Aug 2026· Cancer Epidemiology, Biomarkers and Prevention· 0 citations
Medicine
TL;DR
An elevated risk of early-onset rectal cancer was suggested in individuals with high birth weight in a nested case-control study that evaluated the association between high birth weight and eoCRC in a nested case-control study.
Abstract
Background: Early-onset colorectal cancer (eoCRC), particularly rectal cancer, is increasing. We evaluated the association between high birth weight and eoCRC in a nested case-control study. Methods: We included patients aged 15–49 years diagnosed with colorectal adenocarcinoma at Kaiser Permanente Southern California (2009–2021). Cancer-free controls were matched 10:1 on age, sex, and length of health plan membership. Record linkage with California Department of Public Health’s birth registry was performed. Conditional logistic regression was used to evaluate associations between high birth weight, measured using (1) macrosomia (birth weight >4,000grams), and (2) large for gestational age (LGA; birth weight above the 90th percentile for gestational age and sex), and overall eoCRC, colon, and rectal cancer. Two-stage model adjustments were performed: first adjusting for pre-specified potential confounders, then adjusting for potential intermediates. Results: Of 1,400 eligible cases and matched 13,608 controls, 471 eoCRC cases (mean diagnosis age: 41.1 years) and 1,931 controls with linked birth certificate were included. Adjusted odds ratio (OR) for eoCRC was 1.32 (95% CI: 0.95–1.84) for macrosomia and 1.38 (0.97–1.98) for LGA. Macrosomia and LGA were associated with a marginal, non-statistically significant elevated risk of rectal cancer [OR (95%CI): 1.69 (0.97–2.97) and 1.81 (0.96–3.41), respectively], but not colon cancer [OR (95%CI): 1.18 (0.78–1.80) and 1.20 (0.77–1.86) for macrosomia and LGA, respectively]. Conclusions: An elevated risk of early-onset rectal cancer was suggested in individuals with high birth weight. Impact: The impact of intrauterine conditions on eoCRC risk should be further evaluated.
Traditional environmental risk factors and established common genetic variants are not associated with the rising incidence of early-onset colorectal cancer, and drivers of early-onset disease might include novel environmental exposures or early-life factors beyond traditional risk assessment.
Anmol Nigam, Chidiebere Onongaya, Pravin Meshram et al.· Diseases of the Colon & Rect...· 0 citations
Current evidence on early-onset colorectal cancer epidemiology, biology, clinical presentation, screening, and treatment is summarized, and emerging directions including liquid biopsy, artificial intelligence, and microbiome-based strategies are highlighted.
Ahmed Sohaib, Ashwaq Salami, Wesal Alghwyeen et al.· Integrated Oncology Diagnost...· 0 citations
The global EOPC burden among WCBA and its links to core metabolic determinants are delineated, providing an evidence base to guide targeted interventions in this priority population and support progress toward international development goals.
Jiaxing Li, Jing Luo, Qi-Hui Hu et al.· PLoS ONE· 0 citations
Background: Early-onset colorectal cancer (EOCRC), diagnosed in adults younger than 50 years, has increased at approximately 1.5–2.0% per year in both high-income and South Asian populations. The independent and joint roles of ultra-processed food (UPF) consumption, cumulative antibiotic exposure, and systemic inflammation have not been examined in resource-limited settings.
Methods: We conducted a retrospective 1:2 matched case-control study at the Bolan Medical Complex / Sandeman Provincial Hospital, Quetta (2018–2026). Cases (n=174) were adults aged 18–49 with histologically confirmed colorectal adenocarcinoma (ICD-10 C18–C20); controls (n=348) were matched on age (±2 years), sex, race/ethnicity, BMI category, and index year. UPF intake was measured via a validated 28-item NOVA-adapted food frequency questionnaire. Antibiotic exposure was extracted from the pharmacy database. Inflammation markers (hsCRP, ESR, fecal calprotectin) were retrieved from the electronic health record. Conditional logistic regression estimated adjusted odds ratios. Mediation analysis quantified the proportion of the UPF–EOCRC association mediated by hsCRP elevation. STROBE guidelines were followed.
Results: High UPF intake (top tertile, ≥9.8 servings/day) was independently associated with 65% higher odds of EOCRC (aOR 1.65; 95% CI 1.21–2.26). Cumulative antibiotic exposure ≥3 courses was associated with aOR 1.47 (95% CI 1.09–1.99). A statistically significant multiplicative interaction was observed between high UPF and ≥3 antibiotic courses (combined aOR 2.98; interaction OR 1.89; p=0.031). Elevated hsCRP mediated 24.3% (95% CI 12.1–38.6%) of the UPF–EOCRC association. Associations were stronger for distal/rectal tumours (aOR 1.82) than proximal tumours (aOR 1.31; p-heterogeneity=0.042) and amplified in the lowest SES quartile (aOR 2.04).
Conclusions: High UPF intake and cumulative antibiotic exposure independently and synergistically increase odds of EOCRC, with a substantial proportion mediated through systemic inflammation. These findings identify actionable targets for dietary counselling, antibiotic stewardship, and risk-stratified screening in young South Asian adults.
Basit Ur Rehman, Fareed Ullah, Ahmed Shahbaz et al.· Pakistan Journal of Gastroen...· 0 citations
Background: The incidence of early-onset colorectal cancer (eoCRC), diagnosed at age <50 years, is increasing in the United States. Prior studies using national and state cancer databases have observed higher eoCRC mortality after diagnosis among non-Hispanic Black (NHB) patients. These studies, however, often did not account for insurance status, access to care, and comorbidity burden, which may contribute to the observed disparities. We examined the associations between race and ethnicity and neighborhood-level socioeconomic status [measured by the neighborhood deprivation index (NDI)] and survival among persons with eoCRC in a large integrated healthcare delivery system whose racially/ethnically diverse members have standardized access to care. Methods: We included Kaiser Permanente Southern California (KPSC) members diagnosed with eoCRC (age 15-49 years) between 2009-2020 and followed them through 12/31/2023. Patients with <12 months of prior KPSC membership, an unspecific CRC site, or other/unknown race/ethnicity were excluded. Bivariate and multivariable Cox models were used to estimate hazard ratios (HRs) for the associations between race/ethnicity and NDI and all-cause and CRC-specific mortality. Multivariable models were adjusted for age at diagnosis, sex, Charlson comorbidity score, obesity, stage at diagnosis, cancer site, and histologic subtype. Subgroup analyses were conducted by stage at diagnosis (localized vs. advanced). Results: Of 1,695 eoCRC cases included, we observed 465 deaths (among those with known cause, 417 (90.3%) were CRC-specific). The mean follow-up time was 6.8 years. In the adjusted models, NHB and non-Hispanic Asian/Pacific Islander (NH API) patients, but not Hispanic patients, had significantly higher all-cause mortality [HR=1.62, 95% CI: 1.14-2.29; HR=1.44 (1.08-1.93), respectively] compared with non-Hispanic White (NHW) patients. In the subgroup analyses, race and ethnicity were not associated with all-cause mortality among patients with localized disease. However, among patients diagnosed with advanced disease, NHB patients had a significantly higher risk of all-cause mortality compared with NHW patients (HR=1.54, 95% CI: 1.07-2.22, p=0.02). Similar findings were observed for CRC-specific mortality, overall and by cancer stage. NDI was not significantly associated with all-cause or CRC-specific mortality. Conclusions: In this insured population, NHB race and ethnicity were associated with increased risk of CRC-specific mortality among those diagnosed with advanced stage eoCRC. However, the number of NHB patients diagnosed at distant stages was small. Therefore, future research is needed to confirm these findings and better understand potential survival disparities.
T. Habeshian, Lan-Fang Xu, K. Cannavale et al.· Journal of Colon and Rectal...· 0 citations
BACKGROUND
/Aims: Few studies have explored how family history of colorectal cancer (CRC) affects CRC incidence in inflammatory bowel disease (IBD). We estimated CRC incidence rates (IRs) and IR differences, by family history of CRC, and the interaction between IBD and family history.
METHODS
Nationwide, register-based cohort study 1996-2023, including patients with IBD and matched (age, sex, parish, year) comparators from the general population. The exposure was family history, defined as the number of first-degree relatives (parent, sibling, or child) and their age at CRC diagnosis (<50 or ≥50 years).
RESULTS
During a median follow-up of 11 years, 1,882 CRC events occurred in 124,387 patients with IBD (IR 1.17[95%CI:1.12-1.23]/1,000 person-years) and 14,177 CRC events in 1,213,641 comparators (IR 0.88[95%CI:0.86-0.89]/1,000 person-years). In IBD, the greatest CRC risk increase was seen in those with ≥2 affected relatives: 2.69(95%CI:0.60-4.78) additional cases per 1,000 person-years versus no family history, while risk increase with early-onset CRC heredity was modest: 0.42(95%CI: -0.47-1.31)/1,000 person-years. The IRs were comparable between patients and matched comparators with the same family history, except among those without family history of CRC, where the CRC incidence was higher in IBD. The relative effect of family history was weaker in IBD, where the baseline CRC risk was already elevated.
CONCLUSION
On the absolute scale, family history of CRC increased CRC incidence similarly in IBD and matched comparators, with the greatest increase in individuals with multiple affected relatives. Guidelines advise special attention to patients with family history of early-onset CRC; our findings raise the question if surveillance strategies should instead prioritize patients with multiple affected relatives.
Å. H. Everhov, Kári Kristjánsson, J. Ludvigsson et al.· Gastroenterology· 0 citations
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