Risk Of Sporadic Colorectal Cancer Research Articles

High serum riboflavin is associated with the risk of sporadic colorectal cancer

BackgroundExperimental results indicate that riboflavin is involved in tumorigenesis. Data regarding the relationship between riboflavin and colorectal cancer (CRC) are limited, and findings vary between observational studies. DesignThis was a case–control retrospective study. ObjectiveThis study aimed to evaluate the associations between serum riboflavin level and sporadic CRC risk. MethodsIn total, 389 participants were enrolled in this study – including 83 CRC patients without family history and 306 healthy controls – between January 2020 and March 2021 at the Department of Colorectal Surgery and Endoscope Center at Xinhua Hospital, Shanghai Jiao Tong University School of Medicine. Age, sex, body mass index, history of polyps, disease conditions (e.g., diabetes), medications, and eight other vitamins were used as confounding factors. Adjusted smoothing spline plots, subgroup analysis, and multivariate logistic regression analysis were conducted to estimate the relative risk between serum riboflavin levels and sporadic CRC risk. After fully adjusting for the confounding factors, an increased risk of colorectal cancer was suggested for individuals with higher levels of serum riboflavin (OR = 1.08 (1.01, 1.15), p = 0.03) in a dose–response relationship. ConclusionsOur results support the hypothesis that higher levels of riboflavin may play a role in facilitating colorectal carcinogenesis. The finding of high levels of circulating riboflavin in patients with CRC warrants further investigation.

Can butyrate prevent colon cancer? The AusFAP study: A randomised, crossover clinical trial

Increased colonic butyrate from microbial fermentation of fibre may protect from colorectal cancer (CRC). Dietary butyrylated high amylose maize starch (HAMSB) delivers butyrate to the large bowel. The objective of this clinical trial (AusFAP) is to evaluate potential chemoprotective effects of HAMSB on polyposis in individuals with a genetic form of colon cancer, Familial Adenomatous Polyposis (FAP).The study is a multi-site, double blind, randomised, placebo-controlled crossover trial undertaken at major hospitals in Australia. After a baseline endoscopy participants consume either 40g/day of HAMSB or placebo (low amylose maize) starch for 26 weeks. After another endoscopic examination participants consume the alternate starch for 26 weeks. A third endoscopy at 52 weeks is followed by 26 weeks' washout and a final endoscopy at 78 weeks. Primary outcome measure is the global large bowel polyp number. Secondary measures include global polyp size counts, and number and size of polyps at two tattoo sites: one cleared of polyps at baseline, and another safely chosen with polyps left in situ during the study. Other secondary outcome measures include the effects of intervention on cellular proliferation in colonic biopsies, faecal measures including short chain fatty acid concentrations, and participants’ dietary intakes. Generalized linear mixed models analysis will be used to estimate differences in primary outcomes between intervention and placebo periods.This study represents the first clinical evaluation of the effects of increased colonic butyrate on polyp burden in FAP which, if effective, may translate to lower risk of sporadic CRC in the community.Australian New Zealand Clinical Trials Registry Number: 12612000804886.

Adequate vitamin D level associated with reduced risk of sporadic colorectal cancer.

The effect of vitamin D level pertinent to colorectal cancer incidence, progression, or mortality risk is complicated, and study findings are mixed. Therefore, we evaluated whether serum vitamin D [25-hydroxyvitamin D, 25(OH)D] is associated with the incidence of sporadic colorectal cancer (CRC). This study is a retrospective analysis of the relationship between serum 25(OH)D level and the risk of CRC. Age, sex, body mass index, history of polyp, disease conditions (i.e., diabetes), medications, and other eight vitamins were used as confounding factors. A total of 389 participants were enrolled in this study, including comprising 83 CRC patients without a family history and 306 healthy controls, between January 2020 and March 2021 at the Department of Colorectal Surgery and Endoscope Center at the Xinhua Hospital, Shanghai Jiao Tong University School of Medicine. Adjusted smoothing spline plots, subgroup analysis, and multivariate logistic regression analysis were conducted to estimate the relative risk between serum 25(OH)D and sporadic CRC risk. After fully adjusting the confounding factors, it was found that circulating 25(OH)D played a protective role in patients with CRC (OR = 0.76 [0.63, 0.92], p = 0.004) and that an adequate vitamin D level was significantly associated with a reduced CRC risk compared to vitamin D deficiency or sufficiency (OR = 0.31 [0.11, 0.9], p = 0.03). According to this study, statins did not affect the potential protective effects of vitamin D (OR = 1.02 [0.97, 1.08], p = 0.44) and may account for the inverse association between serum 25(OH)D and colorectal cancer. An adequate level of serum 25(OH)D was associated with a reduced CRC risk, especially for the elderly. The finding on the absence of protective effect of vitamin D in the statin use subgroup, suggests it may be one of the substantial contributing confounders, and warrants further investigation.

Association of CHEK2 I157T and SULT1A1 R213H genetic variants with risk of sporadic colorectal cancer in a sample of Egyptian patients

BackgroundRecent research proposed an association between functional defects involving CHEK2 I157T and SULT1A1 R213H variants and increased incidence of several types of cancer. A total of 86 unrelated colorectal cancer patients attending the Surgical Oncology Department were recruited in the study. The second group of 152 healthy age- and sex-matched volunteers were included as controls. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) was applied for genotyping. Chi-square test was applied to compare genotype and allele frequencies in the studied groups. The purpose of the present study was to evaluate the association between CHEK2 I157T and SULT1A1 R213H polymorphisms and colorectal cancer.ResultsNo significant differences in genotypes were detected between cases and controls in the present study for both CHEK2 I157T and SULT1A1 R213H polymorphisms (χ2 = 1.839; P = 0.399/χ2 = 2.831; P = 0.243), respectively. Likewise, discrepancies in allele frequency for the wild-type or mutant alleles were non-statistically significant in CHEK2 I157T and SULT1A1 R213H (χ2 = 1.231; P = 0.267/χ2 = 0.180; P = 0.671), respectively.ConclusionsResults of the current study propose that CHEK2 I157T and SULT1A1 R213H polymorphisms are not associated with CRC development in Egyptian population. Further future studies on the functional implications of these polymorphisms are strongly recommended.

Periodontal disease as a risk factor for sporadic colorectal cancer: results from COLDENT study

Colorectal cancer remains the top leading cancer worldwide. Accumulating evidence suggests periodontal pathogens are involved in colorectal carcinogenesis, indicating the need for high-quality epidemiological evidence linking periodontal disease (PD) and colorectal cancer (CRC). Thus, we conducted the first population-based case–control study that was specifically designed to investigate the association between compromised oral health and sporadic CRC. A total of 348 incident cases of colon or rectal cancer, and 310 age and sex frequency-matched controls, from the Montreal island and Laval population participated in the study. Data were collected on PD and on several CRC risk factors using validated questionnaires. A life-course approach was used to document long-term history regarding lifestyle factors. Multivariable unconditional logistic regression analysis was used to estimate the rate ratio (RR) quantifying the association between CRC and PD. Results showed that the rate of new diagnosis of CRC in persons with a positive history of PD was 1.45 times higher than in those with a negative history of PD adjusting for age, sex, BMI, education, income, diabetes, family history of CRC, regular use of non-steroidal anti-inflammatory drugs, lifetime cumulative smoking, lifetime consumption of red meats, processed meats, and alcoholic drinks, and lifetime total physical activity score (adjusted RR = 1.45; 95% CI 1.04–2.01; p = 0.026). Our results support the hypothesis of an association between PD and sporadic CRC risk.

High Serum Riboflavin Associates with Risk of Sporadic Colorectal Cancer

High Serum Riboflavin Associates with Risk of Sporadic Colorectal Cancer

Racism Is a Modifiable Risk Factor: Relationships Among Race, Ethnicity, and Colorectal Cancer Outcomes

Racism Is a Modifiable Risk Factor: Relationships Among Race, Ethnicity, and Colorectal Cancer Outcomes

Which bacterial toxins are worthy of validation as markers in colorectal cancer screening? A critical review.

Appropriate screening of early asymptomatic cases can reduce the disease burden and mortality rate of sporadic colorectal cancer (CRC) significantly. Currently, fecal occult blood testing (FOBT) is able to detect up to 80% of asymptomatic cases in the population aged 50+. Therefore, there is still a demand for new screening tests that would complement FOBT, mainly by detecting at least a part of the FOBT-negative CRC and adenoma cases, or possibly by identifying person at increased risk of sporadic CRC in order to offer them tailored follow-up. Among the potential markers studied, our knowledge has advanced at most in toxigenic gram-negative bacteria. In this review, we assess their potential critically and recommend those best suited for prospective evaluation of their true ability to increase the sensitivity of FOBT when combined during general population screening. In our opinion, colibactin and Bacteroides fragilis toxin are the best candidates, possibly complemented by the cytotoxic necrotizing factor (CNF).

The Association between Cyclin D1 (CCND1) rs9344 AA Genotype and Increased Risk of Colorectal Cancer in An Iranian Population

Background: Colorectal cancer (CRC) is a globally growing disease with a steady decrease in the age of incidence. Pathogenesis of this cancer stems from a complex interaction between environmental factors and genetic predisposition. Among genetic factors, high activity of cyclin D1gene is prominent. A polymorphism (G870A) in exon 4 of cyclin D1 is responsible for a variant transcript with longer half-life and may culminate in uncontrollable cellular growth, thereby contributing to cancer development. Method: This case-control study evaluated the frequency of CCND1 G870A polymorphism and risk of sporadic CRC in an Iranian population. The study population comprised 50 CRC patients and 50 CRC-free controls selected on the basis of colonoscopy examination. For genotyping, we performed polymerase chain reaction – restriction fragment length polymorphism analysis (PCR-RFLP). Result: AA genotype frequencies compared to GA+GG genotype frequencies between cases and controls showed that AA genotype frequency in the case group was significantly higher than the control group (AA vs. GG + GA: OR= 2.25, 95% CI: 1.13-5.54, P=0.04). Allele A frequency was 57% in patients and 46% in healthy subjects. Statistical analysis showed that the odds ratio of carriers with allele A for risk of CRC was 1.55 more than G allele carriers (OR=1.55, 95% CI: 0.856-2.828). Moreover, physical activity in cases was significantly less than controls (P=0.001). We further observed that the subjects in the case group used fewer non-steroidal antiinflammatory drugs compared to healthy controls (P=0.02). Analysis of body mass index (BMI) between cases and controls revealed that the average of BMI in cases was higher than the controls (P =0.04). Conclusion: Our results showed that individuals carrying the AA genotype ran a higher risk of developing CRC compared to GG genotype.

Rs12904 polymorphism in the 3'-untranslated region of ephrin A1 ligand and the risk of sporadic colorectal cancer in the Iranian population.

Colorectal cancer (CRC) is rated as the second cause of cancer death. Genetic determinants are considered as driving forces in the development of sporadic CRC. Single-nucleotide polymorphisms (SNPs), due to their abundance in the human genome with collectively huge effect on cellular signaling pathways, are attributed as the main genetic factor in disease susceptibility including cancers. MicroRNAs are contributing to posttranslational gene regulation. They exert their regulatory function by binding to their specific recognition sequences located at 3'-untranslated region (UTR) of mRNAs. In the present study, we have elucidated the role of rs12904, a naturally occurring SNP, in the recognition site of miR200c in the 3'UTR of ephrin A1 ligand gene, in the development of sporadic CRC in the Iranian population. A case-control study using 152 CRC patients and 160 noncancerous counterparts was conducted to determine the rs12904 genotypes using polymerase chain reaction-restriction fragment length polymorphism method. The results revealed no significant association between the rs12904 and sporadic CRC (odds ratio = 0.97, 95% confidence interval = 0.70-1.34). The frequency of genotypes and also alleles of the mentioned polymorphism were not significantly different between case and control groups (P = 0.765 and P = 0.847, respectively). The results suggest that this polymorphism probably has not a crucial role in the Iranian CRC risk and is not an important potential risk factor in molecular diagnostics of mentioned disease among the Iranian population.

The association between survivin -31G>C polymorphism and susceptibility to sporadic colorectal cancer in a Southern Chinese population.

The case-control study aimed to investigate the association between the -31G>C polymorphism in the promoter of survivin gene and the susceptibility to sporadic colorectal cancer (CRC) in a Southern Chinese population. The study was carried out on 711 healthy controls and 702 CRC cases of a Southern Chinese population. Survivin gene -31G>C genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. The association between CRC risk and -31G>C genetic polymorphism was estimated using an unconditional logistic regression model. The number of CC genotype carried in CRC patients was much higher than those of controls (P < 0.001). Compared with CC genotypes, GC, GG genotypes and -31G wild-type genotypes (i.e., GC + GG) had a significantly decreased risk of CRC (P < 0.001). In addition, survivin -31G wild-type genotypes were not associated with decreased risk of sporadic CRC patients with body mass index (BMI) ≥28.0 kg/m2, family cancer history, and premenopausal. Survivin -31G>C polymorphism is associated with sporadic CRC risk in the Southern Chinese population. The -31G wild-type genotypes and GC, GG genotypes are the independent protective factors against sporadic CRC excluding those with a BMI ≥28.0 kg/m2, family cancer history, and premenopausal.

MiR-30a promoter variation contributes to the increased risk of colorectal cancer in an Iranian population.

Cytochrome P450 family 24 subfamily A member 1 (CYP24A1) gene is overexpressed in many cancers including colorectal cancer (CRC) and correlated with tumor invasion, lymph node metastasis, and the reduced overall survival. We predicted that miR-30a and miR-125a regulate the CYp24A1 gene expression. Therefore, we performed a case-control study using 800 individuals, including 389 patients with CRC and 411 noncancer controls to evaluate the association between miR-30a rs2222722 and miR-125a rs12976445 polymorphisms, located at in the promoter region, and the risk of sporadic CRC in an Iranian population. The genotyping assay for both polymorphisms was performed using Tetra-primer amplification refractory mutation systems polymerase chain reaction. The results indicated that the frequency of the miR-30a rs2222722 CT genotype was significantly different in the studied groups ( P = 0.0001; odds ratio [OR] = 1.9; 95% confidence interval [CI], 1.39-2.60). Also, a significant difference was observed under the dominant inheritance model ( P = 0.0001; OR = 1.8; 95% CI, 1.33-2.43). The frequency of the miR-30a rs2222722 T allele was significantly associated with increased CRC risk in the studied population ( P = 0.0019; OR = 1.47; 95% CI, 1.15-1.89). Taken together, our study provides preliminary evidence that the rs2222722 polymorphism increases the susceptibility to CRC in an Iranian population. Therefore, the affecting factors on CYP24A1 gene expression such as microRNAs can be considered as risk factors for CRC.

Molecular evaluation of glutathione S transferase family genes in patients with sporadic colorectal cancer.

AIMTo evaluate the association between polymorphisms in glutathione S transferases (GSTs) and the risk of sporadic colorectal cancer (SCRC), tumor progression and the survival of patients.METHODSA case-control study of 970 individuals from the Brazilian population was conducted (232 individuals from the case group with colorectal cancer and 738 individuals from the control group without a history of cancer). PCR multiplex and PCR-RFLP techniques were used to genotype the GST polymorphisms. The tumors were categorized according to the TNM classification: tumor extension (T), affected lymph nodes (N), and presence of metastasis (M). Logistic regression, multiple logistic regression and survival analysis were used to analyze the data. The results are presented in terms of odds ratio (OR) and 95% confidence interval (CI). The level of significance was set at 5% (P ≤ 0.05).RESULTSAge equal to or over 62 years (OR = 8.79; 95%CI: 5.90-13.09, P < 0.01) and female gender (OR = 2.91; 95%CI: 1.74-4.37; P < 0.01) were associated with increased risk of SCRC. Analysis of the polymorphisms revealed an association between the GSTM1 polymorphisms and a risk of SCRC (OR = 1.45; 95%CI: 1.06-2.00; P = 0.02), as well as between GSTT1 and a reduced risk of the disease (OR = 0.65; 95%CI: 0.43-0.98; P = 0.04). An interaction between the presence of the wild-type allele of GSTP1 Ile105Val polymorphism and tobacco consumption on risk of SCRC (OR = 2.33; 95%CI: 1.34-4.05; P = 0.05) was observed. There was an association between the GSTM1 null genotype and the presence of advanced tumors (OR = 2.33; 95%CI: 1.23-4.41; P = 0.009), as well as increased risk of SCRC in the presence of a combination of GSTT1 non-null/GSTM1 null genotypes (OR = 1.50; 95%CI: 1.03-2.19; P = 0.03) and GSTT1 non-null/GSTM1 null/GSTP1 Val* (OR = 1.85; 95%CI: 1.01-3.36, P = 0.04). Combined GSTT1 non-null/GSTM1 null genotypes (OR = 2.40; 95%CI: 1.19-4.85; P = 0.01) and GSTT1 non-null/GSTM1 null/GSTP1 Val* (OR = 2.92; 95%CI: 1.05-8.12; P = 0.04) were associated with tumor progression. Polymorphisms were not associated with the survival of patients with SCRC.CONCLUSIONFemales aged 62 years or older are more susceptible to SCRC. Polymorphisms of GSTT1 and GSTM1 null genotypes modulated the susceptibility to SCRC in the population studied.

RAD51 135G&gt;C polymorphism and risk of sporadic colorectal cancer in Iranian population

Colorectal cancer (CRC) is among the most common cancers and accounts as the second leading cause of death from cancers in the world. RAD51 plays a crucial role in double-strand breaks repair of DNA. Single nucleotide polymorphisms within this gene could influence on the potential of DNA repair and in consequence on the susceptibility to various tumors such as CRC. This is the first report about the role of RAD51 polymorphisms in Iranian CRC susceptibility. The study was conducted to evaluate the association of 135G>C polymorphism of RAD51 gene with sporadic CRC in a subset of Iranian population. The current case-control study was performed from 2013 to 2015. One hundred patients with sporadic CRC and one hundred controls were enrolled from two referral centers in Isfahan. All samples were genotyped for the RAD51 gene using polymerase chain reaction-restriction fragment length polymorphism assay. The results revealed no significant association between the RAD51 135G>C and sporadic CRC (odds ratio = 0.86, 95% confidence interval = 0.464-1.595). The frequency of genotypes and also alleles of the mentioned polymorphism were not significantly different between case and control groups (P = 0.2 and 0.4, respectively). The results suggest that RAD51 135G>C probably has not a crucial role in Iranian CRC risk and is not an important potential risk factor in molecular diagnostics of mentioned disease among Iranian population.

Polymorphism of Gly39Glu (c.116G>A) hMSH6 is associated with sporadic colorectal cancer development in the Polish population: Preliminary results.

Colorectal cancer (CRC) remains a major source of cancer-related mortality, accounting for 10% of all cancer-related deaths. DNA mismatch repair mechanism (MMR) responsible for correcting errors generated during DNA replication and its deficiency is associated with both hereditary and sporadic CRC. Single-nucleotide polymorphisms (SNPs) are the most common forms of genetic variation, and it has been shown that the SNPs in MMR genes may modify CRC risk. The aim of the study was to determine the relationship between gene polymorphism Glu39Gly (c.116G>A) of the hMSH6 gene and the modulation of the risk of sporadic colorectal cancer in the Polish population. A total of 128 patients with resectable colorectal carcinoma as well as 189 sex-, age-, and ethnicity-matched control subjects without cancer history were enrolled in this study. Patients with a family history of CRC or inflammatory bowel diseases were excluded from this study. The DNA was isolated from peripheral blood lymphocytes of enrolled patients, and gene polymorphisms were analyzed by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR). We observed that the genotype G/A variant of Glu39Gly (c.116G>A) genotype is associated with an increased risk of colorectal cancer (OR 1.65; 95% CI: 1.01-2.69; p = 0.44). The presence of A allele was also significantly higher in patients with CRC (OR 1.57; 95% CI: 1.04-2.38; p = 0.032). When comparing the prevalence of genotypes with clinical staging, genotype G/A and A allele were significantly less frequent in stage III-IV than in I (OR 0.3409; 95% CI: 0.124-0.939; p = 0.0375, and OR 0.4462; 95% CI: 0.201-0.991; p = 0.044, respectively). These findings suggest that hMSH6 Glu39Gly polymorphism is associated with the risk of developing colorectal cancer in the Polish population, probably due to a defective mismatch repair system. The presence of G/A genotype and A allele is, however, associated with less advanced disease.

Genome-wide association study identified copy number variants associated with sporadic colorectal cancer risk

BackgroundMultiple single nucleotide polymorphisms (SNPs) have been associated with colorectal cancer (CRC) risk. The role of structural or copy number variants (CNV) in CRC, however, remained unclear. We investigated the...

MLH1 -93G&gt;A and I219V polymorphisms are susceptible to increased risk of sporadic colorectal cancer in a Turkish population

Colorectal cancer (CRC) comprises approximately 10% of all cancers and is a major cause of cancer-related morbidity and mortality despite current diagnostic and treatment improvements. DNA damage and altered DNA replication through the deregulation of related genes cause genomic instability in sporadic CRC. DNA repair is very complex; many factors play a role to ensure that the restoration of errors occurs during the transfer of genetic material. MutL homolog 1 (MLH1) is one of the vital DNA repair genes responsible for genomic stability. Together with environmental factors, the genetic background may be associated with CRC development; thus, genetic polymorphisms are considered as risk factors. The present prospective case– control study aimed to determine the association between 93G&gt;A and I219V polymorphisms of MLH1 and CRC susceptibility in a Turkish population. The genotyping of 158 patients and 164 age- and sex-matched controls was performed by polymerase chain reaction-restriction fragment length polymorphism. Two variants, 93G&gt;A and I219V, were associated with an increased risk of CRC. Individuals with A allele of 93G&gt;A had an approximately 2-fold risk (OR: 1.92, 95% CI: 1.22–3.04; p&lt;0.01) and those with G allele of I219V had an approximately 3-fold risk (OR: 2.82, 95% CI: 1.76–4.52; p&lt;0.01) of developing CRC. Our results provide novel information for understanding the influence of MLH1 on CRC risk in the Turkish population; however, further studies with a larger number of participants are required.

The association between CCND1 G870A polymorphism and colorectal cancer risk: A meta-analysis.

Background:CyclinD1 (CCND1) is a key cell cycle regulatory protein. A large number of epidemiological studies have assessed the potential correlation between the CCND1 G870A polymorphism and the risk of colorectal cancer (CRC), but their findings have been inconsistent. To obtain a more precise understanding of the association between the G870A polymorphism in the CCND1 gene and the CRC risk, we conducted a more comprehensive meta-analysis.Methodology:We searched PubMed, Ovid, Springer, Weipu, China National Knowledge Infrastructure (CNKI), and Wanfang databases, covering all publications (the last search was updated on January 10, 2017). The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were derived from a fixed effect or random effect model. Statistical analyses were performed using Review Manager 5.3 and STATA 10.0 software.Results:A total of 7276 CRC patients and 9667 controls from 27 publications were included in this meta-analysis. We found that compared with GG homozygote genetic model, AA, AG, AA + AG genetic models of the CCND1 G870A polymorphism were significantly associated with overall CRC risk (AA homozygote genetic model: OR = 1.28, 95% CI = 1.10–1.49; AG heterozygote genetic model: OR = 1.15, 95% CI = 1.06–1.25; AA homozygote + AG heterozygote genetic model: OR = 1.19, 95% CI = 1.07–1.33). Subgroup analyses by ethnicity and cancer location showed that A carriers were consistently associated with a significantly increased risk of CRC in all subsets of participants (Asian and Caucasian; colon cancer and rectal cancer). When stratified by study design, we found a significant association in hospital-based studies (HB), but no significant associations were found in either population-based studies (PB) or family-based studies (FB). According to subgroup analysis by cancer type, the risk of sporadic colorectal cancer (sCRC) and hereditary nonpolyposis colorectal cancer (HNPCC) were not correlated with the CCND1 G870A polymorphism, except AG (AG vs GG: OR = 1.30, 95% CI = 1.11–1.53).Conclusions:This meta-analysis suggests that the CCND1 G870A polymorphism is associated with an increased risk of CRC, especially that A carriers may be a major risk factor for CRC.

Long-term follow-up reveals high incidence of colorectal cancer in Indian patients with inflammatory bowel disease.

As the magnitude of sporadic colorectal cancer (CRC) in India is low, magnitude of CRC in ulcerative colitis (UC) is also considered low. As a result, screening for CRC in UC although advocated may not be followed everywhere. We report our data of UC-related CRC from a low-incidence area of sporadic CRC. A total of 1012 patients with left-sided colitis/pancolitis having more than one full-length colonoscopy performed at least a year after the onset of symptoms were included in retrospective analysis of prospectively maintained case records. In addition, 136 patients with duration of disease >10 years underwent surveillance white-light colonoscopy prospectively during the study period. A total of 1012 individuals were finally included (6542 person-years of follow-up, 68.5% males, disease duration: 6.4 ± 6.8 years). Twenty (1.97%) patients developed CRC. Two (10%) patients developed CRC during the first decade, 10/20 (50%) during the second and 8/20 (40%) after the second decade of disease. The cumulative risk of developing CRC was 1.5%, 7.2% and 23.6% in the first, second and third decade, respectively. Of 136 high-risk UC cases, five (3.6%) had CRC on screening colonoscopy. Disease duration and increasing age of onset were associated with higher risk of CRC. Cumulative risk of CRC in Indian UC patients is as high as 23.6% at 30 years. The risk of CRC increases with increasing age of onset and increasing duration of disease. A low risk of sporadic CRC does not confer a low risk of UC-related CRC, and regular screening is warranted.

The PTPN13 Y2081D (T>G) (rs989902) polymorphism is associated with an increased risk of sporadic colorectal cancer.

Colorectal cancer (CRC) is one of the most common cancers worldwide and, although the majority of cases are sporadic, its development and progression depends on a range of factors: environmental, genetic and epigenetic. A variety of genetic pathways have been described as being crucial in CRC, including protein tyrosine phosphatases (PTPs). PTPN13 (also called FAP-1) is a non-receptor PTP and interacts with a number of important components of growth and apoptosis pathways. It is also involved in the inhibition of Fas-induced apoptosis. The single nucleotide polymorphism genotype at Y2081D (T>G) (rs989902) of PTPN13 exon 39 was determined in DNA extracted from blood samples from 174 sporadic CRC patients and 176 healthy individuals. Also, a meta-analysis was performed based on three articles accessed via the PubMed and ResearchGate databases. The risk of CRC was 2.087 times greater for patients with the GG genotype than for those with the TT genotype (P=0.0475). In the meta-analysis, a significantly increased risk of cancer associated with the G allele was observed in the squamous cell carcinoma of the head and neck subgroup (TT vs GG+GT, OR 1.23, 95% CI [1.02, 1.47], P=0.0258), and a significantly decreased risk in the breast cancer subgroup (TT vs GG+GT, OR 0.63, 95% CI [0.41, 0.96], P=0.0334) and in the CRC subgroup (GT+TT vs GG, OR 0.51, 95% CI [0.41, 0.95], P=0.0333). PTPN13 rs989902 is significantly associated with the risk of CRC in the Polish population. Given that this report provides the first evidence of an association of PTPN13 rs989902 with the risk of CRC in a Caucasian population, further large scale studies are necessary to confirm this finding.