Risk Of Pancreatic Cancer Research Articles

NCCN Guidelines® Insights: Genetic/Familial High-Risk Assessment: Breast, Ovarian, and Pancreatic, Version 2.2024.

The NCCN Guidelines for Genetic/Familial High-Risk Assessment: Breast, Ovarian, and Pancreatic focus primarily on assessment of pathogenic/likely pathogenic (P/LP) variants associated with increased risk of breast, ovarian, pancreatic, and prostate cancer, including BRCA1, BRCA2, CDH1, PALB2, PTEN, and TP53, and recommended approaches to genetic counseling/testing and care strategies in individuals with these P/LP variants. These NCCN Guidelines Insights summarize important updates regarding: (1) a new section for transgender, nonbinary and gender diverse people who have a hereditary predisposition to cancer focused on risk reduction strategies for ovarian cancer, uterine cancer, prostate cancer, and breast cancer; and (2) testing criteria and management associated with TP53 P/LP variants and Li-Fraumeni syndrome.

9O Pancreatic cancer risk in individuals with newly diagnosed diabetes: Insights from the AMORIS cohort in Sweden

9O Pancreatic cancer risk in individuals with newly diagnosed diabetes: Insights from the AMORIS cohort in Sweden

Dietary patterns in relation to incidence rate of pancreatic cancer - the Norwegian women and cancer cohort study.

Despite development in cancer treatment and prevention options during the past few years, cancer of the pancreas remains a diagnosis associated with poor prognosis and limited options for prevention. Diet has proven to be an important risk factor for development of many types of cancer, particularly for cancers of the digestive system. Still, evidence regarding its relation to pancreatic cancer remains ambiguous. To investigate the relationship between diet and pancreatic cancer, an analysis of dietary patterns in participants from the Norwegian Women and Cancer Study (n = 89,156; 305 pancreatic cancer cases) was performed. Cox regression analysis was used for studying possible associations between dietary patterns, derived from principal component analysis, and pancreatic cancer incidence. The four most prominent dietary patterns were identified and described: European pattern, animal food consumers' dietary pattern, traditional Norwegian pattern, and alcohol-abstaining dietary pattern. In analysis without adjustment for confounders, being in the highest tertile of the abstaining dietary pattern was associated with lower risk of pancreatic cancer in comparison to the lowest tertile (hazard ratios [HR]: 0.66, 95% confidence interval [CI]: 0.49-0.89). After additional adjustment for height and smoking status, no dietary pattern was associated with increased pancreatic cancer risk, nor was there any difference in effect estimates between strata of smokers and non-smokers. The results of our current analysis do not support the role of major dietary patterns in the development of pancreatic cancer.

Splicing transcriptome-wide association study to identify splicing events for pancreatic cancer risk.

A large proportion of the heritability of pancreatic cancer risk remains elusive, and the contribution of specific mRNA splicing events to pancreatic cancer susceptibility has not been systematically evaluated. In this study, we performed a large splicing transcriptome-wide association study (spTWAS) using three modeling strategies (Enet, LASSO and MCP) to develop alternative splicing genetic prediction models for identifying novel susceptibility loci and splicing introns for pancreatic cancer risk by assessing 8275 pancreatic cancer cases and 6723 controls of European ancestry. Data from 305 subjects of whom the majority are of European descent in the Genotype-Tissue Expression Project (GTEx) were used and both cis-acting and promoter-enhancer interaction regions were considered to build these models. We identified nine splicing events of seven genes (ABO, UQCRC1, STARD3, ETAA1, CELA3B, LGR4 and SFT2D1) that showed an association of genetically predicted expression with pancreatic cancer risk at a false discovery rate ≤0.05. Of these genes, UQCRC1 and LGR4 have not yet been reported to be associated with pancreatic cancer risk. Fine-mapping analyses supported likely causal associations corresponding to six splicing events of three genes (P4HTM, ABO and PGAP3). Our study identified novel genes and splicing events associated with pancreatic cancer risk, which can improve our understanding of the etiology of this deadly malignancy.

Validation of a real-time biliopancreatic endoscopic ultrasonography analytical device in China: a prospective, single-centre, randomised, controlled trial

Endoscopic ultrasonography (EUS) is a key procedure for the diagnosis of biliopancreatic diseases. However, the performance among EUS endoscopists varies greatly and leads to blind spots during the operation, which can impair the health outcomes of patients. We previously developed an artificial intelligence (AI) device that accurately identified EUS standard stations and significantly reduced the difficulty of ultrasonography image interpretation. In this study, we updated the device (named EUS-IREAD) and validated its performance in improving the quality of EUS procedures. In this single-centre, randomised, controlled trial, we updated EUS-IREAD so it consisted of five learning models to identify eight EUS stations and 24 anatomical structures. The trial was done at the Renmin Hospital of Wuhan University (Wuhan, China) and included patients aged 18 years or older with suspected biliopancreatic (pancreas and biliopancreatic duct) lesions due to clinical symptoms, radiological findings, or laboratory findings, and with a high risk of pancreatic cancer. Patients were randomly assigned (1:1) by a dedicated research assistant using a computer-generated random number series (with a block size of four) to undergo the EUS procedure with or without the assistance of EUS-IREAD. Endoscopists in the EUS-IREAD-assisted group were required to observe all standard stations and anatomical structures according to the prompts by the AI device. Data collectors, the independent data anaylsis team, and patients were masked to group allocation. The primary outcome was the missed scanning rate of standard stations between the two groups, which was assessed in patients who underwent EUS procedure in accordance with the assigned intervention (per protocol). This trial is registered with ClinicalTrials.gov, NCT05457101. Between July 9, 2022, and Feb 28, 2023, 290 patients (mean age 55·93 years [SD 14·06], 152 [52%] male, and 138 [48%] female) were randomly assigned and analysed, including 144 in the EUS-IREAD-assisted group and 146 in the control group. The EUS-IREAD-assisted group had a lower missed scanning rate of stations than the control group (4·5% [SD 0·8] vs 14·3% [1·0], -9·8% [95% CI -12·2 to -7·5]; odds ratio 3·6 [95% Cl 2·6 to 4·9]; p<0·0001). No significant adverse event was found during the study. Our study confirms the capability of EUS-IREAD to monitor the blind spots and reduce the missed rate of stations and structures during EUS procedures. The EUS-IREAD has the potential to play an essential part in EUS quality control. Innovation Team Project of Health Commission of Hubei Province and College-enterprise Deepening Reform Project of Wuhan University.

Fine tuning calcium dynamics by inhibition of Store-operated Calcium Entry as a novel therapeutic approach for the treatment of chronic pancreatitis

Chronic pancreatitis (CP) is a complex inflammatory disorder characterized by progressive fibrosis, leading to pancreatic dysfunction, reduced quality of life and an elevated pancreatic cancer risk. Current therapeutic options for CP are restricted to symptomatic treatment. Using ex vivo and in vivo preclinical disease models, Szabó et al. now explored for the first time the involvement of Store-operated Ca2+ entry (SOCE) in the progression of CP and propose that a selective pharmacological inhibition of the SOCE signaling component Orai1 might serve as specific treatment option for CP[1,2].

Pancreatic Cancer and Detection Methods.

The pancreas is a vital organ with exocrine and endocrine functions. Pancreatitis is an inflammation of the pancreas caused by alcohol consumption and gallstones. This condition can heighten the risk of pancreatic cancer (PC), a challenging disease with a high mortality rate. Genetic and epigenetic factors contribute significantly to PC development, along with other risk factors. Early detection is crucial for improving PC outcomes. Diagnostic methods, including imagining modalities and tissue biopsy, aid in the detection and analysis of PC. In contrast, liquid biopsy (LB) shows promise in early tumor detection by assessing biomarkers in bodily fluids. Understanding the function of the pancreas, associated diseases, risk factors, and available diagnostic methods is essential for effective management and early PC detection. The current clinical examination of PC is challenging due to its asymptomatic early stages and limitations of highly precise diagnostics. Screening is recommended for high-risk populations and individuals with potential benign tumors. Among various PC screening methods, the N-NOSE plus pancreas test stands out with its high AUC of 0.865. Compared to other commercial products, the N-NOSE plus pancreas test offers a cost-effective solution for early detection. However, additional diagnostic tests are required for confirmation. Further research, validation, and the development of non-invasive screening methods and standardized scoring systems are crucial to enhance PC detection and improve patient outcomes. This review outlines the context of pancreatic cancer and the challenges for early detection.

On the Menu: Analyzing the Macronutrients, Micronutrients, Beverages, Dietary Patterns, and Pancreatic Cancer Risk.

This narrative review summarizes the principal findings of observational studies, systematic reviews, and meta-analyses on diet and dietary patterns' role in the risk of pancreatic cancer. Etiologically pancreatic cancer is multifactorial. Evidence exists of an association between nutrients, dietary patterns, and pancreatic cancer. An extensive literature search was conducted on PubMed, Cochrane, and Google Scholar. A thorough search of articles published in English till May 2023 and related to the review was performed. The relationship between all macronutrients, micronutrients, and various dietary patterns with the risk of pancreatic cancer was assessed. It is concluded that a diet high in nutrients like red and processed meat, refined sugars, saturated and monounsaturated fats, alcohol, copper, and a Western dietary pattern can increase the likelihood of pancreatic cancer. Contrary to this, a diet consisting of fruits, vegetables, appropriate quantities of vitamins and minerals, and a Mediterranean dietary pattern is associated with a decreased risk of pancreatic cancer.

Gastroesophageal reflux disease and risk of cancer: Findings from the Korean National Health Screening Cohort.

Little is known about the association of cancers other than esophageal adenocarcinoma with gastroesophageal reflux disease (GERD). This study aimed to examine the association between GERD and the risk of different types of cancer. A cohort study was conducted using data from the National Health Screening Cohort. We included 10,261 GERD patients and 30,783 non-GERD individuals who were matched in a 1:3 ratio by age and sex. All participants were followed-up until cancer diagnosis, death, or end of the study (December 31, 2015). Hazard ratios were calculated using the Cox proportional hazards model, adjusting for smoking and alcohol consumption, physical activity, body mass index, income, area, and Charlson Comorbidity Index. The median follow-up time was 9.9 years. GERD was associated with an increased risk of esophageal (adjusted hazard ratios [aHR] = 3.20 [1.89-5.41]), laryngeal (aHR = 5.42 [2.68-10.96]), and thyroid cancers (aHR = 1.91 [1.55-2.34]) after controlling for all covariates. The results were consistent when examining GERD with esophagitis (K210) and without esophagitis (K219) separately. For thyroid cancer, the results were insignificant after controlling for having ever-received thyroid biopsy procedures. A dose-response relationship was found between GERD and esophageal cancer as well as laryngeal cancer, with patients with a longer duration of GERD treatment showing a stronger effect. In contrast, GERD was associated with a reduced risk of colorectal (aHR = 0.73 [0.59-0.90]), liver (aHR = 0.67 [0.51-0.89]), and pancreatic cancers (aHR = 0.43 [0.24-0.76]), which might have resulted from differences in healthcare utilization between GERD and non-GERD groups. GERD was associated with an increased risk of esophageal and laryngeal cancers. Additionally, early detection and treatment of precancerous lesions among the GERD group could lead to a lower risk of colorectal, liver, and pancreatic cancers.

Pancreatic Cancer and the Family Connection: The Role of Advanced Practitioners in Screening and Educating Genetically At-Risk Individuals.

Pancreatic cancer is the third leading cause of cancer deaths in the United States. It has a 95% mortality rate within 5 years of the initial diagnosis. Pancreatic ductal adenocarcinoma is the most commonly diagnosed histotype. The average age at diagnosis is 70 years. Familial forms of pancreatic cancer have been associated with pathogenic variants in predisposing genes, including ATM, BRCA1, BRCA2, PALB2, CDKN2A, STK11, MLH1, and MSH2. Collecting information on the patient's family history may serve as a primary tool to screen an individual's risk for familial pancreatic cancer. More advanced screening options for individuals at risk include endoscopic ultrasonography, magnetic resonance imaging, and magnetic resonance cholangiopancreatography. Due to pancreatic cancer's high mortality rate, routine screening of individuals at risk for developing familial pancreatic cancer may result in early diagnosis and improved survivability. This review aims to characterize the genetic risk factors associated with pancreatic cancer and recognize available screening options for at-risk individuals.

Multistate Model of the Natural History of Inflammatory Pancreatic Diseases: A Nationwide Population-based Cohort Study

Understanding the nature of inflammatory pancreatic diseases is essential for planning health care system requirements and interventions. The aim of this study was to quantify the trajectories of inflammatory pancreatic diseases and their association with pancreatic cancer in a population-based setting. National health registries were used to identify all Danish residents (18 years or older) in the period from 2000 through 2018 with incident cases of acute pancreatitis (AP), recurrent acute pancreatitis (RAP), chronic pancreatitis (CP), and pancreatic cancer. We used a multistate model to examine transitions from a healthy state to intermediate states of acute pancreatic inflammation (AP and RAP) to chronic states (CP and pancreatic cancer) and, ultimately, death. Results were reported as transition incidence rates per 1000 person-years with 95% CIs. There were 4,663,864 individuals included (mean age, 46 years; 51% were women). During a mean follow-up of 16.8 years, 31,396 individuals were diagnosed with incident AP, 5546 with RAP, 8898 with CP, and 18,182 with pancreatic cancer. The cumulative incidence of pancreatitis (acute and chronic) during the study period was 0.80% (95% CI, 0.79%-0.80%). The transition incidence rates to CP were 12.1 (95% CI, 8.1-18.1) from AP, 46.8 (95% CI, 31.6-69.3) from RAP, and 0.07 (95% CI, 0.04-0.13) from a healthy state. Similar patterns were observed for transitions to pancreatic cancer. Most patients diagnosed with CP (64.2%) and pancreatic cancer (96.4%) transitioned directly from a healthy state. Among patients with pancreatitis, 41.0% (95% CI, 40.5%-41.5%) died during follow-up. The study findings revealed an increased risk of CP and pancreatic cancer in patients with a history of AP. However, most patients with CP and pancreatic cancer transitioned directly from a healthy state.

A blood-based metabolomic signature predictive of risk for pancreatic cancer

Emerging evidence implicates microbiome involvement in the development of pancreatic cancer (PaCa). Here, we investigate whether increases in circulating microbial-related metabolites associate with PaCa risk by applying metabolomics profiling to 172 sera collected within 5 years prior to PaCa diagnosis and 863 matched non-subject sera from participants in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cohort. We develop a three-marker microbial-related metabolite panel to assess 5-year risk of PaCa. The addition of five non-microbial metabolites further improves 5-year risk prediction of PaCa. The combined metabolite panel complements CA19-9, and individuals with a combined metabolite panel+ CA19-9 score in the top 2.5th percentile have absolute 5-year risk estimates of >13%. The risk prediction model basedon circulating microbial and non-microbial metabolites provides a potential tool to identify individualsat high risk of PaCa that would benefit from surveillance and/or from potential cancer interception strategies.

Where the metabolome meets the microbiome for pancreatic cancer detection

Risk prediction tools for pancreatic cancer are urgently sought to facilitate screening. Irajizad etal.1 describe the performance of a risk predication model based on circulating microbial- and non-microbial metabolites for assessment of 5-year pancreatic cancer risk.

Outcomes of the IMMray PanCan-d Test in High-Risk Individuals Undergoing Pancreatic Surveillance: Pragmatic Data and Lessons Learned.

An effective blood-based test for pancreatic cancer (PC) screening has remained elusive. The IMMray PanCan-d is the first commercially available blood-based test specifically designed for early detection of PC; however, outcomes from its use in clinical practice have not been reported. We performed a blinded spike-in study of 100 individuals who had an IMMray PanCan-d test, including 94 high-risk individuals (HRIs) undergoing PC surveillance and six individuals with known PC. Specimens were processed blindly following the commercial laboratory's standardized operating procedure. Positive predictive value (PPV) and negative predictive value (NPV) were calculated. Cohort characteristics included a median age of 63 (IQR, 55-70) years, 57% female, 96% non-Hispanic White, 57% with a pathogenic variant in a PC risk gene (BRCA2 most commonly-18%), and 83% with a family history of PC. Among IMMray PanCan-d results from 94 HRIs undergoing PC surveillance, there was one positive (1%), seven borderlines (7%), 73 negatives (78%), and 13 tests not performed because of low CA19-9 expression (14%). No PC was diagnosed among these HRIs; however, there were two sub-cm pancreatic neuroendocrine tumors, seven clinically diagnosed side branch intraductal papillary mucinous neoplasms ≥1 cm, and a sub-cm solid mass with indeterminate cytology requiring close follow-up; all these individuals had negative IMMray PanCan-d tests. Of the six spiked-in PCs, four (67%) yielded a positive and two (33%) yielded a negative. With an estimated disease prevalence of 2%, the PPV and NPV are 52% and 99%, respectively, if borderline results are considered negative and 12% and 99%, respectively, if borderline tests are considered positive. In clinical practice, IMMray PanCan-d has a robust NPV; however, PPV is dramatically influenced by whether borderline results are characterized as a positive or negative result.

Risk of Pancreatic Cancer and Use of Dipeptidyl Peptidase 4 Inhibitors in Patients with Type 2 Diabetes: A Propensity Score-Matching Analysis.

The effects of dipeptidyl peptidase 4 (DPP-4) inhibitors over the course of long-term treatment remain unclear, and concerns have been raised regarding the role of DPP-4 inhibitors in carcinogenesis in the pancreas. Earlier studies of pancreatic adverse events have reported conflicting results. This study analyzed Korean National Health Insurance Service data from January 2009 to December 2012. Patients who had type 2 diabetes mellitus and took two or more oral glucose-lowering drugs (GLDs) were included. Patients prescribed DPP-4 inhibitors (n=51,482) or other GLDs (n=51,482) were matched at a 1:1 ratio using propensity score matching. The risk of pancreatic cancer was calculated using Kaplan-Meier curves and Cox proportional-hazards regression analysis. During a median follow-up period of 7.95 years, 1,051 new cases of pancreatic cancer were identified. The adjusted hazard ratio (HR) for DPP-4 inhibitor use was 0.99 (95% confidence interval [CI], 0.88 to 1.12) compared with the other GLD group. In an analysis limited to cases diagnosed with pancreatic cancer during hospitalization, the adjusted HR for the use of DPP-4 inhibitors was 1.00 (95% CI, 0.86 to 1.17) compared with patients who took other GLDs. Using the other GLD group as the reference group, no trend was observed for elevated pancreatic cancer risk with increased DPP-4 inhibitor exposure. In this population-based cohort study, DPP-4 inhibitor use over the course of relatively long-term follow-up showed no significant association with an elevated risk of pancreatic cancer.

BRCA genes as candidates for colorectal cancer genetic testing panel: systematic review and meta-analysis

BackgroundBreast cancer susceptibility gene (BRCA) mutation carriers are at an increased risk for breast, ovarian, prostate and pancreatic cancers. However, the role of BRCA is unclear in colorectal cancer; the results regarding the association between BRCA gene mutations and colorectal cancer risk are inconsistent and even controversial. This study aimed to investigate whether BRCA1 and BRCA2 gene mutations are associated with colorectal cancer risk.MethodsIn this systematic review, we searched PubMed/MEDLINE, Embase and Cochrane Library databases, adhering to PRISMA guidelines. Study quality was assessed using the Newcastle–Ottawa Scale (NOS). Unadjusted odds ratios (ORs) were used to estimate the probability of Breast Cancer Type 1 Susceptibility gene (BRCA1) and Breast Cancer Type 2 Susceptibility gene (BRCA2) mutations in colorectal cancer patients. The associations were evaluated using fixed effect models.ResultsFourteen studies were included in the systematic review. Twelve studies, including seven case–control and five cohort studies, were included in the meta-analysis. A significant increase in the frequency of BRCA1 and BRCA2 mutations was observed in patients with colorectal cancer [OR = 1.34, 95% confidence interval (CI) = 1.02–1.76, P = 0.04]. In subgroup analysis, colorectal cancer patients had an increased odds of BRCA1 (OR = 1.48, 95% CI = 1.10–2.01, P = 0.01) and BRCA2 (OR = 1.56, 95% CI = 1.06–2.30, P = 0.02) mutations.ConclusionsBRCA genes are one of the genes that may increase the risk of developing colorectal cancer. Thus, BRCA genes could be potential candidates that may be included in the colorectal cancer genetic testing panel.

The Natural Disease Course of Pancreatic Cyst–Associated Neoplasia, Dysplasia, and Ductal Adenocarcinoma: Results of a Microsimulation Model

Estimates on the progression of precursor lesions to pancreatic cancer (PC) are scarce. We used microsimulation modeling to gain insight into the natural disease course of PC and its precursors. This information is pivotal to explore the efficacy of PC screening. A Microsimulation Screening Analysis model was developed in which pancreatic intraepithelial neoplasms and cysts can evolve from low-grade dysplasia (LGD) to high-grade dysplasia (HGD) to PC. The model was calibrated to Dutch PC incidence data and Japanese precursor prevalence data (autopsy cases without PC) and provides estimates of PC progression (precursor lesion onset and stage duration). Mean LGD state durations of cysts and pancreatic intraepithelial neoplasms were 15.8 years and 17.1 years, respectively. Mean HGD state duration was 5.8 years. For lesions that progress to PC, the mean duration was 4.8-4.9 years for LGD lesions and 4.0-4.1 years for HGD lesions. In 13.7% of individuals who developed PC, the HGD state lasted less than 1 year. The probability that an individual at age 50 years developed PC in the next 20 years was estimated to be 1.8% in the presence of any cyst and 6.1% in case of an LGD mucinous cyst. This 20-year PC risk was estimated to be 5.1% for individuals with an LGD pancreatic intraepithelial neoplasm. Mean duration of HGD lesions before development of PC was estimated to be 4.0 years. This implies a window of opportunity for screening, presuming the availability of a reliable diagnostic test. The probability that an LGD cyst will progress to cancer was predicted to be low.

Association between inflammatory bowel disease and pancreatic cancer: results from the two-sample Mendelian randomization study.

The nuanced relationship between inflammatory bowel disease (IBD) and pancreatic cancer is noticed in recent years. However, the underlying causal effects of these two diseases are still unclear. The two-sample mendelian randomization (MR) was conducted to explore the causal effect of IBD condition on pancreatic cancer. Methods of Wald ratio, inverse variance weighted (IVW), MR-Egger, weighted median, and weighted mode were used to investigate the causal relationship between IBD and pancreatic cancer. Besides, Cochrane's Q test, MR-Egger, and leave-one-out method were further conducted to detect heterogeneity, stability, and pleiotropy of MR results. In the MR analysis, we found Crohn's disease had a significant causal effect on pancreatic cancer. Specifically, Crohn's disease would increase 11.1% the risk of pancreatic cancer by the IVW method (p= 0.022), 33.8% by MR Egger (p= 0.015), by 35.3% by the Weighted model (p= 0.005). Regarding ulcerative colitis, there was no statistically significant causal effect observed on pancreatic cancer (p>0.05). Additionally, the pleiotropic test and Leave-one-out analysis both proved the validity and reliability of the present two-sample MR analyses. This study indicates that IBD, particularly Crohn's disease, is causality associated with increased risk of pancreatic cancer. Our results may help public health managers to make better follow-up surveillance of IBD patients.

CD 133 Gene Polymorphisms as Predictive Markers for Development of Cancer Pancreas

Abstract Background Pancreatic cancer is one of the most aggressive human malignancies, it ranks the fourth leading cause of cancer death in the Western world and the 13th commonest cancer. Aim of the Work The aim of this study is to evaluate the genetic variants CD133 (rs1029728, rs2240688, rs2286455, and rs3130) as possible non-invasive predictive biomarker for Pancreatic cancer in the Egyptian population, this could help to detect the susceptible individuals, diagnose patients earlier, and this improve the therapeutic outcome. Patients and Methods This study was conducted in co-operation between Gastroenterology and Hepatology Department, Ain-Shams University and the Gastroenterology and Hepatology Department, Theodor Bilharz Research Institute “between” september 2020 to march 2021. It included total participants of 133 Results Our study demonstrated that there are three gene polymorphisms showed significant increase in pancreatic cancer group vs. control group, rs2240688 (TT) (65.5%) vs. (44.9%), rs1029728 (AA) (20.2%) vs. (2.0%), and rs3130 (TT) (32.1%) vs. (16.3%) respectively. There is significant increase in rs2240688 (TT), rs1029728 (AG) and rs3130 (TT) with smoking in pancreatic cancer group. And There is significant increase in males in pancreatic cancer group vs. control group in rs3130 (TT) with rs2240688 (TT) polymorphism. While rs2286455 showed no statically significance. The functional polymorphisms rs3130 (CC) and rs2240688 (CC) were found to be higher in control group vs. pancreatic cancer group that may represent a protective value against the disease. So, CD133 gene polymorphisms, rs2240688 (TT) rs1029728 (AA) and rs3130 (TT) could be used as a predictive marker for Pancreatic cancer after validation by larger studies or met analysis. Conclusion We concluded that the Genetic polymorphisms of the CD133 gene were associated with risk of Pancreatic cancer are three polymorphisms and represented as rs2240688 (TT) (65.5%) vs. (44.9%), rs1029728 (AA) (20.2%) vs. (2.0%), and rs3130 (TT) (32.1%) vs. (16.3%) Vs. control group. There is significant increase in rs2240688 (TT), rs1029728 (AG) and rs3130 (TT) with smoking in pancreatic cancer group vs. control group. rs3130 (TT) with rs2240688 (TT) gene polymorphisms showed significant increase in pancreatic cancer group group vs. control in male gender only as. According to the age as a demographic variable, mean age for pancreatic cancer group was 61.5 years with percentage of (76.2%) for age more than 50 years vs. (23.8%) for age less than or equal 50 years these. The functional polymorphisms rs3130 (CC) and rs2240688 (CC) were found to be higher in control group vs. pancreatic cancer group that may represent a protective value against the disease.

FTP7.5 Accuracy of the END-PAC model in predicting the risk of developing pancreatic cancer in patients with new-onset diabetes: a systematic review and meta-analysis

Abstract Objectives to evaluate the accuracy of END-PAC model in predicting the risk of pancreatic cancer in patients with new-onset diabetes (NOD). Methods A systematic review in accordance with PRISMA statement standards was conducted to identify all studies evaluating the accuracy of END-PAC model in predicting the risk of pancreatic cancer in patients with NOD. The number of true positives, false negatives, true negatives, and false positives were used to construct two-by-two tables, coupled forest plots and the summary receiver operating characteristic plots. We estimated summary sensitivity and specificity points using diagnostic random effects model. Results We analysed 26752 patients from four studies. The pooled risk of pancreatic cancer was 0.8% (95% CI 0.6%-1.0%) with median follow-up of 3 years. END-PAC score ≥3 [sensitivity: 55.8% (43.9%-67%); specificity: 82.0% (76.4%-86.5%)] which classifies the patients as high risk was associated with better predictive performance than END-PAC score 1–2 [sensitivity: 22.2% (16.6%-29.2%); specificity: 69.9% (67.3%-72.4%)] and END-PAC score &amp;lt;1 [sensitivity: 18.0% (12.8%-24.6%); specificity: 50.9% (48.6%-53.2%)] which classify the patients as intermediate and low risks, respectively. The quality of the available evidence was moderate to high. Conclusions END-PAC model is promising in predicting the risk of pancreatic cancer in patients with new-onset diabetes. END-PAC score ≥3, which classifies the patients as high risk, has the best predictive performance and should be considered as optimum cut-off value. Future comparative studies are required to evaluate whether application of END-PAC model could improve pancreatic cancer early detection rate, pancreatic cancer resection rate, and pancreatic cancer treatment outcomes.