MSI (Microsatellite instability)

In conclusion, quantitative GC-related histology of nrLNs can serve as a prognostic indicator for MSI-H CRC. Our findings suggest that GC-activated nrLNs may represent B cell-mediated antitumor immunity, independent of tumor-infiltrating T cells and tumor-intrinsic molecular characteristics.

Although outcomes varied depending on the PEM treatment duration and the medical cost setting after disease progression in the SoC group, PEM was suggested to be more cost-effective than SoC at the reference willingness-to-pay threshold of JPY15 million per QALY in Japan.

In the subgroup analysis, SAMD4B mean expression was the highest in the TP53 mutation group, which showed the worst OS. SAMD4B may serve as a novel prognostic biomarker for patients with EC.

We established a DRRG-based prognostic model for CRC and uncovered their links to metabolic regulation, immune infiltration, and metastasis. These findings highlight DRRGs as potential biomarkers and therapeutic targets and suggest that DR-mimicking strategies may benefit CRC management.

These genes were also found to be associated with tumor mutational burden (TMB) and microsatellite instability (MSI) scores. Our findings reveal how these genes contribute to CRC pathogenesis by modulating the immune microenvironment, providing important biomarkers and targets for the development of novel therapeutic strategies.

Among emerging therapies, the novel anti-angiogenic agent fruquintinib has recently demonstrated clinical efficacy in the treatment of mCRC. Based on the data discussed in the present narrative review, the therapeutic landscape of mCRC appears poised for significant evolution in the near future. While numerous challenges and unanswered questions remain, the emergence of innovative therapeutic combinations and agents provides a promising opportunity for improving patient outcomes in mCRC.

This review provides a comprehensive overview of the evolving therapeutic landscape of GEC. It emphasizes the growing role of precision medicine and the integration of emerging clinical data into practice.

Furthermore, FBXW7 alterations contribute to chemoresistance and anti-EGFR therapy resistance but also reveal potential therapeutic vulnerabilities. These findings underscore FBXW7's promise as a prognostic biomarker and a potential target for precision oncology strategies in colorectal cancer.

There existed a positive correlation between E2F2 expression level and Dasatinib sensitivity, negatively related to drug sensitivity of Nelarabine, XK-469, Cyclophosphamide, etc. Pazopanib, Doxorubicin, and Paclitaxel sensitivity was all positively associated with E2F5 expression. According to these analysis and validation results, E2F genes are relevant to the occurrence and progression of various cancers, which may be biomarkers for tumor diagnostics and prognosis. The discovery of new therapeutic targets can lead to reshaping TME to promote tumor-suppressive metastasis rather than tumor-friendly metastasis.

In conclusion, discordance between IHC- and NGS-based MMR/MSI detection is primarily attributable to MSH6 loss with MSH3 compensation and MLH1 promoter methylation. Recognizing these mechanisms is essential for accurate molecular subtyping and clinical decision-making in EC.

The use of prolgolimab in locally advanced dMMR/MSI CRC is associated with high rates of pCR and cCR, allowing for further exploration of organ-sparing approaches in these patients.

The observed toxicity was consistent with the known toxicity profile of immunotherapy and did not lead to discontinuation of therapy. Our case report highlights the need to test for predictive markers in patients with locoregionally advanced rectal cancer in order to identify specific subtypes of the disease that can be treated with immunotherapy with a high probability of achieving clinical complete remission, thereby avoiding potentially risky surgery.