Articles related to SOLID TUMORS

Targeted therapy gene mutations may: (a) encode a protein that can be targeted in a manner distinct from the WT protein; (b) cause abnormal activation of a protein that is druggable but for which mutant-specific targeting has not been achieved; or (c) create novel molecular dependencies that are druggable. This article describe key examples of genetic drivers and associated modes of druggability, considers the clinical and research challenges in the field, and discusses new approaches to maximizing therapeutic benefit of targeted therapies.

The authors analyzed the immune cell infiltrates of head and neck squamous cell carcinoma and colorectal cancers and identified a subset of CD4 Th cells that appear to be directly involved in the anti-tumor immune response.

Phase 1 trial using an autologous CAR-T cell therapy that targets the oncofetal antigen Claudin-6 (CLDN6) — and CARVac (BioNTech), a CLDN6-encoding mRNA-based vaccine designed to enhance CAR T-cell activity. Data show encouraging clinical activity for an investigational CAR T-cell therapy alone or in combination with an amplifying mRNA vaccine for patients with solid tumors.

Results of a MEDLINE review highlight numerous studies across different cancer types indicating that ctDNA-based MRD detection predicts recurrence with high sensitivity and specificity, and with lead times that precede standard imaging by up to 12 months.

The KRASG12C mutation was more prevalent in females and older patients and appeared to be associated with smoking status. KRASG12C tumors exhibited a distinct co-mutation profile and were associated with tumor mutational burden-high status.

Adagrasib 600 mg twice a day was well tolerated and exhibited antitumor activity in patients with advanced solid tumors harboring the KRASG12C mutation.