The identification of fusion genes provides new insights into the initial mechanisms of molecular events implicated in the prostate cancer tumorigenesis. The presence of TEMPRSS2-ETS fusion in up to half of all human prostate cancer makes it perhaps the most common genetic rearrangement in human epithelial tumors. Some data suggest that TMPRSS2-ERG fusion prostate cancers have a more aggressive phenotype, which may affect cancer progression and outcome in localized tumors treated with prostatectomy. This discovery should pave the way towards future targeted therapies.

Lymphangioleiomyomatosis is a rare pulmonary disease encountered almost exclusively in women of reproductive age. Pulmonary involvement is characterized by multiple thin-walled cysts in the lungs, recurrent pneumothorax, obstructive lung disorders, and progression to chronic respiratory failure over a mean period of 10 years. Certainty of diagnosis requires a lung biopsy, but international criteria have been proposed for a diagnosis without such a biopsy. International recommendations were recently issued for the diagnosis and treatment of lymphangioleiomyomatosis. Treatment is principally symptomatic and relies on the management of bronchial obstruction by bronchodilators; of hypoxemia by oxygen therapy; of pleural complications by pleurodesis, most often surgical; and of renal angiomyolipomas by percutaneous embolization in cases of hemorrhagic risk. Hormone treatment is not recommended. Hopes are high for mTor inhibitors (sirolimus and everolimus) and treatment trials are currently underway. Lung transplantation must be considered when chronic respiratory failure occurs in patients younger than 60 years.

In spite of the great advances made on the knowledge of cancer etiology and the significant breakthroughs in terms of treatment, complete remission is obtained in only around half of cancer patients. In fact, therapies that appear successful for some cancers are totally unfruitful for others, and some cancer types still remain incurables. In order to develop new therapies suitable to these tenacious cancers, we need to renew our view on cancer and to revise some old paradigms and "false friends" that can hide unexpected new therapeutic targets. A good example of these paradigms is the role of the cell stress response in tumor progression. Indeed, a number of studies has been devoted to the pivotal tumor suppressor function of some players of this response, of which the p53 protein is the best example. Nevertheless, during tumor progression and metastasis, the cancer cell faces many stresses imposed by tumor microenvironment and its survival will be conditioned by an efficient cell stress response. This review is consecrated to the role played by a pivotal actor of the cell stress response, the p8 protein, during carcinogenesis. We will recapitulate the data available on its different cell functions and the assets p8 confer to the cancer cell in terms of growth, drugs resistance and metastasis formations.

Adrenocortical carcinomas are rare tumors characterized by an aggressive behaviour with a 5-year survival rate below 30%. Until now, surgery is the only curative treatment for tumors confined to the adrenal gland and there is a lack of an effective medical treatment for invasive or metastatic tumors due to the poor knowledge of the mechanisms underlying adrenocortical malignancy. Moreover, histopathology is sometimes insufficient to establish an accurate diagnosis between a benign and a malignant adrenal tumor and a poor indicator of prognosis. In the last decade, the study of rare genetic syndromes associated with adrenocortical carcinomas and the identification of genetic alterations in adrenal tumors has improved our understanding of the pathogenesis of adrenal tumors. The development of molecular predictors of malignancy and of survival could help for histological diagnosis and determination of prognosis. These significant advances are essential to improve adrenocortical carcinoma management. This review summarizes recent advances in the understanding and management of adrenocortical tumors.

The p73 gene encodes a nuclear protein that is highy homologous to p53. p73 also shares some common functions with p53 protein indicating that p73 gene is a p53-like tumor suppressor.

In 1956, the number of chromosomes in humans is set at 46; in 1959, the link between a disability (mongolism) and a chromosomal anomaly (the Down syndrome) is established: human and medical cytogenetics were born. Since then, progress has been remarkable: the techniques of chromosomal and molecular cytogenetics can reach a resolution of the size of a single gene with a pangenomic scope. Practical applications are constantly expanded. The clinical impact is significant, from the genetic counselling in constitutional to the targeted therapies. Fifty years later, cytogenetics can be defined as the science which aims to detect chromosomal abnormalities, whether constitutional or acquired, using chromosomal or molecular techniques aiming to study the arrangement of genes in chromosomes, to quantify the number of gene copy and to look for the presence of gene fusion.

The aim of this study was to characterize the antigenic profile of blasts in acute lymphoblastic leukaemia (ALL) and to determine possible phenotypic aberrancies in a series of 152 patients with acute leukaemia diagnosed non myeloid leukaemia in cytology. Samples were analyzed by EPICS XL flow cytometer (Beckman Coulter) after staining with monoclonal antibodies(Beckman Coulter). Based on criteria of EGIL (European Group of Immunological Leukaemia), cases were classified as: acute lymphoblastic leukaemia (ALL, 52,6%); 75% cases of ALL belong to lymphoid B lineage. 80% of ALL B were CD10 positive, marker of best prognosis. In 10,5% of cases, biphenotypic leukaemia is diagnosed (lymphoid/myeloid). In 25% of cases aberrancies in phenotype were found. Flow cytometry has wide field of applications to characterize blast cells from patients with acute leukaemia: to establish diagnosis of lineage responsible in proliferation, to determine the stage of maturation, to predict prognosis for a better adaptation of adequate treatment, to follow evolution of disease after chemotherapy and to study minimal residual disease.

Birt-Hogg-Dube is a rare syndrome which is sporadic or hereditary with a dominant autosomal transmission. Various organs, in particular the skin, can be affected. In the presently reported case, skin was covered by hundreds of small molluscoid papules corresponding to trichodiscomas, fibrofolliculomas and skin tags.