Articles related to 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.

Sixty patients with EGFR-amplified gastroesophageal adenocarcinoma(GEA) received EGFRi, including 31 of 60 patients (52%) with concurrent chemotherapy. Across treatment lines, patients achieved a 43% objective response rate with a median PFS of 4.6 months. Typical OS with first-line initiation of non-EGFRi therapy in patients with EGFR-amplified GEA is 11.2 months, as determined by analysis of a deidentified clinicogenomic database. Despite this benefit, analysis of that database for January 2011 through December 2020 suggests that only 5% of patients with EGFR-amplified GEA received EGFRi.

The interpretation of genomic sequencing data is complex. Not all tumors have alterations within therapeutically targetable or actionable genes, and not all alterations detected within a therapeutically actionable gene may confer sensitivity to genomic biomarker–linked therapies. ASCO’s expert panel provides a provisional opinion, giving guidance on using genomic sequencing to inform treatment selection for patients with metastatic or advanced solid tumors.

PIK3CA is the most mutated oncogene across many of the common solid tumor types. Consequently, targeting PIK3CA has been of major clinical interest. Initial efforts at have not been promising, however. The limiting factors have primarily been lack of isoform specificity of inhibitors and dose-limiting toxicities. This study evaluates copanlisib, an α and δ isoform–specific phosphoinositide 3-kinase (PI3K) inhibitor, in patients with PIK3CA mutations.