A 2-year post-doctoral position, dedicated to deciphering the mechanisms underlying reduced immunosuppression and improved response to therapies with physical activity in pancreatic cancer, is available in the “Immunity & Cancer” team at the Cancer Research Center of Marseille in France, under the supervision of Dr. Alice Carrier. The position can start on October 1st, 2026.

The CRCM is an international cancer research center affiliated to national (Inserm, CNRS) and local (Aix-Marseille University, Paoli-Calmettes Cancer Institute) institutions, hosting 450 members in 4 Scientific Departments in the South-East of France (https://crcm-marseille.fr/). The CRCM combines excellent research and access to high education in oncology and immunology, state-of-the-art technological support and a collegial set of teams offering a fertile and outstanding environment to develop fundamental, translational or clinical projects for patient benefits. 

Pancreatic ductal adenocarcinoma (PDAC), the most frequent pancreatic cancer, has a very poor prognosis, due to the high percentage of locally advanced or metastatic disease and the limited efficacy of anti-tumor treatments, including immunotherapy. The only curative treatment is surgery associated with chemotherapy, but most resected patients relapse for as yet unknown reasons. Patients with PDAC are often cachectic and sarcopenic (low muscle mass and function), which contributes to their frailty and impairs their response to treatments. Physical activity (PA) programs are now offered to cancer patients to limit sarcopenia, and improve quality of life and therapeutic response.

Two key biological features of PDAC tumors that underly resistance to treatment are a strong metabolic reprogramming in PDAC tumors and an immunosuppressive tumor microenvironment (TME), in which cancer-associated fibroblasts (CAFs) found abundantly are central to the loss of infiltration and function of anti-tumor immune cells. It is now well known in several cancers that metabolic reprogramming concerns also immune cells, in particular T cells that become exhausted in the TME. This remains to be explored in PDAC. 

In this project, we hypothesize that PA could attenuate CAF-induced immunosuppression via metabolic remodeling, thereby improving therapeutic success and helping to prevent relapse. Specific objectives are to study in preclinical models whether and how PA could: 1) attenuate immunosuppression caused by the dialogue between CAFs and anti-tumor immune cells, 2) increase the efficacy of immunotherapy (immune checkpoint inhibitor) combined with chemotherapy, and 3) prevent relapse after a therapeutic response. The candidate will use cutting-edge single-cell analysis technologies to identify the impact of PA on TME immunosuppression. Candidates must have experience in animal experimentation using mouse cancer models, as well as in spectral flow cytometry, multiplex microscopy, and single-cell RNA-seq data analysis.