intestine. These fibroblasts have been characterized for their expression of collagens type I, III and IV, vimentin, fibronectin, alpha-smooth muscle actin, laminin and desmin. The effects of conditioned media of human colon cancer cell lines, HT29, SW1116, LS180 and HCT8R, on the metabolism of these fibroblasts were tested. All the conditioned media stimulate both types of fibroblasts, as reflected by their incorporation of radiolabelled methionine and proline. Normal fibroblasts were highly sensitive to the conditioned media as compared to the activated fibroblasts. Additionally, the production of TGF beta 1 by the four colorectal cancer cell lines has been quantified, and significant qualitative (production of latent and/or active form) and quantitative differences were observed. The effects of the conditioned media of the four tumoral cell lines and exogenous TGF beta 1 on the proliferation of the two types of fibroblasts were compared. Our data indicated that the two types of fibroblasts respond differently to TGF beta 1 whereas they are both growth stimulated by the conditioned media, apart from the LS180 conditioned medium. We conclude that if TGF beta 1 acts in the fibroblastic reaction, additional factors are required.

Cancer is a disease at the DNA level, originating from mutations of genes involved in the regulation of cell proliferation and differentiation: oncogenes and tumor suppressor genes. Only a few proportion of tumors, resulting mainly from germ-line anti-oncogene inactivation, arise in the frame of inherited cancer syndromes with mendelian mode of transmission. There may also be a much larger number of cases who are less strongly predisposed, without evident familial clustering. Genes involved in DNA repair process and in metabolism of carcinogenesis may be responsible. Study of genetic predisposition to cancer have important implications for screening individuals at high-risk in families.

In situ hybridization for the detection of RNAm in ultrathin tissue sections embedded in lowicryl resin is reported. This method proved suitable for both tissues and cell cultures, using either complementary DNA probes or synthetic oligonucleotides, labeled with a radioisotope or biotin. This method seems to strike a satisfactory balance between preservation of cell ultrastructure and sensitivity.

The case described corresponds to a grade G2 urothelial tumor with stage pTa extension (according to the World Health Organisation classification). After transurethral resection of the tumor and treatment by Bacillus Calmette Guerin (BCG), the efficacy of treatment was evaluated by cystoscopy, standard cytology, flow cytometry or image analysis. According to these various methods it has been shown that a normal cystoscopy may or may not be associated with aneuploidy revealed by flow cytometry. Such a case clearly illustrates the value of combining macroscopic examination and a cytologic analysis in particular by flow cytometry in order to increase the accuracy of diagnosis and to evaluate without ambiguity the efficacy of treatment.

Testicular ageing affects at the same time the individual and his lineage. In the individual, vascular, endocrine, blood testis barrier and Sertoli cells changes because of age lead a decrease of spermatozoa number and an alteration in their form and motility. These changes lead a gradual decrease of fertility. In the progeny, paternal ageing is responsible for new dominant autosomic mutations which themselves cause different malformations and perhaps for certain chromosome X linked recessive mutations. Moreover, in animal and man, paternal ageing seems responsible for a gradual lowering in the level of progeny cerebral functions. In man, very youthful age was also related to these effects. Maternal age did not appear to play a part in this event. On the whole, these results pose the problem of the optimum age for fatherhood.

During the last few years, the diagnosis of cutaneous lymphoma has benefited from new techniques. Immunohistochemical staining helps in the early diagnosis of mycosis fungoides and has contributed to a better characterization of non-epidermotropic lymphomas. The possibility of immunohistochemical staining on paraffin-embedded sections has facilitated its execution. CD 30 antigen expression seems to have a prognostic value for nonepidermotropic giant T-cell lymphomas. The prognostic value of expression of one of the two types of T-cell receptors for the antigen, alpha/beta or gamma/delta, remains to be established. The anti-V region antibodies may constitute a marker of clonality for some T-cell lymphomas and demonstrate that in some cases of mycosis fungoides the infiltrate is strictly intraepidermal. Genotype determination represents an advance in the diagnosis of certain nonepidermotropic lymphomas which cannot be characterized on the basis of immunohistochemical data alone. On the other hand, the Southern blot test has been unable to solve the difficult problem of the early diagnosis of mycosis fungoides. Polymerase chain reaction is a novel and very promising technique the usefulness of which remains to be determined. It can already be predicted that it will confront the clinicians with a problem: the significance of demonstrating very small clonal populations. A better knowledge of various cytokines makes it easier to understand the course of cutaneous lymphomas. Finally, advances in molecular biology techniques in the field of retroviruses suggest that defective retroviruses might be the cause of some cutaneous lymphomas.

The authors report a case of familial Stuve-Wiedemann syndrome where the diagnosis was made in utero. Following this case the authors discuss the management of short femur discovered by ultrasound. The analysis of the morphology, the ultrasound appearance and the radiographic appearance (X-ray of the uterine contents) may make it possible sometimes to diagnose the syndrome. An important element is a study of the genealogy to discover the way in which a large number of these bone diseases are transmitted. The prognosis for life is very variable according to the severity of the syndrome.

Cutaneous pseudolymphomas are benign hyperplastic lymphoproliferative reactions that simulate cutaneous malignant lymphomas clinically and/or histologically. The differentiation between cutaneous pseudolymphomas and primary cutaneous lymphomas is often very difficult, but is important because it may have therapeutic consequences. The term pseudolymphoma does not refer to a specific disease, but to a heterogeneous group of pseudo-B-cell lymphomas and pseudo-T-cell lymphomas. In this review the definitions and classification of cutaneous pseudo-B-cell lymphomas and pseudo-T-cell lymphomas will be discussed, with emphasis on the changing concepts that have resulted from the introduction of new diagnostic methods. The various differential diagnostic criteria that have resulted from these concepts will be presented.

Tumorigenesis is caused by abnormal proliferation of cells that escape regulatory mechanisms. Most of the molecular events leading to the formation of tumors are still largely unknown. In this paper, experimental data supporting a causative role for cellular genes, termed oncogenes, in the formation of tumors of the nervous system are reviewed. Two types of oncogenes are described: dominant oncogenes, characterized by the fact that one abnormal copy of the gene is sufficient to induce tumorigenesis, and recessive oncogenes which require the inactivation of both copies of the gene to lead to tumor formation. The role of recessive oncogenes in tumorigenesis of the nervous system is illustrated by molecular studies of meningiomas and neurinomas. The mutation of one, and perhaps two loci on chromosome 22, has indeed been shown to be most probably the causative molecular event in the growth of these two tumors when they occur either in their sporadic form, or in neurofibromatosis type 2. All the available data support the proposition of systematically analyzing a large number of tumors to eventually correlate clinical phenotype and evolution, to the genetic abnormalities observed. Furthermore, the understanding of the normal and pathological function of oncogenes should lead to future therapeutical improvements.