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Prior small reports have postulated a link between gastrointestinal polyposis and childhood and young adulthood cancer (CYAC) treatment (therapy-associated polyposis; TAP), but this remains a poorly understood phenomenon. The aim of this study was to describe the phenotypic spectrum of TAP in a multi-institutional cohort. TAP cases were identified from eight high-risk cancer centers. Cases were defined as patients with ≥10 gastrointestinal polyps without known causative germline alteration or hereditary colorectal cancer predisposition syndrome who had a history of prior treatment with chemotherapy and/or radiotherapy for CYAC. A total of 34 TAP cases were included (original CYAC: 27 Hodgkin lymphoma, three neuroblastoma, one acute myeloid leukemia, one medulloblastoma, one nephroblastoma, and one non-Hodgkin lymphoma). Gastrointestinal polyposis was first detected at a median of 27 years (interquartile range, 20–33) after CYAC treatment. A total of 12 of 34 (35%) TAP cases had ≥50 colorectal polyps. A total of 32 of 34 (94%) had >1 histologic polyp type. A total of 25 of 34 (74%) had clinical features suggestive of ≥1 colorectal cancer predisposition syndrome [e.g., attenuated familial adenomatous polyposis (FAP), serrated polyposis syndrome, extracolonic manifestations of FAP, mismatch repair–deficient colorectal cancer, or hamartomatous polyposis] including 8 of 34 (24%) with features of multiple such syndromes. TAP is an apparently acquired phenomenon that should be considered in patients who develop significant polyposis without known causative germline alteration but who have had prior treatment for a CYAC. Patients with TAP have features that may mimic various hereditary colorectal cancer syndromes, suggesting multiple concurrent biologic mechanisms, and recognition of this diagnosis may have implications for cancer risk and screening.

Supplementary Tables S1 - S12. Supplementary Table S1. Prioritization of candidate FPC susceptibility genes by private heterozygous PTVs. Supplementary Table S2. FPC patients harboring a private PTVs ASXL1, DNMT3A, and TET2. Supplementary Table S3. 87 genes analyzed in-depth in FPC patients and kindreds. Supplementary Table S4. Deleterious variants in FPC patients and kindreds. Supplementary Table S5. FPC samples with more than one deleterious variant. Supplementary Table S6. Deleterious variants in BCCS samples. Supplementary Table S7. Deleterious variants in FPC kindreds and BCCS samples. Supplementary Table S8. Differences in deleterious variants between FPC kindreds with three or more affected members and BCCS samples. Supplementary Table S9. Private heterozygous PTVs present in all sequenced affected members of a kindred. Supplementary Table S10. Deleterious variants shared between affected members of an FPC kindred. Supplementary Table S11. Somatic mutations in FPC patient tumors. Supplementary Table S12. Summary of somatic mutation data for FPC patient tumors by gene.

Supplementary Table 3 shows types of surgical resection

Supplementary Table 1 shows number of TAP cases per site

Supplementary Table 2 shows individual case-level data (clinical history, genetic testing, secondary cancers)

CCR Translation for This Article from Colorectal Cancers with Microsatellite Instability Display Unique miRNA Profiles

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The role of socioeconomic status and race on cancer survivorship has been identified, however, the role of neighborhood disadvantage and race in cancer survivorship has not been well studied. This analysis aimed to evaluate the relationship between a comprehensive measure of neighborhood-level social disadvantage and cancer survivorship in the racially diverse population of metropolitan Detroit. We calculated overall and cancer-specific survival for 11,367 Non-Hispanic Black (NHB) and 29,481 Non-Hispanic White (NHW) individuals with breast, colorectal, lung, and prostate cancer using data from the Metropolitan Detroit Cancer Surveillance System. Neighborhood socioeconomic disadvantage was measured by the Area Deprivation Index (ADI) at the census block group level using data from the Census Bureau’s American Community Survey. Associations between ADI and survival were estimated using Cox proportional hazards mixed-effects models accounting for geographic grouping and adjusting for demographic, clinical, and treatment factors. Among all participants, an increase in ADI quartile was associated with increased overall mortality for all four cancer sites in multivariable models adjusting for race, age at diagnosis, stage, treatment, and Gleason score (prostate only). When stratifying by race, these associations remained among breast (NHW: Hazard Ratio (HR)=1.10, 95% Confidence Interval (CI) 1.05-1.15, p Citation Format: Natalie G. Snider, Theresa Hastert, Mrudula Nair, Madhav KC, Julie Ruterbusch, Ann Schwartz, Ed Peters, Elena Stoffel, Laura Rozek, Kristen Purrington. Evaluating racial disparities in cancer survivorship via the role of area-level socioeconomic disadvantage in metropolitan Detroit [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr A019.