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Unraveling MSI-H/dMMR Cancers: Biology and Treatment Advances
- Deficiency in DNA mismatch repair (dMMR) leads to microsatellite instability-high (MSI-H) status, impacting cancer development and treatment outcomes.
- Endometrial and colorectal malignancies exhibit prevalent MSI-H/dMMR phenotypes, influencing tumor biology and therapeutic response to immune-checkpoint inhibitors (ICIs).
- Hereditary syndromes like Lynch syndrome contribute to MSI-H/dMMR cancers, necessitating personalized treatment and genetic counseling.
- MSI-H/dMMR tumors demonstrate enhanced immunogenicity, making them susceptible to ICIs and paving the way for novel immunotherapies.
- Histology-agnostic efficacy of ICIs in MSI-H/dMMR cancers highlights the potential of precision oncology in targeting molecular vulnerabilities.
- Molecular profiling and histotype-specific contexts play crucial roles in devising treatment regimens for MSI-H/dMMR tumors.
- Impaired DNA repair mechanisms in MSI-H/dMMR cancers lead to microsatellite instability, detected through diagnostic assays.
- MSI-H/dMMR status serves as a predictive biomarker for ICI responsiveness, guiding therapeutic decision-making in colorectal, endometrial, and other cancers.
- Therapeutic approaches for MSI-H/dMMR tumors include immune-checkpoint inhibitors and exploration of combinatorial regimens to optimize patient outcomes.
- Challenges in immunotherapy response variation among MSI-H/dMMR tumors prompt investigations into resistance mechanisms and alternative therapeutic targets.
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