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Breast cancer (BC) is one of the most common causes of cancer in the world and the second leading cause of cancer deaths among women. Mortality is associated mainly with the development of metastases. Identification of the mechanisms involved in metastasis formation is, therefore, a major public health issue.

La relation entre syndrome métabolique (SM) et cancer de la prostate (CaP) demeure controversée et très peu d’études se sont adressées aux populations d’ascendance africaine.

Le cancer de la prostate de risque intermédiaire est désormais classé en pronostic favorable et défavorable, en fonction du score ISUP, du PSA, du toucher rectal et du pourcentage de biopsies positives. Notre objectif était d’évaluer l’apport de l’imagerie et des biopsies ciblées pour améliorer cette classification à partir de l’analyse du stade histopathologique après prostatectomie totale.

In most cases, metastatic breast cancer remains an incurable disease. A PIK3CA mutation is detected in 30-40% of all hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2-) advanced breast cancers. PIK3CA activating mutations have been linked to endocrine resistance.

It is well known that the intestine absorbs nutrients, electrolytes, and water. Chikina et al. recently demonstrated that it is also able to sense, recognize, and block the absorption of toxins through a very sophisticated interactive cellular cooperation between novel subpopulations of macrophages and epithelial cells.

Background: Clinical benefit from programmed cell death 1 receptor (PD-1) inhibitors relies on reinvigoration of endogenous antitumor immunity. Nonetheless, robust immunological markers, based on circulating immune cell subsets associated with therapeutic efficacy are yet to be validated.

Emerging data suggest that the combination of MEK inhibitors and immunotherapeutic agents may result in improved efficacy in melanoma. We evaluated whether combining MEK inhibition and immune checkpoint inhibition was more efficacious than immune checkpoint inhibition alone in patients with previously untreated BRAFV600 wild-type advanced melanoma.

Purpose: Report results of the phase Ib dose-escalation/expansion study of triplet therapy with cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor (ribociclib), mTOR inhibitor (everolimus), and endocrine therapy (exemestane).

Triple-negative breast cancer (TNBC) heterogeneity represents one of the main obstacles to precision medicine for this disease. Recent concordant transcriptomics studies have shown that TNBC could be divided into at least three subtypes with potential therapeutic implications.