The rapid development of cancer genomics is due to important progresses in oncogenesis, human genome sequencing and emergence of new technologies in genome and transcriptome analysis. In this context, the aim of the French program 'Cartes d'Identites des Tumeurs--Molecular Portraits of Tumors' is to build a public data base containing a pan genome assessment of genome and transcriptome alterations in the major types of tumors as well as in relevant normal cells and experimental models. Data mining is done in the context of genome annotations and clinical and biological informations attached to the enrolled samples. The goal of the program is to define new tests useful for diagnostic procedures in clinical laboratories and new targets for biological treatments of tumors.

The authors report the association of ureteric tumour and colon carcinomas in the context of hereditary predisposition to HNPCC colon cancer (hereditary non polyposis colon cancer). The recall the diagnostic criteria of HNPCC syndrome and emphasize the importance of guiding the clinical interview of patients with upper urinary tract tumours in order to detect a family history and the presence of gastrointestinal tumours.

Recent improvement in the understanding of the mechanisms involved in the response to ionizing radiation have made it possible to identify new therapeutic targets to increase the anti-tumor efficacy or, alternatively, to decrease the effect on normal tissues. These approaches included targeting genes involved in the regulation of radio-induced DNA-repair and cell death as well as genes involved in the regulation of radio-induced apoptosis. Many other molecular targets have been recently identified to potentially interfere with the response to ionizing radiation, such as some cell membrane growth factor receptors (EGFr, TGFb) or molecules involved in intra-cellular signal transduction pathways, cell cycle regulation, etc. In addition, other promising ways to modulate radiation-induced response concern extracellular or tissue factors such as hypoxia and angiogenesis.

Two distinct clinical syndromes have been associated with the p11.12 region of the short arm of chromosome 8: stem-cell myeloproliferative disorder (B-or T-cell lymphoblastic leukemia/lymphoma with myeloid hyperplasia and peripheral blood eosinophilia) and acute myeloid leukemia (myelomonocytic or monocytic with erythrophagocytosis). The FGFR1 and MOZ genes are rearranged in these diseases and encode one of the four fibroblast growth factor receptors and a member of a novel histone acetyltransferase family, respectively. The predicted fusion proteins that are putatively oncogenic - FOP-FGFR1, CEP110-FGFR1, and FIM-FGFR1 - and - MOZ-CBP, MOZ-p300, and MOZ-TIF2 - lead to tumorigenesis through distinct pathways. The constitutive kinase activity triggered by dimerization mediated by the protein-protein interaction motifs of the FGFR1 protein partner regardless of external stimuli and the delocalization of the fusion proteins compared to their normal counterparts may lead to tumorigenesis presumably by inducing inappropriate recruitment in the cytoplasm of signaling substrates. Currently, little is known about the precise role of MOZ in the regulation of gene transcription. However, all the aberrant proteins described to date retain the MOZ histone acetyltransferase domain fused to that of the transcription coactivators CBP, p300, and TIF2. The fusion of two acetyltransferases whose activity may be mistargetted or misregulated could be a critical event in leukemogenesis. The increasing number of translocations affecting FGFR1 and MOZ strongly suggest their involvement in oncogenic processes and point to these proteins as potential therapeutical targets.

The interaction between Fas and its ligand (Fas-L) leads to Fas-positive cell apoptosis. Our objective was to study a new mechanism of tumor escape involving these molecules, the so-called "counterattack".

Genetic alterations in the p53 protein may induce serum anti-p53 antibodies. The aim of this study was to assess the prevalence of serum anti-p53 antibodies in a large series of Western patients with hepatocellular carcinoma and the prognostic value of these antibodies on survival.