Cancer immunotherapy biomarkers and CHD1/MAP3K7 deletion in predicting immunotherapy response New insights into dual-gene deletion, tumor response to immunotherapy, and emerging immunotherapy success predictors Understand how CHD1 and MAP3K7 co-deletion could guide personalized cancer treatment and precision oncology decisions

What You'll Learn:

• How CHD1 and MAP3K7 co-deletion functions as a potential cancer immunotherapy biomarker to predict which patients may benefit most from treatment
• Why CHD1+MAP3K7 co-deletion appears in roughly 8% of primary and 15% of metastatic prostate tumors, and how that prevalence shapes clinical and research priorities
• What preclinical mouse data reveal about a 5-fold increase in CD8+ T-cell infiltration and a 6-fold rise in STING pathway transcripts in dual-deleted tumors
• How a Johns Hopkins pembrolizumab cohort (n=57) showed a 33% objective response rate in dual-deleted tumors versus 7% in non-deleted tumors, and why this signal still requires independent validation
• Practical ways these findings could inform biomarker development, patient stratification, and immunotherapy trial design in prostate cancer and other solid tumors
• How CHD1/MAP3K7 deletion research integrates with existing biomarkers for cancer treatment, including PD-L1, MSI, and TMB, in predicting immunotherapy response
• Key methodological and translational challenges that must be addressed before CHD1/MAP3K7 co-deletion can be used as a routine immunotherapy success predictor in the clinic