We reassessed the use of DNA flow cytometry in bladder cancers on the basis of our research and already published findings. We discuss technical aspects underlying the validity of the results. Currently, the validity of DNA flow cytometry is established by parametric analysis of the DNA content of tumor cells found in the course of multiple biopsies of the tumor. In addition, we examine the results obtained with bladder washings and, in some cases, the results of biopsies of the bladder mucosa which may appear normal under cystoscopy. The complementarity of these examinations appears to be essential. Our experience confirms the results already published, suggesting that the frequency of DNA aneuploidy increases significantly according to the grade and the tumor stage. However, clinical interpretation of DNA flow cytometry results calls for some caution. There is a general consensus not to use these results in the screening of bladder cancers. However, DNA flow cytometry is particularly useful in the follow-up of carcinoma in situ since DNA aneuploidy is almost always present. DNA flow cytometry is also useful in the stratification of superficial grade 2 tumors. Finally, during the follow-up of invasive tumors, the persistence or appearance of DNA aneuploidy may be attributed to therapeutic resistance.

In France, invasive bladder cancer is the more frequent urologic malignancy after prostate carcinoma. Treatment of bladder cancer is radical cystectomy. New therapeutic approaches such as chemoradiation combination for a conservative procedure, neoadjuvant or adjuvant chemotherapy are still developing. In this way, a rigorous selection of patients is needed. This selection is based on prognostic criteria that could be divided into four groups: i) the volume of the tumor including the tumor infiltration depth, the nodal status, the presence or not of hydronephrosis and the residual tumor mass after transuretral resection; ii) the histologic aspects of the tumor including histologic grading, the presence or not of an epidermoid metaplasia, of in situ carcinoma or of thrombi; iii) the expression of tumor markers (tissue polypeptide antigen, bladder tumor antigen); iv) the biologic aspects of the tumor as ploidy, cytogenetic abnormalities, expression of Ki67, expression of oncogenes or tumor suppressor genes, expression of tumor antigens or growth factor receptors. This paper reviews the prognostic value of the various parameters.

Segmental neurofibromatosis (NF V) is ten times less frequent than Recklinghausen disease. Would the risk of visceral involvement in this uncommon form of neurofibromatosis warrant systematic imaging procedures?

The myelodysplastic syndromes (MDS) are a heterogeneous group of disorders characterized by peripheral blood cytopenias with a hypercellular bone marrow exhibiting dyspoiesis. The predominant in elderly patients are associated with a high risk of progression to acute myelogenous leukemia. The etiology of MDS is unknown in most cases. About 10% of MDSs are secondary. MDS are classified by the French American British (FAB) classification into five subgroups. The incidence of the disorders is difficult to estimate but it seems to be increasing. Clonal cytogenetic aberrations are found in 30 to 50% of de novo MDS. The only currative treatment for MDS is allogeneic bone marrow transplantation.

Tumor differentiation, myometrial invasion and lymph node metastasis are the most important prognostic factors in endometrial carcinoma. Tumor stage, positive peritoneal cytology, obesity and race seems to be also prognostic factors. The surgical treatment of stage I and II endometrial carcinoma is hysterectomy with bilateral adnexectomy and pelvic lymphadenectomy (obturator group). This procedure can be performed by laparotomy or laparoscopy.

The tumour biology of non-small cell bronchial cancer integrates recent developments and a dynamic schema of the phenomena of tumour progression and diffusion of the metastatic disease. There is no leap of known biological disruption between Stage II and Stage III. The latter is defined by anatomical criteria and is a transition in the continuum of the natural history of these cancers. The moto for the tumour progression is the genotypic instability and phenotypic diversification. Metastatic microscopic disease constitutes the first cause of failure in the treatment of Stage III non-small cell bronchial cancer. Among prognostic factors for survival emphasis is placed on the alterations of p53 expression, different types of aneuploidy, anomalies of the expression of cellular adhesion molecules and finally, tumour diversification towards a metastatic phenotype.

Von Hippel-Lindau (VHL) disease is a genetic disease predisposing to the development of various tumours (haemangioblastomas of the neuraxis and retina, tumours of the membranous labyrinth, renal clear cell carcinomas or cysts, phaeochromocytomas, pancreatic cysts or tumours, epididymal cystadenomas), affecting one in 36,000 people. Renal cancer constitutes one of the main causes of death. The VHL gene, situated at 3p25-26, is a tumour suppressor gene which plays a major role in regulation of VEGF transcription and expression. The germ cell mutation can be identified in 70% of patients. Somatic mutations of the VHL gene are also responsible for sporadic clear cell carcinomas. In the urological setting, any patient presenting with "sporadic" bilateral clear cell renal cancer or detected at an early age, or bilateral epididymal cystadenomas, should be investigated for the presence of VHL disease.

We report a case associating NF1 with multiple sclerosis. There are only seven cases of this association, so that it might be interpreted as resulting from chance. However, although the association is weak, it might be non fortuitous, owing to a particularity of the NF1 gene that embedded oligodendrocyte-myelin glycoprotein gene, even if the responsibility of structural genes of myelin have not been implicated in susceptibility to multiple sclerosis.

The granulocytic sarcoma is a rare and extramedullary tumor, which is composed of granulocytic precursor cells. The diagnosis remains difficult. Infectious disease are often associated with leukemic processes. Combination of clinical, radiological and pathological findings are useful for diagnosis. On gross examination, the tumor appears green. The detection of myeloperoxidases and the presence of immature eosinophils can help histological analysis. Granulocytic sarcoma occurs before or during an acute leukemia. It is treated like an acute leukemia. Prognostic is greatly improved by early diagnosis and treatment. The lack of cytogenetic abnormalities is associated with a prolonged survival. We describe a new case of rapidly growing pleural granulocytic sarcoma. The uncommon modifications of chromosome 5 long arm in this case could explain the immature eosinophil reaction in that tumor.

Parathyroid cancer is very rare in chronic renal failure. Only twelve cases have been described, but the actual incidence might be under estimated. Monoclonal proliferation have been demonstrated in hyperplasic parathyroid glands of uremic patients and the diagnosis between benign or malignant tumor may be difficult. Evidence for a deletion of the "Retinoblastoma Tumor Suppressor gene" (RB gene) is helpful for the diagnosis of parathyroid cancer, especially in the absence of dissemination. A 46-years old male patient on dialysis since 1989 for polycystic kidney disease developed a refractory and persistent hyperparathyroidism after parathyroidectomy with vascular and osteoarticular complications. Liver nodules were localised by sestaultrasonography. MIBI radionucleid scan and were confirmed by CT-scan, and ultrasonography. Diagnosis of parathyroid cancer was confirmed by the immuno-histochemical study of the biopsied liver nodules and the histopathological review of the removed parathyroid glands.

An unusual endometrial stromal sarcoma is described in a 50-year-old patient. The distinctive feature of this case is the focal occurrence of sex cord-like pattern and rhabdoid appearance of tumor cells. Rhabdoid cells have an eosinophilic cytoplasm and a vesicular nucleus with a prominent nucleolus. Immunohistochemistry showed positive cytoplasmic staining for both cytokeratin and vimentin, and ultrastructural examination identified tumor cells with abundant cytoplasmic intermediate filaments. To our knowledge, only one case of endometrial stromal sarcoma with this unusual morphological association has been reported in the literature.

In January 1997, PCR genomic analysis of the TSG101 gene showed frequent large intragenic deletions. The investigators used a small cohort of sporadic breast cancers. Li et al. proposed human TSG101 as a breast tumor suppressor gene. Since then, several teams have worked on large series of breast cancers, using a variety of techniques. They have shown that intragenic deletion, if it exists at all, is rare. Is TSG101 a tumor gene or an impostor?

Human telomeres are guanine-rich regions (TTAGGG) located at the end of chromosomes that protect them against aberrant recombination and protect DNA from exonuclease degradation. Telomeres maintenance is performed by telomerase, a RNA-dependent DNA polymerase. Telomerase is over-expressed in a large number of cancers that have short telomeres whereas it is not expressed in somatic cells that have long telomeres. Therefore, this differential gives a rational for further evaluation of telomerase and telomeres as targets for identification of new anticancer drugs. Current strategies aim to identify new drugs with specific activity against telomerase and telomeres. In this review we will discuss the biological and clinical approaches as well as relevant tumor models for studying the biological effects of telomerase inhibition and telomere targeting in vitro and in vivo.

Triploidies are pregnancies that show a 69 chromosome karyotype. This chromosomal abnormality gives rise to early abortion in most cases. Triploid pregnancies, after the first three months, become molar pregnancies (molar changes inside the placenta with identifiable embryonic structures and a preeclampsia) or non molar pregnancies (isolated intauterin growth retardation). Several possibilities concerning the origin of the additional set of chromosomes exist: dispermy (the most common), diandry and digyny. The maternal and fetal clinical manifestations of this chromosomal abnormality are very diverse, which explains the difficulty of finding and recognizing this pathology. Mac Fadden's classification does not explain all the phenotypic triploid physiopathology. Formal diagnosis of triploidy depends on the fetal karyotype. The better the maternal prognosis is, the worst the fetal prognosis is. Postnatal life expectancy is not more than a few weeks. In most cases, maternal associated complications disappear with the molar evacuation. The risk of post molar tumor is discussed. However, good management of triploidy is based on an early diagnosis, before birth if that is possible.

Cytogenetic anomalies described in colo-rectal tumors are numerous. Despite the complexity and the number of the anomalies observed, a combined study of their frequency and of the stage of prognosis of the tumors suggests that the evolution from colonic adenoma to carcinoma often follows a sequence of events comprising a 5q15-22 deletion (DCC), and a 17p deletion (P53). It even seems likely that in many cases, these events are not constant and that others might lead to the same phenotypic transformation. Chromosome 1 involvement in structural rearrangements has been demonstrated in numerous forms of cancers, malignant blood disorders and in solid tumors. In colorectal adenocarcinoma anomalies have been described on short and/or long arms. In a case of adenoma with mild dysplasia a deletion of the distal part of the short arm of chromosome 1 was observed as an isolated cytogenetic anomaly, suggesting it would be an early, perhaps triggering, event for the tumour development. A cytogenetic study in a series of colo-rectal tumours, researches on loss of heterozygosity and microsatellite instability lead to consider deletions at chromosome 1p as an early event in human colorectal tumourigenesis.