Case report: Immune response characterization of a pseudoprogression in a PD-L1-negative, TMB-low, co-mutated metastatic NSCLC.

A patient with a PD-L1-negative, TMB-low, co-mutated metastatic non-small cell lung cancer (NSCLC) experienced a multisite radiological progression at 3 months after initiation of chemoimmunotherapy as first-line treatment for metastatic disease. After the radiological progression, while she was not undergoing treatment, the patient had spontaneous lesions shrinkage and further achieved a prolonged complete response. Genomic and transcriptomic data collected at baseline and at the time of pseudoprogression allowed us to biologically characterize this rare response pattern.

Using immunogenic cell death to improve anticancer efficacy of immune checkpoint inhibitors: From basic science to clinical application.

Even though the discovery of immune checkpoint inhibitors (ICIs) has revolutionized cancer treatment, a high proportion of patients do not respond. Moreover, some types of cancers are refractory to these treatments. Thus, the need to find predictive biomarkers of efficacy and to evaluate the association with other treatments, such as chemotherapy or radiotherapy, appears to be essential.

Associating Immunotherapy and Targeted Therapies: Facts and Hopes.

Immune-checkpoint inhibitors (ICI), particularly inhibitors of the PD-1/PD-L1 (Programmed Death 1/Programmed Death-Ligand 1) axis, have modified the management of many types of cancer over the last 10 years. However, both intrinsic and acquired resistance are major clinical issues with these therapies, and only a few patients are cured by ICI monotherapy. To overcome resistance, the concept of combining ICIs with other therapies is emerging and supported by many preclinical trials.

Tumor Immunogenic Cell Death as a Mediator of Intratumor CD8 T-Cell Recruitment.

The success of anticancer treatments relies on a long-term response which can be mediated by the immune system. Thus, the concept of immunogenic cell death (ICD) describes the capacity of dying cancer cells, under chemotherapy or physical stress, to express or release danger-associated molecular patterns (DAMPs). These DAMPs are essential to activate dendritic cells (DCs) and to stimulate an antigen presentation to CD8 cytotoxic cells.

Downregulation of Elovl5 promotes breast cancer metastasis through a lipid-droplet accumulation-mediated induction of TGF-β receptors.

Metastatic breast cancer cannot be cured, and alteration of fatty acid metabolism contributes to tumor progression and metastasis. Here, we were interested in the elongation of very long-chain fatty acids protein 5 (Elovl5) in breast cancer. We observed that breast cancer tumors had a lower expression of Elovl5 than normal breast tissues.