Prostatic cancer is the second most frequent cancer in men in industrialised countries. The histological analysis of its initial development demonstrates the existence of precancerous lesions, PIN. The initial presence of several different cell populations accounts for the development of contingents of hormone-sensitive and hormone-resistant cells. The presence of numerous neuroendocrine cells appears to be a factor of poor prognosis. Hormones are intimately involved in the development of prostatic cancer and are an integral part of its treatment. Progress in molecular biology has furthered out knowledge of this disease. In particular, growth factors such as EGF and FGF are particularly involved and are starting to have a clinical application. The oncogene and anti-oncogene system is currently being explored (particularly p53 abd BCL 2). They are the basis for carcinogenesis and analysis of these factors will allow a better approach to the mechanisms of tumour induction and development.

Prostatic cancer is the second most frequent cancer in men in France. It is a serious disease with a relative 5-year survival of 42%. Although the incidence of latent forms appears to be constant throughout the world, the incidence of clinical forms varies from country to country and according to race. These aspects are in favour of a dual mechanism of prostatic carcinogenesis: initiation of a cellular modification, which may be transmitted genetically according to an autosomal dominant mode, but whose expression may be influenced by the environment, and successive steps of transformation (epigenetic factors) which are essentially environment-dependent. The main identified risk factors essentially consist of a direct family history, age and a diet rich in animal fats. In contrast, neither the presence of benign prostatic hypertrophy, nor the characteristics of the sex life or a history of vasectomy appear to influence the incidence of prostatic cancer. The main epidemiological data currently available are presented.

Tobacco is responsible for 80 to 90% lung cancer cases in industrialized countries. However, genetic factors are likely to be involved in lung cancer susceptibility. Some degree of familial aggregation of lung cancer is evidenced in most family studies. On the other hand, many tobacco carcinogens are metabolised by enzymes of the P450 cytochrome family. Two enzymes of cytochrome P450, CYP1A1 and CYP1A2, are inducible by tobacco carcinogens, and animal studies evidenced a genetic polymorphism of CYP1A1 associated with tumour occurrence after administration of a polycyclic aromatic hydrocarbon. In humans, an association between lung cancer and some P450 polymorphisms (CYP1A1, CYP2D6, CYP2E1) was suggested but the results of epidemiologic studies are discordant and difficult to interpret. In addition, there is a polymorphism of glutathione S-transferase isoenzyme (GSTM1) involved in carcinogen elimination; an association between this polymorphism and lung cancer has also been reported. Further studies on combined effects of these polymorphisms should allow an identification of sub-groups of individuals at high risk of lung cancer.

Presenting 3 personally examined cases, the authors underline the incidence and the characteristics of pheochromocytoma associated with Von Hippel Lindau disease. In conclusion, a systematic screening for Von Hippel Lindau disease-often unrecognized to day-must be done in every patient presenting with pheochromocytoma.

CYFRA is a new marker which measures a fragment of cytokeratin 19 in the serum by an immune radiometric method. The test is based on the preservation of the cytokeratin expression on the epithelial cells during the course of malignant transformation. In immuno-histochemistry the antibodies which selectively recognise cytokeratin react with all histological types of bronchial cancer. The presence of cytokeratin in the serum of patients suffering from cancer would be linked to their liberation during the course of cellular death. The threshold of specificity for CYFRA 21-1 is 3.3.3.6 ng/ml in a population suffering from benign respiratory diseases. The study performed in bronchial cancer produced the following conclusions: the marker is, above all, useful for epidermoid cancer; it is more discriminating than other markers to separate bronchial cancers and non-malignant respiratory disease. An elevated level of CYFRA 21-1 is predictive of advanced disease but does not permit any prediction as to inoperability. In 65% of cases, variations of CYFRA 21-1 are concordant with the stage of the disease during chemotherapy. Finally, elevated levels of CYFRA 21-1 predict a poor prognosis independent of the state of the disease.

This presentation allows us to understand the terminology used for oncogenesis by Molecular Biology investigators. Thanks to the minute description of the normal physiology of the cell cycle, its regulatory mechanisms and growth stimulating and inhibiting effects, we are able to understand the language used. We are now able to fill the gap in our knowledge and to establish the increasingly necessary relationship between routine practice and Molecular Biology.

We described a case of squamous cell carcinoma of the vulva in a patient with Morris' syndrome. In these patients, there is an increased risk of gonadal neoplasms. On the contrary, neoplasms originating from the vulvo-vaginal tract are very rare. Neoplasms arising from the neovagina have been reported. Therefore, a continued periodic surveillance of the external genitalia and the vagina is indicated.

Prognosis factors such as mutated or amplified oncogenes are used in the treatment of breast cancer. We have recently shown that the members of the PEA3 group (ER81, ERM and PEA3) from the transcription factor family of the ets genes are overexpressed in breast cancer tumors arising from MMTV-neu transgenic animals. Moreover, we have shown that ER81, and in a lesser extent ERM and PEA3, are not expressed in the estrogen and/or progesterone receptor-positive mammary cancer cell lines, whereas they are expressed in the receptor negative ones. Our research interest in now focused on the role(s) of these oncogenes in the development and the regulation of breast tumors.

The role of estrogens as promoters of breast carcinogenesis has been well established while their action in tumor invasion appears more complex. Breast cancer cells without estrogen receptor (ER) are generally less differentiated and more aggressive than those containing function ER. Moreover the reexpression of ER by transfection in ER-negative cell lines inhibit their metastatic potential. These results suggest a protective role of ER in the metastatic progression of breast cancers. Studies of the underlying mechanisms of this effect may open new therapeutical strategies.

Numerous acquired genetical mutations are now well described by molecular biology and seem to be related to tumour progression. K-RAS mutation is of interest in colorectal cancer where it could be correlated to an aggressive tumoral behaviour leading to a high risk of recurrence or metastasis.

T cell prolymphocytic leukemia (T PLL) is a rare variant of mature lympho-proliferative disorder. The main physical sign is a gross splenic enlargement contrasting with no enlargement of lymph nodes. Skin involvement is found in 30 p. 100 cases. Twenty-one cases of cutaneous lesions of PLL have been reported, mainly with T PLL, only 2 cases of B PLL: Clinical lesions are polymorphous; histology shows a dermal prolymphocytic infiltrate. The main cytogenetic abnormalities are: translocation (14; 14) (q11; q32), inversion of chromosome 14 (q11; q32), isochromosome 8q.

A 14-year-old girl consulted for multiple breast nodules which were found to result from Cowden's disease, also called multiple hamartomatosis. Mammography and sonography examinations were completed with nuclear magnetic resonance imaging after injection of paramagnetic contrast product. Cowden's disease is a rare condition resulting in the development of tumors in genodermatous tissue; The cause remains unknown. In cases involving the breast, cutaneous lesions are markers of precancerous development since cancer occurs in 28 to 30% of these cases.