In spite of important progress in the local treatment of uveal melanoma, the most frequent primitive intraocular tumor, 15%-30% of patients still die because of tumor metastasis. This tumor is characterized by constitutive chemoresistance, thwarting any attempt to control it using the usual chemotherapy protocols. The chemoresistance of uveal melanoma is mainly due to the typical multidrug resistance phenotype (MDR), which is linked to overexpression of membrane proteins that actively extrude anticancer drugs from the cell. Typical MDR is particularly complex in this tumor since several chemoresistance-related proteins are simultaneously produced. The negative prognostic significance of the overexpression of P-glycoprotein, the main representative among the typical MDR-related proteins, was shown in uveal melanoma. The atypical MDR phenotype, which refers to other chemoresistance mechanisms such as resistance to apoptosis also contributes to the chemoresistance of uveal melanoma. Thanks to the recent progress in molecular biology, the chemosensitization strategies of gene therapy approaches, which aim at weakening the pathological activity of MDR genes in cancer cells, are currently on the rise. This approach will disrupt current therapeutic strategies and necessarily improve and standardize the methods used to characterize the chemoresistance profile of this cancer. Indeed, we will have to know the genes to be targeted for each melanoma in order to induce cell chemosensitivity.

Experimental evidence indicates that n-3 fatty acids, especially the long-chain polyunsaturated fatty acids, unlike n-6 fatty acids could prevent cancer development. This survey shows that fatty acids could act through several mechanisms including the production of reactive oxygen species, the modulation of gene expression and signal transduction pathways, or the eicosanoid biosynthesis. Human genetics has underlined several polymorphisms in genes identified as possible targets of fatty acids which suggests that the link between nutritional intake and cancer prevention, especially the eventual anti-carcinogenic effects of n-3 fatty acids, depends on the genetic background. Further studies are needed to evaluate the effects of fatty acids on angiogenesis which represents a marker of a poor prognosis in cancer. Finally, the use of genomic technologies combined with nutritional strategies could provide a more understanding of the effects of n-3 fatty acid intake on cancer prevention.

Malignant glioma are especially difficult to model in vivo. Here we review the most recent strategies for designing relevant models of glioma. These should greatly contribute to identification of new tumor regulating molecules and facilitate testing of inhibitors to be used in therapeutical trials as well as the drug resistance that they might confer.

It is estimated that 100 to 200 genes in the human genome are imprinted. These are expressed only from one parental allele, although having the same DNA sequence. Several of the known imprinted genes have been shown to be involved in fetal and placental growth, and imprinting defects can lead to embryonic, developmental defects as well as cancer. This mechanism of gene regulation probably emerged 150 million years ago in mammals. The reasons for the appearance and maintenance of this phenomenon throughout evolution are still controversial.

A key challenge in clinical proteomic of cancer is the identification of biomarkers that would allow early detection, diagnosis and monitor progression of the disease to improve long-term survival of patients. Recent advances in proteomic instrumentation and computational methodologies offer unique chance to rapidly identify these new candidate markers or pattern of markers. The combination of retentate affinity chromatography and surfaced-enhanced laser desorption/ionization time-of-flight (SELDI-TOF) mass spectrometry is one of the most interesting new approaches for cancer diagnostic using proteomic profiling. This review aims to summarize the results of studies that have used this new technology method for the early diagnosis of human cancer. Despite promising results, the use of the proteomic profiling as a diagnostic tool brought some controversies and technical problems and still requires some efforts to be standardised and validated.

The jugulotympanic paragangliomas (JTP) represents the most frequent tumour of the middle ear but also of the temporal bone, after the acoustic neurinoma. The management of these vascular tumours remains uncleared. The purpose of this study was to report our experience about JTP in the CHU of Grenoble.

We report the case of a 8-year-old girl diagnosed with myelodysplastic syndrome. This case was morphologically characterized by the presence of bundle of Auer rods in the neutrophils. The evolution of the disease was marked by a quick transformation in a acute myeloid leukaemia with t(8;21) refractory to treatment. We reviewed the literature for clinical, biological and therapeutic features of this rare childhood hemopathy.

The genetic bases of inherited predisposition to cancer are now established. The aim of our study is to value the knowledge, attitude and behavior of the general population about the inherited predisposition to cancer. Our study involved a population of 200 individuals. Without any history of cancer. The mean age of our population was 37.5 years (18 to 74 years). The education level was low in 62.5% of cases (illiterate or primary education). About knowledge: heredity was considered a predisposing factor to cancer by 42.5% of the respondents. About attitude: we noted a cancerophobia in 82% of cases. 86.5% of our respondents trought that an early diagnosis increased the chance of recovery. About behavior: 72.5% of the studied population wishd to know if they were predisposed to develop cancer. In case of pregnancy, 79% wished to know if the foetus wasa cancer gene predisposition carrier. 28% would keep this foetus in case of positive genetic testing. These results are encouraging to develop oncogenetic counselling in Tunisia.

Our work aims at defining by microarray gene expression profiles in different thyroid tumors: hyperfunctioning autonomous adenomas, and sporadic and post-Chernobyl papillary cancers. Gene expression analysis in hyperfunctioning autonomous adenomas allowed us to identify genes involved in various physiological processes of the thyroid. Concerning papillary cancers, gene expression profiling in post-Chernobyl and sporadic papillary carcinomas could not identify a specific gene expression signature allowing to distinguish both tumors although such a signature exists for autonomous adenomas and carcinomas. This suggests that both cancers represent the same disease, and that there is unlikely to be a molecular signature for radiation-induced thyroid cancer.

Bovine leukemia virus (BLV) is a retrovirus responsible for lymphoproliferative disorders in ruminants. The comprehensive study of this model system permitted the identification of genetic determinants required for leukemogenesis, the quantification of the dynamic parameters responsible for cell accumulation and the elaboration of novel therapeutic approaches in human.

Genomic imprinting is a process that appeared in mammals. This phenomenon blocks the normal development of parthenogenic and androgenic conceptuses, that is to say benign ovarian teratomas and hydatidiform moles respectively. Pathological modifications of these conceptuses depend on whether the chromosomes come from the mother or father. These pathologies are associated with an accidental anomaly during gametogenesis and/or fertilizing. These reproductive anomalies are sporadic and some familial cases may exist suggesting a genetic control of such diseases. The human andro- and parthenogenetic conceptuses, but more frequently the moles, may be invasive (choriocarcinoma). An imbalance of the imprinting genes may initiate the deregulation of other genes, including oncogenes and anti-oncogenes, which can explain the cancerous modification. Immunological and environmental factors must be also considered (presence of the only paternal chromosomes in the choriocarcinoma). Numerous works on this subject are published and some recent important discoveries underline the roles of genes HOX, Tim P3, E-cad and p-16, and the recurrent chromosome anomalies 7q21+and 8p21- in the mole to choriocarcinoma processing. Although these phenomena are complex and heterogeneous, the andro- and parthenogenote conceptuses are particularly interesting models with which to understand developmental disorders and cancerous progression.

Oncological family history allows to estimate an empirical risk to develop malignant tumors. Nowadays family history is crucial to determine the indication to perform screening of cancer predisposing genes. Five to 10% of all cancers are the result of highly penetrant genes. Most of the genes responsible for familial cancer syndromes have been characterized. It is now feasible, by a simple blood sample, to detect germ-line alterations of these genes and to identify the at risk individuals. Specific screening and preventive strategies are recommended in the management of these high risk individuals.