[Update of guidelines of the AFSOS, SFRO, SFH, SFNCM, SFCE, GFRP for the management of radio-induced nausea and vomiting].

Background: Radiation-induced nausea and vomiting have mutiple clinical consequences: delay or refusal of irradiation (decreased antineoplastic efficacy of irradiation), altered quality of life, dehydration, malnutrition, interruption of treatment, decompensation of comorbidities and aspiration. These guidelines aim at defining good clinical practices for management of radiation-induced nausea and vomiting (RINV).

Methods: AFSOS, SFRO, SFH, SFNEP, SFCE and GFRP applied an expert consensus methodology to propose updated guidelines.

The Interleukin-17 Family of Cytokines in Breast Cancer.

Breast cancer (BC) is the most common cancer in women worldwide and remains a major cause of mortality with an expected 137,000 death this year in Europe. Standard management of metastatic BC comprises hormonotherapy, chemotherapy, and targeted therapies. Cyclin dependent kinase (CDK) and mammalian target of rapamycin (mTOR) inhibitors have recently proved their efficiency in hormonal receptor expressing BC.

Targeting the Tumor Microenvironment: The Protumor Effects of IL-17 Related to Cancer Type.

The inflammatory process contributes to immune tolerance as well as to tumor progression and metastasis. By releasing extracellular signals, cancerous cells constantly shape their surrounding microenvironment through their interactions with infiltrating immune cells, stromal cells and components of extracellular matrix. Recently, the pro-inflammatory interleukin 17 (IL-17)-producing T helper lymphocytes, the Th17 cells, and the IL-17/IL-17 receptor (IL-17R) axis gained special attention.

IL-17E synergizes with EGF and confers in vitro resistance to EGFR-targeted therapies in TNBC cells.

Estrogen receptor-, progesterone receptor- and HER2-negative breast cancers, also known as triple-negative breast cancers (TNBCs), have poor prognoses and are refractory to current therapeutic agents, including epidermal growth factor receptor (EGFR) inhibitors. Resistance to anti-EGFR therapeutic agents is often associated with sustained kinase phosphorylation, which promotes EGFR activation and translocation to the nucleus and prevents these agents from acting on their targets. The mechanisms underlying this resistance have not been fully elucidated.