To evaluate whether adjusted computed tomography (CT) scan image-based radiomics combined with immune genomic expression can achieve accurate stratification of cancer recurrence and identify potential therapeutic targets in stage III colorectal cancer (CRC), this cohort study enrolled 71 patients with postoperative stage III CRC. Based on preoperative CT scans, radiomic features were extracted and selected to build pixel image data using covariate-adjusted tensor classification in the high-dimension (CATCH) model. The differentially expressed RNA genes, as radiomic covariates, were identified by cancer recurrence. Predictive models were built using the pixel image and immune genomic expression factors, and the area under the curve (AUC) and F1 score were used to evaluate their performance. Significantly adjusted radiomic features were selected to predict recurrence. The association between the significantly adjusted radiomic features and immune gene expression was also investigated. Overall, 1037 radiomic features were converted into 33 × 32-pixel image data. Thirty differentially expressed genes were identified. We performed 100 iterations of 3-fold cross-validation to evaluate the performance of the CATCH model, which showed a high sensitivity of 0.66 and an F1 score of 0.69. The area under the curve (AUC) was 0.56. Overall, ten adjusted radiomic features were significantly associated with cancer recurrence in the CATCH model. All of these methods are texture-associated radiomics. Compared with non-adjusted radiomics, 7 out of 10 adjusted radiomic features influenced recurrence-free survival. The adjusted radiomic features were positively associated with PECAM1, PRDM1, AIF1, IL10, ISG20, and TLR8 expression. We provide individualized cancer therapeutic strategies based on adjusted radiomic features in recurrent stage III CRC. Adjusted CT scan image-based radiomics with immune genomic expression covariates using the CATCH model can efficiently predict cancer recurrence. The correlation between adjusted radiomic features and immune genomic expression can provide biological relevance and individualized therapeutic targets.

Lynch syndrome is caused by a germline mutation in mismatch repair (MMR) genes, leading to the loss of expression of MMR heterodimers, either MLH1/PMS2 or MSH2/MSH6, or isolated loss of PMS2 or MSH6. Concurrent loss of both heterodimers is uncommon, and patients carrying pathogenic variants affecting different MMR genes are rare, leading to the lack of cancer screening recommendation for these patients. Case presentation: Here, we reported a female with a family history of Lynch syndrome with MLH1 c.676C > T mutation. She developed endometrial cancer at 37 years old, with loss of MLH1/PMS2 expression. Immunohistochemical staining on tumor samples incidentally detected the additional loss of MSH6 expression. Whole exome sequencing on genomic DNA from peripheral blood revealed MSH6 c.2731C > T mutation, which was confirmed to be inherited from her mother, who had an early-onset ascending colon cancer without cancer family history. This is a rare case of the Lynch syndrome harboring germline mutations simultaneously in two different MMR genes inherited from two families with Lynch syndrome. The diagnosis of endometrial cancer at the age less than 40 years is uncommon for Lynch syndrome-related endometrial cancer. This suggests an earlier cancer screening for patients carrying two MMR mutations.