Risk Of Gastrointestinal Cancer Research Articles

Association Between Type 1 Diabetes Mellitus and Incident Gastrointestinal Cancer in Korean Population: A Nationwide Retrospective Cohort Study.

The age-standardised incidence ratio of gastrointestinal cancers in type 1 diabetes (T1D) patients has been reported to be higher than that in the general population. After adjusting for shared risk factors, we aimed to explore the association between T1D and gastrointestinal cancer and examine how this relationship varies by age and sex. This retrospective cohort study included 268,179 participants from the Korean National Health Insurance Service-National Sample Cohort. The primary outcome is the incident of gastrointestinal cancers, based on diagnostic codes. Multivariate Cox regression analyses were performed to assess the association between T1D and gastrointestinal cancers. Of the 268,179 participants, 2681 had T1D at baseline and were followed for 12.98 (± 2.92) years. Compared with non-T1D, T1D patients had a significantly increased risk of all gastrointestinal cancer (adjusted hazard ratio [aHR]: 1.403, 95% confidence interval [CI]: 1.253-1.573). T1D patients increased risks of oesophageal cancer (aHR: 1.864, 95% CI: 1.038-3.349), gastric cancer (aHR: 1.313, 95% CI: 1.066-1.616), colon cancer (aHR: 1.365, 95% CI: 1.110-1.678), liver cancer (aHR: 1.388, 95% CI: 1.115-1.727), and pancreatic cancer (aHR: 1.716, 95% CI: 1.182-2.492). The consistency of this association persisted among both male and female, with its strength increasing with older age. The risk of gastrointestinal cancer was significantly increased in T1D patients. Older male T1D patients exhibit a higher risk, suggesting the need for targeted attention in their care.

Effect of smoking on the risk of gastrointestinal cancer after cholecystectomy: A national population-based cohort study.

The role of smoking in the incidence of colorectal cancer (CRC) or gastric cancer (GC) in populations undergoing cholecystectomy has not been investigated. To evaluate the effect of smoking on CRC or GC development in cholecystectomy patients. A total of 174874 patients who underwent cholecystectomy between January 1, 2010 and December 31, 2017 were identified using the Korean National Health Insurance Service claims database. These patients were matched 1:1 with members of a healthy population according to age and sex. CRC or GC risk after cholecystectomy and the association between smoking and CRC or GC risk in cholecystectomy patients were evaluated using adjusted hazard ratios (HRs) and 95%CIs. The risks of CRC (adjusted HR: 1.15; 95%CI: 1.06-1.25; P = 0.0013) and GC (adjusted HR: 1.11; 95%CI: 1.01-1.22; P = 0.0027) were significantly higher in cholecystectomy patients. In the population who underwent cholecystectomy, both CRC and GC risk were higher in those who had smoked compared to those who had never smoked. For both cancers, the risk tended to increase in the order of non-smokers, ex-smokers, and current smokers. In addition, a positive correlation was observed between the amount of smoking and the risks of both CRC and GC. Careful follow-up and screening should be performed, focusing on the increased risk of gastrointestinal cancer in the cholecystectomy group, particularly considering the individual smoking habits.

Metabolic dysfunction‐associated steatotic liver disease and MetALD increases the risk of liver cancer and gastrointestinal cancer: A nationwide cohort study

SummaryBackgroundThe new nomenclature of metabolic dysfunction‐associated steatotic liver disease (MASLD) substituting nonalcoholic fatty liver disease was proposed along with a new category of MASLD with increased alcohol intake (MetALD).AimsWe aimed to explore the cancer risk by MASLD and MetALD.MethodsThis nationwide cohort study included 3,596,709 participants who underwent a health check‐up in 2011 in South Korea. Steatotic liver disease (SLD) was defined as a fatty liver index ≥30. Participants were categorized into four exclusive groups: MASLD, MetALD, other combination aetiology and no SLD. The subdistribution hazard ratio (SHR) was calculated using the Fine–Gray model after adjusting other variables.ResultsDuring the 33.9 million person‐years of follow‐up, 285,845 participants (7.9%) developed cancers. Compared with no SLD, MASLD, MetALD and other combination aetiology had an increased risk of all cancer. Liver cancer risk escalated from no SLD to MASLD (SHR, 1.16; 95% CI, 1.12–1.21), MetALD (SHR, 2.06; 95% CI, 1.92–2.20) and other combination aetiology (SHR, 8.16; 95% CI, 7.69–8.67). Gastrointestinal cancers including oesophagus, stomach, colorectal, biliary and pancreas cancers increased in MASLD (SHR, 1.13; 95% CI, 1.11–1.15), MetALD (SHR, 1.17; 95% CI, 1.14–1.21) and other combination aetiology (SHR, 1.09; 95% CI, 1.05–1.13). A modest increase in lung cancer and hormone‐sensitive cancer was observed with MASLD.ConclusionsThis study showed that MASLD and MetALD are associated with an increased risk of cancer, particularly liver and gastrointestinal cancers. The findings build new evidence for the clinical outcomes of MetALD while highlighting the importance of managing alcohol intake properly in MASLD and MetALD.

Regular whole blood donation and gastrointestinal, breast, colorectal and haematological cancer risk among blood donors in Australia

AbstractBackground and ObjectivesSeveral studies have suggested that blood donors have lower risk of gastrointestinal and breast cancers, whereas some have indicated an increased risk of haematological cancers. We examined these associations by appropriately adjusting the ‘healthy donor effect’ (HDE).Materials and MethodsWe examined the risk of gastrointestinal/colorectal, breast and haematological cancers in regular high‐frequency whole blood (WB) donors using the Sax Institute's 45 and Up Study data linked with blood donation and other health‐related data. We calculated 5‐year cancer risks, risk differences and risk ratios. To mitigate HDE, we used 5‐year qualification period to select the exposure groups, and applied statistical adjustments using inverse probability weighting, along with other advanced doubly robust g‐methods.ResultsWe identified 2867 (42.4%) as regular high‐frequency and 3888 (57.6%) as low‐frequency donors. The inverse probability weighted 5‐year risk difference between high and low‐frequency donors for gastrointestinal/colorectal cancer was 0.2% (95% CI, −0.1% to 0.5%) with a risk ratio of 1.25 (0.83–1.68). For breast cancer, the risk difference was −0.2% (−0.9% to 0.4%), with a risk ratio of 0.87 (0.48–1.26). Regarding haematological cancers, the risk difference was 0.0% (−0.3% to 0.5%) with a risk ratio of 0.97 (0.55–1.40). Our doubly robust estimators targeted minimum loss‐based estimator (TMLE) and sequentially doubly robust (SDR) estimator, yielded similar results, but none of the findings were statistically significant.ConclusionAfter applying methods to mitigate the HDE, we did not find any statistically significant differences in the risk of gastrointestinal/colorectal, breast and haematological cancers between regular high‐frequency and low‐frequency WB donors.

CYP2D6, CYP2E1 Gene Polymorphisms and Gastrointestinal Cancer Risk in Rural Maharashtra: A Hospital Based Case-Control Study.

Cytochrome P450 (CYP) is a family phase I metabolizing enzymes important in xenobiotics metabolism. Genetic polymorphisms of CYPs have been comprehensively studied for their association with a range of diseases including cancer risk. In this study we assessed single nucleotide polymorphism (SNP) CYP2D6 and CYP2E1 genes and their role in gastrointestinal (GI) cancer susceptibility in the rural population of Maharashtra. Genotyping of CYP2D6*4, CYP2E1*5B, CYP2E1*6, CYP2E1*7B genes among 200 GI cancer cases and equal number of controls was studied by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The Odds ratio (OR) with 95% confidence interval and p-value were evaluated to get the level of association of polymorphisms with risk of GI cancer, where p ≤0.005 was considered as statistically significant. After the analysis of CYP2D6 and CYP2E1 gene polymorphisms, we noticed that CYP2D6*4 (rs3892097) with heterozygous genotype (G/C) showed negative association with GI cancer risk (OR=0.43, 95% CI: 0.25-0.74; p=0.002) and CYP2E1*6 (rs6413432) variant genotype showed positive association (OR=2.85, 95% CI: 1.40-5.81; p=0.003) showed positive association with GI cancer risk in studied population. The findings obtained from this study concluded that the polymorphic CYP2D6 was negatively associated; however CYP2E1*6 polymorphism was significantly associated with GI cancer risk in studied population.

O72 ASSOCIATION BETWEEN CUMULATIVE BLOOD PRESSURE AND RISK OF GASTEROINTESTINAL CANCER

Objective: We aimed to examine the association between cumulative blood pressure (cumBP) and risk of gastrointestinal cancer. Methods: The Kailuan study is a prospective cohort study based on community. CumBP (mmHg year) was calculated as follows: cumBP = [(BP1 + BP2)/2 time1-2] + [(BP2 + BP3)/2 time2-3]. All participants were into four groups according to the quartiles of cumBP. The association between quartiles of cumBP or duration of hypertension and gastrointestinal cancer was assessed by the Cox proportional hazards models (hazard ratios [HRs], 95%confidence intervals [CI]). Results: During the median follow-up time of 11 years, a total of 624 (0.95%) participants gastrointestinal cancer occurred among 65,734 participants. The Kaplan-Meier curves showed that higher quartiles on cumulative systolic blood pressure (cumSBP), cumulative diastolic blood pressure (cumDBP) and cumulative pulse pressure (cumPP) or duration of hypertension are strongly associated with an increased risk of gastrointestinal cancer. After adjusting for covariables, compared with the lowest quartile of cumSBP, cumDBP and cumPP, the HRs (95%CI) of gastrointestinal cancer in highest quartiles were 1.96 (1.44-2.67), 1.29 (0.98-1.71), and 2.18 (1.62-2.92), respectively. Furthermore, compared to those with hypertension unexposed, participants with a 6 years exposure duration of hypertension had 1.37-fold higher risk of gastrointestinal cancer. Conclusions: The higher exposure of cumSBP, cumPP and duration of hypertension are associated with an increased risk of gastrointestinal cancer. Striving to control long-term SBP, PP and hypertension across the life course, and avoiding to develop hypertension by keeping good pathways such as health lifestyles could be of enormous benefit for gastrointestinal cancer risk reduction.

Pediatric Cancer Screening in Hereditary Gastrointestinal Cancer Risk Syndromes: An Update from the AACR Childhood Cancer Predisposition Working Group.

Gastrointestinal (GI) polyposis and cancer in pediatric patients is frequently due to an underlying hereditary cancer risk syndrome requiring ongoing cancer screening. Identification of at-risk patients through family history, clinical features of a syndrome, or symptom onset ensures appropriate cancer risk assessment and management in childhood and beyond. In this 2024 perspective, we outline updates to the hereditary GI cancer screening guidelines first published by the American Association of Cancer Research Pediatric Cancer Predisposition Workshop in 2017. These guidelines consider existing recommendations by pediatric and adult gastroenterology consortia to ensure alignment with gastroenterology practices in managing polyposis conditions. We specifically address the recommendations for pediatric screening in familial adenomatous polyposis, Peutz-Jeghers syndrome, and juvenile polyposis syndrome. Further, we emphasize the importance of multidisciplinary care and partnership with gastroenterology, as it is crucial in management of children and families with these conditions.

Food biodiversity and gastrointestinal cancer risk in nine European countries: Analysis within a prospective cohort study

BackgroundFood biodiversity in human diets has potential co-benefits for both public health and sustainable food systems. However, current evidence on the potential relationship between food biodiversity and cancer risk, and particularly gastrointestinal cancers typically related to diet, remains limited. This study evaluated how dietary species richness (DSR) was associated with gastrointestinal cancer risk in a pan-European population. MethodsAssociations between DSR and subsequent gastrointestinal cancer risk were examined among 450,111 adults enrolled in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC, initiated in 1992), free of cancer at baseline. Usual dietary intakes were assessed at recruitment with country-specific dietary questionnaires. DSR of an individual’s yearly diet was calculated based on the absolute number of unique biological species in each food and drink item. Associations between DSR and cancer risk were assessed by multivariable Cox proportional hazards regression models. FindingsDuring a median follow-up time of 14.1 years (SD=3.9), 10,705 participants were diagnosed with gastrointestinal cancer. Hazard ratios (HRs) and 95 % confidence intervals (CIs) comparing overall gastrointestinal cancer risk in the highest versus lowest quintiles of DSR indicated inverse associations in multivariable-adjusted models [HR (95 % CI): 0.77 (0.69–0.87); P-value < 0·0001] (Table 2). Specifically, inverse associations were observed between DSR and oesophageal squamous cell carcinoma, proximal colon, colorectal, and liver cancer risk (p-trend<0.05 for all cancer types). InterpretationGreater food biodiversity in the diet may lower the risk of certain gastrointestinal cancers. Further research is needed to replicate these novel findings and to understand potential mechanisms.

Peutz-Jeghers syndrome: A case series

IntroductionPeutz-Jeghers syndrome (PJS) is a rare hereditary disorder characterized by gastrointestinal hamartomatous polyps, due to mutation of the STK11/LKB1 gene located on chromosome 19p. The polyps are most commonly found in the small bowel followed by colon. Case presentationOur case series includes 4 patients, three being male and one female. Each of them either presented with abdominal pain and other associated symptoms. Oral cavity and lip melanin pigmentation were common. CT abdomen revealed multiple large jejunal, ileal, gastric and colon polyps. Cancer was found in one patient. Different surgical approaches were adopted. All recovered well. DiscussionPJS is an autosomal dominant disorder with an estimated incidence of 1:50,000 to 1:200,000 cases with a significant family history. Mostly found in small bowel followed by colon, it can also occur in a rare organ like gall bladder as evident in our case. PJS carries a substantial risk for gastrointestinal cancer. The treatment modality depends on the site of polyp, mode of presentation and availability of the expertise. ConclusionPJS is a common disease in our part which is usually observed in teen age groups male. They have a varied presentation, from intestinal obstruction (due to intussusception) to GI bleeding. Colonic malignancy at young age may be the first presentation of the disease. Observation of melanin pigmentations on lips helps diagnose the disease; and one should always look at this findings in a young patient with pain abdomen or in intestinal obstruction to confirm/exclude the disease.

Difference in Gastrointestinal Cancer Risk and Mortality by Dietary Pattern Analysis: A Systematic Review and Meta-Analysis.

Several studies have demonstrated that dietary patterns identified by a posteriori and hybrid methods are associated with gastrointestinal (GI) cancer risk and mortality. These studies applied different methods for analyzing dietary data and reported inconsistent findings. This systematic review and meta-analysis were aimed to determine the association between dietary patterns, derived using principal component analysis (PCA) and reduced rank regression (RRR), and GI cancer risk and GI cancer-caused mortality. Articles published up to June 2023 in English were eligible for inclusion. The Medline, SCOPUS, Cochrane Library, CINHAL, PsycINFO, ProQuest, and Web of Sciences databases were used to identify prospective studies. The Preferred Reporting Item for Systematic Review and Meta-analysis Protocol 2020 was used to report results. A total of 28 studies were eligible for inclusion. Varied approaches to deriving dietary patterns were used, including PCA (n = 22), RRR (n = 2), combined PCA and RRR (n = 1), cluster analysis (CA; n = 2) and combined PCA and CA (n = 1). Two dietary patterns, "healthy" and "unhealthy," were derived using PCA and RRR. The healthy dietary pattern was characterized by a higher intake of fruits, whole grains, legumes, vegetables, milk, and other dairy products, whereas the unhealthy dietary pattern was characterized by a higher intake of red and processed meat, alcohol, and both refined and sugar-sweetened beverages. The findings indicated that the PCA-derived healthy dietary pattern was associated with an 8% reduced risk (relative risk [RR], 0.92; 95% CI, 0.87-0.98), and the unhealthy dietary pattern was associated with a 14% increased risk (RR, 1.14; 95% CI, 1.07-1.22) of GI cancers. Similarly, the RRR-derived healthy dietary pattern (RR, 0.83; 95% CI, 0.61-1.12) may be associated with reduced risk of GI cancers. In contrast, the RRR-derived unhealthy dietary pattern (RR, 0.93; 95% CI, 0.57-1.52) had no association with a reduced risk of GI cancers. Similarly, evidence suggested that PCA-derived healthy dietary patterns may reduce the risk of death from GI cancers, whereas PCA-derived unhealthy dietary patterns may increase the risk. Findings from prospective studies on the association of PCA-derived dietary patterns and the risk of GI cancers support the evidence of healthy and unhealthy dietary patterns as either protective or risk-increasing factors for GI cancers and for survivorship, respectively. The findings also suggest that the RRR-derived healthy dietary pattern reduces the risk of GI cancers (albeit with low precision), but no association was found for the RRR-derived unhealthy dietary pattern. Prospective studies are required to further clarify disparities in the association between PCA- and RRR-derived dietary patterns and the risk of GI cancers. Systematic review registration: PROSPERO registration no. CRD42022321644.

Improving Insights Into Ultra-processed Food Consumption and Gastrointestinal Cancer Risk.

Improving Insights Into Ultra-processed Food Consumption and Gastrointestinal Cancer Risk.

Two-sample Mendelian randomization analysis of the relationship between periodontitis and risk of upper gastrointestinal cancers.

The aim of the present study is to explore the possible association between periodontitis and upper gastrointestinal (UGI) cancers, including esophageal and gastric cancers, utilizing the Mendelian randomization method. In this research, we utilized the Mendelian randomization method to examine the causal association between periodontitis and UGI cancers. Genome-wide association studies data for periodontitis were obtained from the Gene-Lifestyle Interactions in Dental Endpoints consortium, while UGI cancers' data were accessed from FinnGen's Biobank. After rigorously screening instrumental variables for periodontitis, we analyzed them with UGI cancers primarily using the inverse variance weighted. Finally, to identify outliers, the results were subjected to a leave-one-out sensitivity analysis. Inverse variance weighted (fixed effect) results revealed that periodontitis is a risk factor for gastric cancer (OR = 1.7735, 95% CI: 1.1576 to 2.7170, P = 0.0085). As for esophageal cancer, no statistically significant correlation was observed. Furthermore, no outliers were detected in any of the results. Our two-sample Mendelian randomization study obviously demonstrates a significant positive association between periodontitis and gastric cancer, while no statistically significant correlation was found for esophageal cancer.

Interactive Association of XRCC1, XRCC2, XRCC3, and TP53 Gene Polymorphisms With Gastrointestinal Cancer Risk: Insights From a Hospital-Based Case-Control Study.

Gastrointestinal (GI) cancer presents a significant worldwide health burden, influenced by a combination of genetic and environmental factors. This study endeavors to explore the combined effects of the XRCC1, XRCC2, XRCC3, and TP53 genes that contribute to the heightened risk of GI cancer, shedding light on their combined influence on cancer susceptibility. A total of 200 histologically confirmed cases of GI cancerand an equal number of controlswere selected to examine genetic polymorphisms within the XRCC1, XRCC2, XRCC3, and TP53 genes using the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP). Odds ratios (OR) with 95% confidence intervals (CI) were calculated to assess the association of these polymorphisms with GI cancer susceptibility, with statistical significance (p ≤ 0.05). Logistic regression analysis confirmed strong evidence of synergistic interactions among specific variant genotypes. Notably, combinations such as heterozygous Arg/Ser+Ser/Ser genotype of TP53 Arg249Ser polymorphism with Arg/Trp+Trp/Trp genotype of XRCC1 Arg194Trp polymorphism (OR=2.64; 95% CI: 1.35-5.18; p=0.004),Arg/Gln+Gln/Gln genotype of XRCC1 at codon 399 (OR=5.04; 95% CI: 2.81-9.05; p=0.0001), Arg/His and His/His genotypes of XRCC2 Arg188His (OR=2.16; 95% CI: 1.06-4.39; p<0.032), and Thr/Met+Met/Met genotype of XRCC3 Thr242Met (OR=3.48; 95% CI: 1.79-6.77; p=0.0002) showed significant associations with GI cancer risk in the study population. The findings indicate a notable association between the combined effect of heterozygous variant genotypes of TP53 and variant genotypes of XRCC1, XRCC2, and XRCC3 on GI cancer risk. However, further research with a larger sample size and broad single nucleotide polymorphism (SNP) spectra is necessary to understand the interaction between genetic variations and environmental factors influencing GI cancer susceptibility.

Inflammatory Bowel Disease in Cytoreductive Surgery and Heated Intraperitoneal Chemotherapy.

Inflammatory bowel diseases (IBDs) pose an increased risk of gastrointestinal cancer with especially worse prognosis. Cytoreductive surgery and heated intraperitoneal chemotherapy (CRS/HIPEC) improves outcomes in selected patients with colorectal peritoneal metastases. Little published data describes the outcomes of CRS/HIPEC in IBD patients. We performed a retrospective review of a prospectively maintained CRS/HIPEC database. Outcomes in patients with and without IBD were compared for short-term outcomes such as hospital/intensive care unit stay, blood loss/transfusions, complications, and reoperations. We also examined oncological outcomes including recurrence, overall (OS), and disease-free survival (DFS). We identified 232 patients that underwent CRS/HIPEC for colorectal or small bowel adenocarcinoma, of which 10 were with IBD. Patients with IBD had lower ASA (p=0.005), less hypertension (p=0.033), and 30% small bowel primary compared to none in the non-IBD cohort (p<0.001). Otherwise, demographic and perioperative characteristics were similar between the groups. The median peritoneal cancer index (PCI) was 7 and similar between the cohorts (p=0.422). Extent of organ resections and peritonectomies performed were similar. Complications occurred in 60.3% of patients (21.2% major), similar between the groups (p=0.744 and p=0.444, respectively). Reoperation rate of 27% was similar between groups (p=0.097). The median OS in the IBD cohort was 19.6 vs 53.2 months in the non-IBD cohort (p = 0.056). The median DFS in the IBD cohort was 4.9 vs 9.4 months in the non-IBD cohort (p=0.174). Cytoreductive surgery and heated intraperitoneal chemotherapy in patients with IBD has similar complication profile and trended towards poorer oncological outcomes as CRS/HIPEC in non-IBD patients.

Oral dysbiosis and risk of gastrointestinal cancers: A systematic review and meta-analysis of longitudinal studies.

Poor oral health and oral dysbiosis were found to be associated with cancers, especially of the gastrointestinal (GI)system. But the cause-and-effect relationship and the effect of the risk are not yet known due to scarcity of literature. Understanding such risk relationship can contribute to an integrated multi-disciplinary approach for GI cancer prevention. The aim of the present systematic review and meta-analysis is to assess the role of oral dysbiosis on increasing the risk of digestive system cancers. To evaluate the effect of poor oral health on increasing the risk of gastrointestinal cancers. We conducted a systematic search following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines in databases PubMed, Elsevier, Wiley's online library and Web of Science from inception to February 2023 to include recent cohort studies that assessed the association between poor oral health and the risk of cancer. We assessed bias using the New Castle Ottawa scale. We used inferential statistics to describe the effect of oral dysbiosis on gastrointestinal cancers. We performed a sub-group analysis to assess the effect of oral conditions on individual cancers. We included 10 longitudinal studies in the meta-analysis. The overall effect size of poor oral health and GI cancer risk was hazard's ratio (HR) =1.30 (95% CI: [1.14, 1.46]) (p<0.001) (I2 = 68.78). Sub-group analysis indicated that poor oral health increases the risk of esophageal cancer HR=1.61 (95% CI: [1.37, 1.85]), stomach cancer HR=1.33 (95% CI: [1.08, 1.58]), pancreatic cancer HR=1.90 (95%CI; [1.29, 2.50]) and colorectal and hepatocellular carcinoma HR=1.16 (95% CI: [1.08, 1.23]). The meta-analysis indicated that poor oral health was significantly associated with increasing the risk of GI cancers.

Bile Acid Diarrhea Is Associated With an Increased Incidence of Gastrointestinal Cancers.

Bile acid diarrhea (BAD) is an underrecognized and socially debilitating disease caused by high concentrations of bile acids in the colon. Bile acids directly and indirectly promote carcinogenesis. In this article, we investigated whether individuals with BAD have an increased risk of gastrointestinal (GI) cancers. By using the Danish health registries, adult individuals with BAD were identified by International Classification of Diseases 10th revision code K90.8 or referral to the diagnostic ⁷⁵selenium-homotaurocholic acid test followed by prescription of a bile acid sequestrant within 365 days (n = 5,245). Age- and sex-matched individuals without BAD were included for comparison (n = 52,450). We analyzed the cumulative incidence of GI cancers after BAD diagnosis and the odds ratios (ORs) of GI cancer 8 and 15 years before BAD diagnosis/matching. Cumulative incidence of GI cancer 6 years after BAD diagnosis/matching was 1.6% in the BAD group and 1.1% in controls ( P = 0.01). The ORs of total GI cancer 8 and 15 years before BAD diagnosis were 6.16 (5.08-7.48) and 5.19 (4.28-6.29), respectively. Furthermore, 47 individuals with BAD (0.9%) and 250 (0.5%) controls died of GI cancer. This nationwide cohort study indicates an association between BAD and GI cancers. We found both a higher incidence of GI cancer after BAD diagnosis compared with controls and increased OR of GI cancer before BAD diagnosis. Bearing in mind the underdiagnosis of BAD, the delay of BAD diagnosis, and the carcinogenic effect of bile acids, these findings warrant further investigations of the risk of GI cancer in individuals with BAD.

The current infection with Helicobacter pylori and association with upper gastrointestinal lesions and risk of upper gastrointestinal cancer: Insights from multicenter population-based cohort study.

The relationship between Helicobacter pylori (H. pylori) infection and upper gastrointestinal (UGI) cancers is complex. This multicenter, population-based cohort study conducted in seven areas in China aimed to assess the correlation between current H. pylori infection and the severity of UGI lesions, as well as its association with the risk of gastric cancer (GC) and esophageal cancer (EC). From 2015 to 2017, 27,085 participants (aged 40-69) completed a standardized questionnaire, and underwent a 13C-urea breath test. Then a subset underwent UGI endoscopy to assess the UGI lesion detection rates. All individuals were followed up until December 2021 to calculate the hazard ratios (HRs) for UGI cancers. H. pylori infection prevalence was 45.9%, and among endoscopy participants, 22.2% had gastric lesions, 19.2% had esophageal lesions. Higher detection rates of gastric lesions were noted in the H. pylori-positive population across all lesion severity levels. Over a median follow-up of 6.3 years, 104 EC and 179 GC cases were observed, including 103 non-cardia gastric cancer (NCGC) cases and 76 cardia gastric cancer (CGC) cases. H. pylori-infected individuals exhibited a 1.78-fold increased risk of GC (HR 1.78, 95% confidence interval [CI] 1.32-2.40) but no significant increase in EC risk (HR 1.07, 95% CI 0.73-1.57). Notably, there was a higher risk for both NCGC and CGC in H. pylori-infected individuals. This population-based cohort study provides valuable evidence supporting the association between current H. pylori infection and the risk of both NCGC and CGC. These findings contribute to the empirical basis for risk stratification and recommendations for UGI cancer screening.

Understanding Elderly Chinese Cancer Patients in a Multicultural Clinical Setting: Embracing Mortality and Addressing Misperceptions of Vulnerability.

Chinese patients face higher risks of gastrointestinal (GI) cancers and greater cancer-related deaths than Canadian-born patients. The older population encounters barriers to quality healthcare, impacting their well-being and survival. Previous studies highlighted Chinese immigrant perceptions of not requiring healthcare support. During the COVID-19 pandemic, their underutilization of healthcare services garnered attention. The present study explores the experiences of older Chinese cancer patients to improve culturally sensitive cancer care. A total of twenty interviews carried out in Cantonese and Mandarin were conducted with Chinese immigrants, aged 60 or above, diagnosed with Stage 3 or 4 GI cancer. These interviews were transcribed verbatim, translated, and subjected to qualitative descriptive analysis. Among older Chinese immigrant patients, a phenomenon termed "Premature Acceptance: Normalizing Death and Dying" was observed. This involved four key themes: 1. acceptance and letting go, 2. family first, 3. self-sufficiency, and 4. barriers to supportive care. Participants displayed an early acceptance of their own mortality, prioritizing family prosperity over their own quality of life. Older Chinese patients normalize the reality of facing death amidst cancer. They adopt a pragmatic outlook, acknowledging life-saving treatments while willingly sacrificing their own support needs to ease family burdens. Efforts to enhance health literacy require culturally sensitive programs tailored to address language barriers and differing values among this population. A strengths-based approach emphasizing family support and practical aspects of care may help build resilience and improve symptom management, thereby enhancing their engagement with healthcare services.

The Burden of Overweight and Obesity-Associated Gastrointestinal Cancers in Low and Lower-Middle-Income Countries: A Global Burden of Disease 2019 Analysis.

Obesity is associated with cancer, including gastrointestinal (GI). Data from low (LICs) and lower-middle-income countries (MICs) are limited. We utilized data from the Global Burden of Disease Study 2019 to determine the mortality from GI cancer risk of high body mass index (BMI) in these countries. Mortality rates of GI cancers from high BMI increased in LICs and lower MICs, while burdens decreased or remained stable in high and middle-income countries. The GI cancer-related burden from high BMI increased in LICs and lower MICs, necessitating a concerted effort to tackle the obesity pandemic.

VEGF-2578C/A, -460T/C Polymorphisms and Gastrointestinal Tract Cancer Risk: An Updated Meta-Analysis.

Functional polymorphisms in the vascular endothelial growth factor (VEGF) alter the susceptibility toward different gastrointestinal tract (GIT) cancers. In this study, we explored the association of VEGF-2578C/A and VEGF-460T/C polymorphisms with esophageal cancer (EC) risk. In total, 330 patients with EC and 330 controls for VEGF-2578C/A polymorphism and 316 patients with EC and 316 controls for VEGF-460T/C polymorphism were genotyped. AA genotype (p = 0.01) and A allele (p = 0.02) of VEGF-2578C/A and CC genotype (p = 0.04) and C allele (p = 0.04) of VEGF-460T/C polymorphism were significantly associated with an increased risk of EC. VEGF-2578C/A and VEGF-460T/C polymorphisms have been studied in different GIT cancers, but results are inconclusive. Therefore, we performed a meta-analysis to assess the association of these polymorphisms with the risk of GIT cancers. The PubMed, ScienceDirect, and Google Scholar databases were used to search the articles. Twenty-one studies on VEGF-2578C/A and 20 studies on VEGF-460T/C polymorphism were included in this meta-analysis. VEGF-2578C/A polymorphism was associated with the decreased risk of GIT cancer in the overall population under the overdominant model (p = 0.009). A significant association of VEGF-2578C/A polymorphism with GIT cancer risk has been observed in the middle easterners, Caucasians, and Asians under different genetic models. VEGF-460T/C polymorphism was significantly associated with an increased risk of GIT cancers in Caucasians. Stratification of the data on the basis of cancer type showed a significant association of VEGF-2578C/A polymorphism with the risk of gallbladder cancer, whereas VEGF-460T/C polymorphism was associated with the risk of hepatocellular cancer, gastric cancer, and colorectal cancer. Our meta-analysis suggested that VEGF-2578C/A and VEGF-460T/C polymorphisms were associated with GIT cancer risk.