Prophylactic mastectomy is an effective, although controversial strategy to reduce the risk of breast cancer in women carrying a BRCA1/2 mutation. A multidisciplinary pre- and post-operative clinical management is recommended for women who consider or undergo this surgery, because of its radical and irreversible nature as well as its possible impact on quality of life.

Since over a century, medical literature has reported cases of viral infections leading to tumour regression. This phenomenon, now understood, can be exploited for cancer therapy. It involves viruses defined as "oncolytic". These viruses, either wild-type or genetically engineered, replicate preferentially in malignant cells. They induce tumour regression through various mechanisms including direct cell lysis and stimulation of an anti-tumour immune response. Several oncolytic viruses have reached late-stage clinical investigation and could be approved soon for treating certain neoplasms. While already promising, there is still room for improvement and various genetic, immunological, and pharmacological strategies are currently under development to increase their therapeutic efficacy.

Malignant transformation of hepatic adenoma (HA) is now a well-documented phenomenon. Recent pathological and immunophenotypic studies have identified several subtypes with different prognoses. In many cases the HA subtype can be determined by modern radiological methods, including contrast-enhanced ultrasonography (CEUS) and magnetic resonance imaging (MRI). Based on a series of 26 cases of HA studied with CEUS, MR1 histopathology and immunochemistry, we propose tailored therapeutic options. Watchful waiting is appropriate in some cases, while others require biopsy or resection. Management is more conservative than in previous years.

FGFR3 mutation leads to a constitutive activation of the receptor 3 to Fibroblast Growth Factor. This mutation is early in urothelial carcinogenesis and is strongly associated to low grade papillary tumors. Multiple regional epigenetic silencing (MRES) phenotype corresponds to the transcriptional inactivation of chromosomal regions in muscle invasive bladder cancer, and is strongly associated to the molecular signature of carcinoma in situ. These alterations could be targeted by new specific therapies.

Microsatellite instability (MSI) phenotype occurs in approximately 15 to 24% of colorectal cancer (CRC) patients and may be sporadic or hereditary. It reflects a mutator phenotype in the tumor due to a lack of mismatch repair system. MSI is indeed one of the characteristics of CRCs occurring in Lynch syndrome and some sporadic cases. CRCs with MSI have a better prognosis than CRCs with microsatellite stability (MSS). This is explained partly by a more important anti-tumor immune response and by apoptosis of tumor cells in which mutations accumulate. However, in some retrospective studies, microsatellite instability in stage II CRCs was associated with no benefit to or even a deleterious effect of 5-FU alone based adjuvant therapy. Nevertheless, results obtained in stage III CRCs with FOLFOX type adjuvant chemotherapy remain favorable in retrospective studies.

Diagnosis of brain metastases should aim to identify anatomoclinical entities for which a specific treatment is more accurate. Growing numbers of targeted therapies have shown to be effective against specific cancers. Several studies have reported that targeted therapies are capable of reducing brain metastases in melanoma or non small cell lung cancer (NSCLC), sometimes with a high dramatic response. These results have clearly impacted routine neuropathological practice, leading to multidisciplinary strategy management of brain metastases tissues. In accordance with the recommendations of French National Cancer Institute (INCa), the pathologist develops appropriate strategies for molecular and immunohistochemical analysis, in order to provide results as soon as possible.

The success of radiotherapy mainly depends on the total administered dose. This dose must be homogenously delivered onto the tumor and must preserve the surrounding healthy tissue. However, several patients are hypersensitive to ionizing radiations and may develop important radiation-induced early and late side effects. The prediction of these side effects remains currently impossible, involving to limit the given dose with the risk to decrease the therapeutic benefit for patients. Therefore, one of the major challenges in radiobiology is to accurately predict tumour radioresistance and to determine normal tissue radiosensitivity to tailor treatment. Several studies have been carried out and different predictive assays have been described in this field. However, none of them showed significant results for clinical use. For several years, many technological advances in proteomic fields have been performed in order to identify new biomarkers. After a brief description of the main characteristics of tumor radioresistance and normal tissue radiosensitivity, we will develop in this review the different approaches proposed so far to identify predictive tools of radiotherapy outcome. We will then analyze in detail how proteomic studies can improve the understanding of mechanisms associated with radiosensitivity of healthy tissue and radioresistance of tumor cells and how they could highlight new predictive biomarkers in radiobiology.

Two major pathways are described in bladder carcinogenesis: one for invasive or high grade tumors characterized by alteration of the p53 tumor suppressor gene and the other for non-invasive tumors or low grade involving mutations FGFR3. The objective of our study was to validate the research in the urine of mutations in these two genes in patients with a bladder tumor.

The natural history of ductal carcinoma in situ (DCIS) is not fully elucidated, but it is recognized that DCIS is the true precursor of invasive carcinoma. Studies could show that DCIS is as heterogeneous as invasive ductal carcinoma, yet, they were unable to predict which DCIS will progress to invasion. Several biomarkers were also demonstrated to have a certain prognostic value. However, except for estrogen receptors and HER2, biomarkers are not yet widely used in clinical practice since their predictive value has not proven to be better than the grade and the classical classifying systems of DCIS. Identifying biomarkers for risk of invasiveness in DCIS could be of great value to help high risk patients through the management of their disease and to avoid overtreatment in low risk patients.