Introduction
Pancreatic cancer is a highly malignant digestive tumor with a five-year survival rate of approximately 13%.1 According to statistics from the National Cancer Center, pancreatic cancer ranks 8th in tumor incidence and 6th in mortality in China,2 mainly due to the difficulty of early diagnosis. Notably, the evolution from pancreatic intraepithelial neoplasia (PanIN) to invasive carcinoma spans approximately 21 years, offering a critical window of opportunity for early detection and intervention.3 This extended premalignant phase underscores the potential of screening to improve outcomes by identifying curable precursor lesions or early-stage disease.
Despite this opportunity, the rate of early diagnosis of pancreatic cancer in China remains considerably lower than that in developed countries, and systematic surveillance programs for high-risk populations have not yet been widely implemented.4 In addition to the recognized benefits of early detection, a growing body of evidence has highlighted the potential harms associated with screening, including overdiagnosis, procedural risks, the psychological burden of long-term surveillance, and the risk of overtreatment.5 These considerations underscore the importance of a balanced approach that weighs benefits against potential harms and accounts for real-world feasibility.
In 2021, the Chinese Consensus on Early Screening and Surveillance for Pancreatic Cancer in High-risk Individuals was established to provide initial guidance for clinical practice in China.6 This consensus aims to integrate published evidence with practical considerations regarding feasibility, resource allocation, and patient-centered care, offering guidance for early screening and surveillance in high-risk populations.
Methods
Overview and rationale
To address the unmet need for standardized guidance on early pancreatic cancer screening in China, the Pancreatic Disease Collaborative Group of the Chinese Society of Digestive Endoscopy convened a multidisciplinary panel of national experts. This consensus was developed following a systematic review of the available evidence and a modified Delphi process.
Panel composition and conflict of interest management
The expert panel comprised 53 specialists in pancreatic disease diagnosis and treatment, representing 17 provincial-level administrative regions across China. The panel included gastroenterologists (n = 45), pancreatic surgeons (n = 6), radiologists (n = 1), and pathologists (n = 1), ensuring broad multidisciplinary input. Prior to participation, all experts completed a standardized disclosure form declaring any potential conflicts of interest (financial or professional) related to the consensus topic. No expert reported a significant conflict requiring recusal from voting, and all disclosures were reviewed by the steering committee. The funding source had no role in the design, conduct, data collection, analysis, or interpretation of this consensus, nor in the writing of the report or the decision to submit the findings for publication.
Evidence identification and appraisal
A systematic literature search was conducted using PubMed, EMBASE, the China National Knowledge Infrastructure, and the China Science Periodical Database. The search strategy combined terms related to pancreatic ductal adenocarcinoma (PDAC), early diagnosis, new-onset diabetes, chronic pancreatitis, cystic pancreatic tumors, familial pancreatic cancer, screening, biomarkers, and risk stratification.
Inclusion criteria were as follows: (1) studies involving human subjects; (2) publications in English or Chinese; and (3) original research articles (randomized controlled trials, cohort studies, case-control studies, or systematic reviews/meta-analyses). Conference abstracts and opinion pieces were excluded. Two independent reviewers screened titles and abstracts, with disagreements resolved by consensus or by a third reviewer. Full-text articles were assessed for eligibility, and data were extracted using a standardized form.
The quality of evidence for each critical outcome was appraised using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) framework, resulting in four certainty levels: high (A), moderate (B), low (C), and very low (D) (Table 1).
Table 1Levels of certainty of evidence
| Certainty of evidence | Definition | Research type |
|---|
| High certainty (A) | The true effect is similar to the estimated effect | RCT; observational study upgraded by 2 levels |
| Moderate certainty (B) | The true effect is likely close to the estimated effect | RCT downgraded by 1 level; observational study upgraded by 1 level |
| Low certainty (C) | The true effect may be substantially different from the estimated effect | RCT downgraded by 2 levels; observational study |
| Very low certainty (D) | The true effect is likely substantially different from the estimated effect | RCT downgraded by 3 levels; observational study downgraded by 1 level; case series and case reports |
Consensus development
A modified Delphi method was employed to achieve consensus on the recommendations. The process comprised the following steps:
Draft preparation: Based on the evidence summary, a writing group from the Department of Gastroenterology at Nanjing Drum Tower Hospital prepared an initial draft of the recommendations and a summary of the supporting literature.
First voting round: An online questionnaire was distributed to all 53 panel members. For each statement, experts were asked: (1) âIs the statement clearly formulated?â (Yes/No); and (2) âDo you agree with the statement?â (Strongly Agree, Agree, Uncertain, Disagree, Strongly Disagree). Experts could abstain from voting on any statement with which they felt unfamiliar. Statements for which >5% of respondents considered the formulation unclear were revised by the writing group.
Second voting round: The revised draft, along with anonymized results from the first round, was circulated to all panel members for a second vote. A total of 27 experts participated in the second round.
Definition of consensus: Consensus was defined a priori as â¥75% agreement (either Strongly Agree + Agree â¥75%, or Strongly Disagree + Disagree â¥75%) among voting members. Statements not reaching this threshold after the second round were either revised based on qualitative feedback or excluded.
Formulation of recommendations
In formulating the final recommendations, the panel considered not only the certainty of the evidence (GRADE) but also the balance between benefits and harms, the burden of interventions on patients, the diversity of patient values and preferences, the costs and rational use of healthcare resources, and the equity and feasibility of implementation in the Chinese healthcare context. Each recommendation was rated as either âstrongâ or âweakâ based on the GRADE framework.7 A strong recommendation indicates that most informed patients would choose the recommended course of action and that the recommendation can be adopted as policy in most circumstances (Table 2). Table 3 summarizes all recommendations along with their evidence strength and recommendation strength.
Table 2Levels of recommendation strength
| Recommendation strength | Definition |
|---|
| Strong | The intervention clearly demonstrates that benefits outweigh harms or harms outweigh benefits |
| Weak | The balance between benefits and harms is uncertain or equivalent |
Table 3Consolidated table of all recommendations
| Recommendations | Certainty of evidence | Recommendation strength |
|---|
| Recommendation 1 | The detection of stage I pancreatic cancer and high-grade PanIN is the goal of early pancreatic cancer screening | A | Strong recommendation |
| Recommendation 2 | Do not screen asymptomatic non-high-risk individuals for pancreatic cancer | C | Weak recommendation |
| Recommendation 3 | Early screening for pancreatic cancer is recommended in the following high-risk populations: individuals at high risk for hereditary pancreatic cancer, patients with new-onset diabetes, patients with chronic pancreatitis, and individuals with pancreatic cystic neoplasms | B | Strong recommendation |
| Recommendation 4 | Early screening for pancreatic cancer is recommended for individuals with a family history of pancreatic cancer, defined as having at least two first-degree relatives affected by pancreatic cancer | B | Strong recommendation |
| Recommendation 5 | Early screening for pancreatic cancer is recommended for all patients with PeutzâJeghers syndrome (germline STK11 pathogenic variant carriers) and all germline CDKN2A pathogenic variant carriers, irrespective of family history of pancreatic cancer | A | Strong recommendation |
| Recommendation 6 | Pancreatic cancer surveillance should be considered for pathogenic variant carriers in BRCA1, BRCA2, PALB2, ATM, MLH1, MSH2, or MSH6 who have at least one first-degree relative affected by pancreatic cancer | â* | â* |
| Recommendation 7 | Early screening for pancreatic cancer is recommended in patients with new-onset diabetes who are over 50 years of age and present with a BMI below 25 kg/m2 and/or unexplained weight loss exceeding 3.6 kg within 2 years | B | Weak recommendation |
| Recommendation 8 | Early screening for pancreatic cancer is recommended in individuals with new-onset diabetes who are at high risk for hereditary pancreatic cancer, irrespective of age | C | Weak recommendation |
| Recommendation 9 | Early screening for pancreatic cancer is recommended for patients with hereditary chronic pancreatitis who carry PRSS1 mutations. It is not recommended for those with hereditary chronic pancreatitis due to other genetic mutations or for patients with sporadic chronic pancreatitis | C | Weak recommendation |
| Recommendation 10 | For patients with chronic pancreatitis of unknown etiology, gene mutation testing, especially PRSS1 mutation testing, is recommended | C | Weak recommendation |
| Recommendation 11 | Patients with BD-IPMN should undergo pancreatic cancer screening upon diagnosis. Patients with MCN, SPN, cNET, MD-IPMN, or MT-IPMN should be referred for MDT discussion and considered for elective surgical resection | C | Weak recommendation |
| Recommendation 12 | For individuals with a family history of pancreatic cancer, screening should begin at age 50 or 10 years younger than the age at diagnosis of the youngest affected first-degree relative, whichever is earlier. For those with PeutzâJeghers syndrome, screening is recommended to start at age 35. CDKN2A mutation carriers should begin screening at age 40. For carriers of pathogenic variants in BRCA1, BRCA2, PALB2, ATM, MLH1, MSH2, or MSH6 who also have an affected first-degree relative, the starting age is 50 or 10 years earlier than the youngest affected relative, whichever comes first | â* | â* |
| Recommendation 13 | For patients with new-onset diabetes who meet the criteria for monitoring, enrollment in a surveillance program is recommended immediately following diagnosis | C | Weak recommendation |
| Recommendation 14 | For patients with chronic pancreatitis who meet the criteria for monitoring, screening for pancreatic cancer should begin at age 40 | C | Weak recommendation |
| Recommendation 15 | For BD-IPMN, early screening for pancreatic cancer should be initiated immediately following diagnosis, irrespective of age at diagnosis | C | Weak recommendation |
| Recommendation 16 | For high-risk individuals undergoing surveillance, the interval should be 12 months in the absence of pancreatic abnormalities. The interval may be shortened to 3â6 months if any of the following is present: (1) a solid lesion <10 mm or a suspected solid lesion; (2) a main pancreatic duct diameter of 5â9.9 mm; or (3) in the absence of a definite solid lesion, focal main pancreatic duct stricture or focal dilation â¥6 mm. These criteria are not mutually exclusive | â* | â* |
| Recommendation 17 | For patients with BD-IPMN without worrisome features, surveillance intervals are determined by cyst size: 12 months for cysts <2 cm and 6 months for cysts 2â3 cm. If worrisome features develop, including new-onset diabetes, recurrent IPMN-related pancreatitis, cyst â¥3 cm, enhancing mural nodules <5 mm, thickened cyst walls, main pancreatic duct 5â9.9 mm, duct changes with distal atrophy, elevated CA19-9, rapid growth (>5 mm/2 years), or lymphadenopathy, the interval should be shortened to 3â6 months. These features constitute relative indications for surgery, which may be undertaken after multidisciplinary discussion and consideration of patient preferences | B | Strong recommendation |
| Recommendation 18 | Postoperative surveillance should be individualized according to the resected lesion, pathological findings, residual pancreatic abnormalities, and whether the patient is fit for additional treatment. No single surveillance schedule should be applied to all postoperative patients | â* | â* |
| Recommendation 19 | For initial assessment, fasting blood glucose and/or HbA1c and pancreatic imaging with MRI/MRCP and/or EUS are recommended; CT may be used when clinically indicated. Serum CA19-9 should not be used as a stand-alone screening test and may be considered as an adjunct when clinical or imaging findings are concerning | â* | â* |
| Recommendation 20 | During follow-up, fasting blood glucose and/or HbA1c and imaging with MRI/MRCP and/or EUS should be monitored; CT may be used when clinically indicated. CA19-9 may be used as an adjunct when suspicious clinical or imaging findings are present. Pancreatoscopy may be considered selectively at experienced centers when conventional imaging and EUS are inconclusive, main pancreatic duct involvement remains suspected, and the result is expected to change management; it is not recommended routinely for all patients with IPMN | â* | â* |
| Recommendation 21 | During follow-up, EUS-guided tissue acquisition may be considered for a solid pancreatic lesion or a cystic lesion with worrisome features or high-risk stigmata when tissue diagnosis is expected to change management. In an asymptomatic main pancreatic duct stricture without a definite mass, EUS-FNA should not be automatic; further evaluation should be individualized at an experienced center | â* | â* |
| Recommendation 22 | For patients in whom EUS-FNA pathology results are malignant or suspicious for malignancy, scheduled surgical resection is strongly recommended after MDT discussion | A | Strong recommendation |
| Recommendation 23 | For patients with a solid lesion >10 mm in diameter or main pancreatic duct narrowing or dilation â¥10 mm whose lesion nature cannot be definitively determined by EUS-FNA, MDT discussion and surgical exploration are recommended to clarify the diagnosis, with resection performed if indicated | B | Strong recommendation |
| Recommendation 24 | For patients with BD-IPMN with high-risk stigmata, including a solid lesion, tumor-related obstructive jaundice, enhancing mural nodules â¥5 mm, or a main pancreatic duct â¥10 mm, surgical resection is recommended following MDT discussion | B | Strong recommendation |
| Recommendation 25 | Patients are advised to stop smoking, avoid excessive alcohol consumption, maintain a balanced diet and healthy body weight, and engage in regular physical activity | â* | â* |
| Recommendation 26 | Pancreatic cancer monitoring for the four high-risk populations that meet the screening criteria should be conducted at pancreatic specialty centers | C | Strong recommendation |
Results
Recommendation 1: The detection of stage I pancreatic cancer and high-grade PanIN is the goal of early pancreatic cancer screening. (Certainty of evidence: A; Recommendation strength: Strong recommendation)
Goals of early screening for pancreatic cancer
Stage I pancreatic cancer is defined as disease confined to the pancreas, with a maximum tumor diameter â¤4 cm and no evidence of lymph node or distant metastasis. These tumors are considered resectable, and radical resection followed by adjuvant chemotherapy has been shown to significantly improve overall survival.8 Prospective cohort studies have demonstrated that the majority of pancreatic cancers detected through surveillance of high-risk individuals are resectable at diagnosis.9â11 These findings underscore early screening as a key strategy to enhance both survival and cure rates for pancreatic cancer.12
PanIN represents a well-established precursor lesion of pancreatic cancer.13 Whole-genome sequencing also demonstrates substantial genetic heterogeneity among familial pancreatic cancers.14 Clinicopathological studies show that high-grade PanIN is more strongly associated with invasive PDAC than low-grade PanIN.15 In contrast, low-grade PanIN at the pancreatic transection margin did not adversely affect outcomes after R0 resection in one cohort.16 Under the current binary classification, PanIN is categorized as low-grade or high-grade.17 Accordingly, high-grade PanIN, rather than low-grade PanIN, is a principal precursor target for early detection.
Target groups for early screening of pancreatic cancer
Recommendation 2: Do not screen asymptomatic non-high-risk individuals for pancreatic cancer. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
Recommendation 3: Early screening for pancreatic cancer is recommended in the following high-risk populations: individuals at high risk for hereditary pancreatic cancer, patients with new-onset diabetes, patients with chronic pancreatitis, and individuals with pancreatic cystic neoplasms. (Certainty of evidence: B; Recommendation strength: Strong recommendation) The incidence of pancreatic cancer is not high in China, with an annual incidence of approximately 8.41/100,000.4 There are currently no reports on the benefits of pancreatic cancer screening in the general population. Early pancreatic cancer screening may increase the psychological burden on screened populations.18 Therefore, based on cost-effectiveness considerations, pancreatic cancer screening is not recommended for asymptomatic, non-high-risk individuals.
Several well-established risk factors are associated with an increased risk of pancreatic cancer, including hereditary susceptibility,19 new-onset diabetes mellitus,20,21 chronic pancreatitis,22,23 and pancreatic cystic neoplasms.24â26 Because pancreatic cancer is uncommon in the general population, risk-enriched surveillance is generally considered more feasible than population-wide screening.27
Individuals at high risk for hereditary pancreatic cancer
Recommendation 4: Early screening for pancreatic cancer is recommended for individuals with a family history of pancreatic cancer, defined as having at least two first-degree relatives affected by pancreatic cancer. (Certainty of evidence: B; Recommendation strength: Strong recommendation)
Recommendation 5: Early screening for pancreatic cancer is recommended for all patients with PeutzâJeghers syndrome (germline STK11 pathogenic variant carriers) and all germline CDKN2A pathogenic variant carriers, irrespective of family history of pancreatic cancer. (Certainty of evidence: A; Recommendation strength: Strong recommendation)
Recommendation 6 (editorially updated): Pancreatic cancer surveillance should be considered for pathogenic variant carriers in BRCA1, BRCA2, PALB2, ATM, MLH1, MSH2, or MSH6 who have at least one first-degree relative affected by pancreatic cancer. Individuals at high risk for hereditary pancreatic cancer include those with a qualifying family history or a germline pathogenic variant in a recognized pancreatic cancer susceptibility gene.10 Familial pancreatic cancer is commonly defined by at least two affected first-degree relatives in the same kindred.28 Registry data show that risk increases with the number and closeness of affected relatives and with younger age at diagnosis.28â31
Several genetic syndromes have also been linked to an increased risk of pancreatic cancer. Patients with PeutzâJeghers syndrome (STK11 gene mutation carriers) have a 132-fold increased risk of developing pancreatic cancer compared with the general population, with a mean age at onset of 40.8 years.32 Germline CDKN2A pathogenic variant carriers face a 13- to 39-fold increased risk.33,34 Long-term follow-up of high-risk individuals has confirmed a higher detection rate of pancreatic cancer among carriers of these high-risk gene mutations.10 Therefore, this consensus recommends early screening for pancreatic cancer for all patients with PeutzâJeghers syndrome and CDKN2A pathogenic variant carriers, regardless of family history.
Clinical studies have evaluated pancreatic cancer risk associated with BRCA1, BRCA2, PALB2, ATM, MLH1, MSH2, and MSH6 (Table 4).32â41 The magnitude of risk varies across genes: BRCA1/2 and PALB2 carriers have an approximately 2- to 9-fold increased risk;38â40 ATM carriers have an estimated 6.5-fold increased risk;41 and mismatch repair gene carriers have also shown increased risk.36 The original consensus included APC carriers in surveillance eligibility. However, a 2025 competing-risk analysis of 1,357 adults with familial adenomatous polyposis estimated a cumulative PDAC risk of 0.7% by age 70 (95% CI, 0.3â1.8) and an RR of 2.2 (95% CI, 0.9â5.7), below the commonly used 5% surveillance threshold; surveillance solely on the basis of APC/FAP was therefore not recommended.42 A recent Chinese cohort found pathogenic or likely pathogenic germline variants in 9.3% of unselected pancreatic cancer patients, with therapeutically relevant variants in 5.2%, predominantly involving homologous-recombination genes.43 Family history remains a risk modifier, although a multicenter study found that most pathogenic-variant carriers who developed PDAC did not have an affected first- or second-degree relative.44
Table 4Risk of pancreatic cancer for carriers of specific gene mutations
| Gene mutations | Representative diseases | Risk of pancreatic cancer |
|---|
| STK11 | Peutz-Jeghers syndrome | RR = 132 (95% CI, 44â261)32 |
| CDKN2A | Familial atypical multiple mole melanoma syndrome | RR = 13â3933,34 |
| BRCA1, BRCA2 | Hereditary breast and ovarian cancer syndrome | RR = 2â938,40 |
| PALB2 | Fanconi anemia | RR = 2.37 (95% CI, 1.24â4.50)39 |
| ATM | Ataxia-telangiectasia | RR = 6.5 (95% CI, 4.5â9.5)41 |
| MLH1, MSH2, MSH6 | Lynch syndrome | HR = 8.6 (95% CI, 4.7â15.7)36 |
| APC | Familial adenomatous polyposis | Cumulative risk by age 70 = 0.7% (95% CI, 0.3â1.8); RR = 2.2 (95% CI, 0.9â5.7)42 |
New-onset diabetes
Recommendation 7: Early screening for pancreatic cancer is recommended in patients with new-onset diabetes who are over 50 years of age and present with a BMI below 25 kg/m2 and/or unexplained weight loss exceeding 3.6 kg within 2 years. (Certainty of evidence: B; Recommendation strength: Weak recommendation)
Recommendation 8: Early screening for pancreatic cancer is recommended in individuals with new-onset diabetes who are at high risk for hereditary pancreatic cancer, irrespective of age. (Certainty of evidence: C; Recommendation strength: Weak recommendation) A growing body of evidence indicates that new-onset diabetes can be an early manifestation of occult pancreatic cancer. Prospective cohort protocols have emphasized standardized ascertainment of incident diabetes.45 In the absence of unequivocal hyperglycemia, current clinical standards require confirmatory testing rather than diagnosis from a single abnormal HbA1c or fasting plasma glucose result.46 The cited 2026 prospective cohort instead used a study-specific operational definition of glycemically defined new-onset diabetes: a recent diabetes-range HbA1c or fasting plasma glucose result, a preceding measurement within two years below the diabetes threshold, and no prior diagnosis or treatment.47 In 18,838 participants meeting that operational definition, the 3-year cumulative incidence of pancreatic cancer was 0.62% after race adjustment, and diabetes preceded clinical cancer diagnosis by an average of eight months.47 Delayed recognition of incident hyperglycemia can bias estimates of this association.47,48
While screening all patients with new-onset diabetes for pancreatic cancer is limited by low absolute risk and unfavorable cost-effectiveness, additional risk factors can enrich the population selected for assessment. Patients over 50 years of age with new-onset diabetes have an increased risk of sporadic pancreatic cancer,49 with approximately 0.85% diagnosed within three years in one population-based study.21 Declining BMI or unexplained weight loss can further stratify risk.20,50 In a large population-based study, unintentional weight loss exceeding 3.6 kg within two years was associated with increased pancreatic cancer risk (HR = 6.75), particularly when pre-weight-loss BMI was below 25 kg/m2.51 The END-PAC model combines age, change in body weight, and change in glycemia to identify patients at higher risk.52 A systematic review and meta-analysis of four validation studies (26,752 participants) found that an END-PAC score â¥3 had pooled sensitivity of 55.8% (95% CI, 43.9â67.0) and specificity of 82.0% (95% CI, 76.4â86.5); the authors nevertheless called for further outcome studies.53 A separate Hong Kong cohort model that incorporated acute pancreatitis, medication use, and laboratory variables achieved AUCs of 0.90 for 1-year risk and 0.81 for 3-year risk.54
A prospective study following individuals at high risk for hereditary pancreatic cancer who were screened for pancreatic cancer found that 20% of these screened high-risk individuals had abnormal fasting glucose, and one patient was diagnosed with new-onset diabetes.55 If a patient has a family history of pancreatic cancer, a history of diabetes, and a history of smoking, the risk of developing pancreatic cancer is more than 10 times that of the general population.56 Therefore, this consensus recommends that patients with new-onset diabetes among individuals at high risk for hereditary pancreatic cancer should undergo early screening for pancreatic cancer.
Chronic pancreatitis
Recommendation 9: Early screening for pancreatic cancer is recommended for patients with hereditary chronic pancreatitis who carry PRSS1 mutations. It is not recommended for those with hereditary chronic pancreatitis caused by other genetic mutations or for patients with sporadic chronic pancreatitis. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
Recommendation 10: For patients with chronic pancreatitis of unknown etiology, genetic mutation testing, especially PRSS1 mutation testing, is recommended. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
Chronic pancreatitis is an inflammatory process in which the pancreatic parenchyma is gradually replaced by fibrous tissue, causing irreversible changes in pancreatic function and morphology.57 For patients with chronic pancreatitis, the risk of developing pancreatic cancer is approximately seven times that of unaffected individuals.58,59 A multicenter retrospective study initiated by the Chinese Chronic Pancreatitis Research Group found that the prevalence of chronic pancreatitis increased year by year from 1996 to 2003, rising from 3.08 to 13.52 per 100,000 population,60 which is consistent with trends observed in Western countries.57 Patients with chronic pancreatitis in China are mainly idiopathic (76.6%), followed by alcoholic (18.8%), abnormal pancreatic duct anatomy (2.9%), and hereditary (1.2%) etiologies.61 Pancreatic inflammation and injury can drive acinar-to-ductal metaplasia and gradually progress to pancreatic cancer.23 A large 1993 multicenter cohort study of 1,552 patients with chronic pancreatitis across six countries reported cumulative pancreatic cancer risks of 1.8% at 10 years and 4% at 20 years.62 In the Chinese population, the cumulative incidence rates were 0.6%, 1.0%, and 1.3% at 3, 5, and 10 years, respectively.63,64 Notably, an episode of acute pancreatitis, regardless of etiology, significantly increases the risk of pancreatic cancer within 3â10 years,65 and when acute pancreatitis is the initial presentation of pancreatic cancer, it often manifests as mild or recurrent episodes.66 The risk rises with increasing frequency of acute pancreatitis episodes and is further amplified in the presence of chronic pancreatitis.65 In addition, new-onset diabetes in patients with chronic pancreatitis is an important warning sign. Such diabetes may precede pancreatic cancer, with a particularly high carcinogenic risk in elderly patients presenting with sudden weight loss and severe hyperglycemia.58,67 Given these associations, chronic pancreatitis should be considered a high-risk condition warranting inclusion in early pancreatic cancer screening programs.
Alcohol exposure and smoking are important non-genetic contributors to chronic pancreatitis.68 Hereditary pancreatitis is rare, with an estimated prevalence of 0.13â0.57 per 100,000 individuals.69,70 In China, hereditary disease accounted for approximately 1.2% of chronic pancreatitis etiologies in one multicenter series.61 It is characterized by earlier onset and a substantially higher pancreatic cancer risk than many other etiologies. It follows an autosomal dominant inheritance pattern, commonly involving functional PRSS1 variants such as p.R122H and p.N29I.71 Among PRSS1 mutation carriers, cumulative pancreatic cancer risk has been estimated at 44% within 70 years after symptom onset.22 Hereditary pancreatitis should be considered when chronic pancreatitis is familial or remains unexplained after routine evaluation; genetic testing, particularly for PRSS1, may then be appropriate.72
Approximately 51.4% of patients with chronic pancreatitis carry susceptibility gene mutations.73 In addition to PRSS1, these include chymotrypsin C (CTRC),74 cystic fibrosis transmembrane conductance regulator (CFTR),75 carboxypeptidase A1 (CPA1),76 and serine protease inhibitor Kazal type 1 (SPINK1),77 all of which are strongly associated with early-onset chronic pancreatitis. A recent study identified SEC16A as a susceptibility gene for chronic pancreatitis in Chinese patients. Carriers of SEC16A variants developed chronic pancreatitis approximately five years earlier than noncarriers, a predisposition mediated by disrupted ER-to-Golgi transport and ER stress.78 In addition, the carboxyl ester lipase (CEL)-HYB hybrid gene was recently identified as a risk factor for chronic pancreatitis,79 but CEL-HYB and CPA1 do not appear to contribute to disease susceptibility in Asian populations.80,81 A prospective study in a Chinese cohort showed that among patients with chronic pancreatitis, SPINK1 mutation carriers did not have an increased risk of pancreatic cancer compared with noncarriers.64 Currently, aside from PRSS1, there is insufficient evidence linking other susceptibility genes, including SPINK1, CFTR, CTRC, CPA1, SEC16A, and CEL-HYB, to pancreatic cancer risk.82,83 Therefore, routine pancreatic cancer screening is not recommended for patients carrying mutations in these genes.
Pancreatic cystic tumors
Recommendation 11: Patients with branch duct (BD)-intraductal papillary mucinous neoplasms (IPMN) should undergo pancreatic cancer screening upon diagnosis. Patients with mucinous cystic neoplasms (MCN), solid pseudopapillary neoplasms (SPN), cystic neuroendocrine tumors (cNET), main duct (MD)-IPMN, or mixed type (MT)-IPMN should be referred for multidisciplinary team (MDT) discussion and considered for elective surgical resection. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
With widespread imaging, incidental pancreatic cysts are increasingly detected, particularly in older adults.84,85 Patients with pancreatic cystic lesions have a higher pancreatic cancer risk than the general population in longitudinal studies.24,26 Malignant potential varies substantially by histological type.86 Mucin-producing pancreatic cystic neoplasms, principally IPMN and MCN, carry clinically important malignant potential.25 IPMN may progress to invasive carcinoma or coexist with a conventional PDAC elsewhere in the pancreas.87 IPMN is classified as main-duct, branch-duct, or mixed-type disease.86 Reported malignancy risk is higher for main-duct and mixed-type IPMN than for branch-duct IPMN, although estimates vary among studies.88 SPN and cystic neuroendocrine tumors also have malignant potential,89 whereas serous cystadenomas and several other nonmucinous cysts usually require intervention only when symptoms, diagnostic uncertainty, or other clinical concerns arise.90
Given the variable malignant potential of pancreatic cystic lesions, management should be lesion-specific and should integrate imaging features, symptoms, surgical fitness, life expectancy, and patient preferences. Domestic and international guidelines support surveillance for BD-IPMN and multidisciplinary evaluation of MCN, SPN, cystic neuroendocrine tumors, main-duct IPMN, and mixed-type IPMN; resection should follow lesion-specific criteria rather than diagnosis alone.91â94 Because accurate subtyping may be difficult, evaluation at a center with pancreatic multidisciplinary expertise is appropriate when diagnosis or management remains uncertain.
Starting age for early screening of pancreatic cancer
Recommendation 12 (editorially updated): For individuals with a family history of pancreatic cancer, screening should begin at age 50 or 10 years younger than the age at diagnosis of the youngest affected first-degree relative, whichever is earlier. For those with PeutzâJeghers syndrome, screening is recommended to start at age 35. CDKN2A mutation carriers should begin screening at age 40. For carriers of pathogenic variants in BRCA1, BRCA2, PALB2, ATM, MLH1, MSH2, or MSH6 who also have an affected first-degree relative, the starting age is 50 or 10 years earlier than the youngest affected relative, whichever comes first.
Recommendation 13: For patients with new-onset diabetes who meet the criteria for monitoring, enrollment in a surveillance program is recommended immediately following diagnosis. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
Recommendation 14: For patients with chronic pancreatitis who meet the criteria for monitoring, screening for pancreatic cancer should begin at age 40. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
Recommendation 15: For BD-IPMN, early screening for pancreatic cancer should be initiated immediately following diagnosis, irrespective of age at diagnosis. (Certainty of evidence: C; Recommendation strength: Weak recommendation)
For individuals with a family history of pancreatic cancer (without known susceptibility gene mutations), most cases are diagnosed after the age of 55, although the average age at diagnosis is earlier than that of individuals without a family history.9,35,95 Some experts suggest that screening for this group can begin at age 55.19 For individuals with CDKN2A mutations or PeutzâJeghers syndrome, the average age at pancreatic cancer diagnosis is even younger. Among CDKN2A mutation carriers, 16% are diagnosed before age 45, while patients with PeutzâJeghers syndrome are typically diagnosed in their 30s to 40s.28 Long-term surveillance of high-risk individuals has revealed a cumulative incidence of pancreatic cancer of 9.3% in susceptibility gene mutation carriers, including CDKN2A, LKB1/STK11, BRCA2, BRCA1, PALB2, TP53, MLH1, MSH2, MSH6, and ATM, with a median age at diagnosis of 61 years (range: 50â78 years).10
Several prospective cohort studies have confirmed that new-onset diabetes is an early manifestation of pancreatic cancer, with over 25% of patients developing new-onset diabetes within 1â3 years prior to cancer diagnosis.96,97 Studies have shown that the median latency from new-onset diabetes to clinical diagnosis of pancreatic cancer is 8.1 months, with 30.5% of patients diagnosed within 0â4 months and 31.3% within 4â12 months following diagnosis of new-onset diabetes.47 The median delay from onset of new-onset diabetes to clinical diagnosis is 6.5 months, and approximately 33% of cases remain unrecognized prior to the diagnosis of pancreatic cancer.96
For patients with chronic pancreatitis, the current international consensus is to start pancreatic cancer screening after age 40, particularly for those with PRSS1 mutations.98 One study found that among 402 chronic pancreatitis patients, 5 developed pancreatic cancer, with an average age at diagnosis of 50.9 ± 10.1 years.99 Another study involving 581 chronic pancreatitis patients identified six cases of pancreatic cancer, with an average interval of approximately 5.0 years from chronic pancreatitis diagnosis to pancreatic cancer diagnosis.100 According to the European Registry of Hereditary Pancreatitis and Pancreatic Cancer study, 26 of 418 cases (6%) in a cohort of hereditary pancreatitis patients were diagnosed with pancreatic cancer, and risk increased from age 40.22 A follow-up study of 497 hereditary pancreatitis patients found that 19 developed pancreatic cancer, with only 3 cases occurring before age 40, all of whom were smokers.101 These findings suggest that there is limited benefit in conducting pancreatic cancer screening in chronic pancreatitis patients younger than 40 years, and therefore screening is not recommended in this age group.
Large cohort studies have demonstrated that BD-IPMNs carry a measurable risk of malignant progression that warrants surveillance from the time of diagnosis. A competing risk analysis of 926 presumed BD-IPMNs without worrisome features or high-risk stigmata found a 5-year cumulative incidence of relevant changes (including development of worrisome features, high-risk stigmata, or pancreatic malignancy) of 17.83%, with 1.6% developing pancreatic malignancy during follow-up.102 Importantly, while age and comorbidities significantly influence competing mortality risks, malignant potential exists across all age groups, supporting surveillance initiation at diagnosis regardless of age. Another long-term cohort study demonstrated that the risk of progression to worrisome features or high-risk stigmata is evident at 1 year (3.7%), with cumulative rates reaching 23.4% at 5 years and 43.3% at 10 years after diagnosis.103
Follow-up intervals for individuals at high risk for pancreatic cancer
Recommendation 16 (editorially clarified): For high-risk individuals undergoing surveillance, the interval should be 12 months in the absence of pancreatic abnormalities. The interval may be shortened to 3â6 months if any of the following is present: (1) a solid lesion <10 mm or a suspected solid lesion; (2) a main pancreatic duct diameter of 5â9.9 mm; or (3) in the absence of a definite solid lesion, focal main pancreatic duct stricture or focal dilation â¥6 mm. These criteria are not mutually exclusive. CAPS, AGA, and ASGE guidance generally supports annual surveillance when no concerning pancreatic abnormality is present, with shorter intervals determined by the type and severity of an abnormal finding.19,28,104 For chronic pancreatitis, international guidance limits surveillance to selected hereditary pancreatitis populations and specialist centers and does not establish a single interval for all chronic pancreatitis patients.98
Recommendation 17: For patients with BD-IPMN without worrisome features, surveillance intervals are determined by cyst size: 12 months for cysts <2 cm and 6 months for cysts 2â3 cm. If worrisome features develop, including new-onset diabetes, recurrent IPMN-related pancreatitis, cyst â¥3 cm, enhancing mural nodules <5 mm, thickened cyst walls, main pancreatic duct dilation of 5â9.9 mm, ductal changes with distal atrophy, elevated carbohydrate antigen 19â9 (CA19-9), rapid growth (>5 mm/2 years), or lymphadenopathy, the interval should be shortened to 3â6 months. These features constitute relative indications for surgery, which may be undertaken after multidisciplinary discussion and consideration of patient preferences. (Certainty of evidence: B; Recommendation strength: Strong recommendation)
Recommendation 18 (editorially updated): Postoperative surveillance should be individualized according to the resected lesion, pathological findings, residual pancreatic abnormalities, and whether the patient is fit for additional treatment. No single surveillance schedule should be applied to all postoperative patients.
The follow-up strategy for BD-IPMN remains controversial. Existing guidelines define worrisome features and high-risk stigmata.91â94,105 Worrisome features include new-onset diabetes, recurrent pancreatitis caused by IPMN, cyst diameter â¥3 cm, enhancing mural nodules <5 mm, thickened or enhancing cyst walls, main pancreatic duct diameter of 5â9.9 mm, ductal caliber changes with distal pancreatic atrophy, elevated CA19-9, cyst growth >5 mm over 2 years, and lymph node enlargement. High-risk stigmata include obstructive jaundice, enhancing mural nodules â¥5 mm, main pancreatic duct diameter â¥10 mm, and malignant or suspicious cytology on endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA). For BD-IPMN patients, the presence of worrisome features warrants close surveillance at 3â6 month intervals. These features are considered relative surgical indications, and elective resection may be considered after MDT discussion and integration of patient preferences. In contrast, high-risk stigmata constitute absolute surgical indications, and surgery is recommended following MDT evaluation. For patients with cysts <3 cm and no worrisome features or high-risk stigmata, surveillance should be stratified by cyst size: 12-month intervals for cysts <2 cm and 6-month intervals for cysts measuring 2â3 cm.106 Surveillance should be guided by cyst size and morphological changes observed during the initial 6-month follow-up. For patients with small cysts (<20 mm) without morphological changes during the first 5 years, discontinuation of surveillance may be considered in those who are not surgical candidates or whose life expectancy is â¤10 years.107 In patients with presumed BD-IPMN without worrisome features or high-risk stigmata, the risk of pancreatic malignancy after 5 years of stable surveillance is comparable to that of the general population, adjusted for cyst size and age. Discontinuation of surveillance may be justified in individuals aged >75 years with cysts <30 mm, as well as those aged â¥65 years with cysts â¤15 mm, provided stability is maintained over the initial 5-year follow-up period.108
Postoperative surveillance recommendations differ by lesion and guideline. For pancreatic cystic neoplasms, the AGA advises against routine surveillance after resection when high-grade dysplasia or malignancy is absent, whereas European guidance recommends pathology- and lesion-specific follow-up after IPMN resection.92,93 Reviews of premalignant pancreatic cystic lesions likewise emphasize individualized management rather than a uniform postoperative schedule.109 After resection of pancreatic adenocarcinoma, observational evidence suggests that routine imaging follow-up may be associated with longer overall survival than symptom-triggered follow-up in patients eligible for further treatment; this finding should not be generalized to other pathologies.110 The cited literature does not establish twice-yearly CA19-9 and imaging for a low-grade PanIN margin as a universal standard.
Screening modalities for pancreatic cancer in high-risk individuals
Recommendation 19 (editorially updated): For initial assessment, fasting blood glucose and/or HbA1c and pancreatic imaging with MRI/MRCP and/or EUS are recommended; CT may be used when clinically indicated. Serum CA19-9 should not be used as a stand-alone screening test and may be considered as an adjunct when clinical or imaging findings are concerning.
Recommendation 20 (editorially updated): During follow-up, fasting blood glucose and/or HbA1c and imaging with MRI/MRCP and/or EUS should be monitored; CT may be used when clinically indicated. CA19-9 may be used as an adjunct when suspicious clinical or imaging findings are present. Pancreatoscopy may be considered selectively at experienced centers when conventional imaging and EUS are inconclusive, main pancreatic duct involvement remains suspected, and the result is expected to change management; it is not recommended routinely for all patients with IPMN.
Recommendation 21 (editorially updated): During follow-up, EUS-guided tissue acquisition may be considered for a solid pancreatic lesion or a cystic lesion with worrisome features or high-risk stigmata when tissue diagnosis is expected to change management. In an asymptomatic main pancreatic duct stricture without a definite mass, EUS-FNA should not be automatic; further evaluation should be individualized at an experienced center. High-risk individuals undergoing assessment should have fasting blood glucose and/or HbA1c measured, with subsequent monitoring of glycemia and body weight. Longitudinal glycemic changes and elevated HbA1c are associated with pancreatic cancer risk and may contribute to risk assessment.111â114 A systematic review found a linear doseâresponse association between fasting blood glucose and pancreatic cancer incidence.115 CA19-9 may rise before clinical diagnosis, but its limitations preclude use as a stand-alone screening test.116 It may be considered as an adjunct to clinical and imaging assessment when findings are concerning.117
CT, MRI/MRCP, and EUS have complementary roles in pancreatic surveillance. CT is widely available and useful for detecting masses, vascular involvement, and metastatic disease, but it involves ionizing radiation and is less suited to repeated surveillance or detection of some small lesions than MRI and EUS.118â123 Prospective surveillance studies show that EUS and MRI detect complementary pancreatic abnormalities in high-risk individuals.124,125 Long-term BD-IPMN cohorts further show that imaging decisions should account for lesion progression risk over time.126 EUS provides high-resolution assessment of features associated with malignancy, including mural nodules, solid components, and main pancreatic duct abnormalities.88,127 Contrast-enhanced EUS can improve characterization of mural nodules and other suspicious IPMN features.128 Compared with MRI/MRCP, EUS is particularly sensitive for small solid lesions.10,129 When high-grade dysplasia or invasive carcinoma is suspected in IPMN, EUS and selective tissue acquisition may be appropriate at experienced centers.130 Operator dependence remains an important limitation of EUS.131
MRI/MRCP and/or EUS are generally preferred for surveillance because MRI avoids ionizing radiation and characterizes pancreatic parenchyma, ducts, and cysts, while EUS is sensitive for small solid lesions.19,28,104 CT is an alternative or complementary modality when MRI is contraindicated or unavailable, when rapid imaging is required, or for staging, vascular assessment, and preoperative planning. EUS is useful for characterizing suspected lesions, evaluating duct strictures or dilation, and guiding tissue acquisition when the result is expected to alter management. EUS-guided sampling methods have been evaluated for selected solid and cystic lesions.132â134 Cyst-fluid carcinoembryonic antigen and amylase may aid cyst characterization,135,136 and KRAS/GNAS analysis can support identification of mucinous lesions, particularly IPMN.137
Many high-risk individuals who meet pancreatic surveillance criteria, particularly germline-variant carriers, may also require syndrome-specific surveillance for other malignancies. In younger patients with familial or otherwise unexplained chronic pancreatitis, genetic evaluation may be appropriate.71,72 Detecting early pancreatic cancer in patients with unexplained duct stenosis but no definite solid lesion remains challenging. In selected cases, ERCP with pancreatic juice cytology may provide additional diagnostic information.138
Repeated pancreatic juice cytology via endoscopic nasopancreatic drainage has reported sensitivities of 80â100% in selected diagnostic cohorts.139,140 Japanese guidance and clinical studies support serial pancreatic juice cytology as an option in carefully selected patients with ductal abnormalities suspicious for early disease; sampling via the minor papilla has also been described in patients with pancreas divisum.141,142 Pancreatoscopy permits direct visualization and targeted biopsy of suspicious ductal lesions,143,144 and a systematic review found that diagnostic yield may improve when direct visualization is combined with pancreatoscopy-guided biopsy.145 Evidence for assessing main-duct involvement in mixed-type IPMN remains limited.146 Pancreatoscopy should therefore be reserved for experienced centers when CT, MRCP, and EUS are inconclusive and the result is expected to change management. A case report illustrates potential utility for a rare intraductal lesion but does not support routine use.147
Surgical indications for high-risk population of pancreatic cancer
Recommendation 22: For patients with malignant or suspicious EUS-FNA pathology, scheduled surgical resection is strongly recommended after MDT discussion. (Certainty of evidence: A; Recommendation strength: Strong recommendation)
Recommendation 23: For patients with a solid lesion >10 mm or main pancreatic duct narrowing or dilation â¥10 mm, in whom lesion nature cannot be definitively determined by EUS-FNA, MDT discussion and surgical exploration are recommended to clarify the diagnosis, with resection performed if indicated. (Certainty of evidence: B; Recommendation strength: Strong recommendation)
Recommendation 24: For patients with BD-IPMN with high-risk stigmata, including a solid lesion, tumor-related obstructive jaundice, enhancing mural nodules â¥5 mm, or a main pancreatic duct â¥10 mm, surgical resection is recommended following MDT discussion. (Certainty of evidence: B; Recommendation strength: Strong recommendation) Surgical decisions should incorporate staging, resectability, comorbidities, operative risk, life expectancy, and patient preferences.130 Malignant or suspicious cytology should be reported using standardized pancreatobiliary terminology and interpreted in its clinical and imaging context.148 A malignant or suspicious result should prompt multidisciplinary review, confirmation where appropriate, and assessment of fitness and resectability before surgery. When a solid lesion or duct abnormality remains indeterminate after EUS-guided sampling, repeat or alternative diagnostic evaluation and staging should precede consideration of surgical exploration. Management of SPN, cystic neuroendocrine tumor, MCN, main-duct IPMN, and mixed-type IPMN should follow lesion-specific criteria rather than diagnosis alone.94 For main-duct or mixed-type IPMN without enhancing mural nodules and with a main pancreatic duct <10 mm, surveillance rather than immediate surgery may be reasonable in selected patients.149 For BD-IPMN, high-risk stigmata generally support resection after multidisciplinary assessment.92,93,150
In addition to absolute indications, relative surgical indications may also warrant intervention in selected cases. These include worrisome features such as main pancreatic duct dilation of 5â9 mm, cyst growth >5 mm over two years, enhancing mural nodules <5 mm, or thickened/enhancing cyst walls. In such cases, surgery should be considered, particularly when recurrent symptoms such as pancreatitis affect quality of life or in younger patients with multiple worrisome features. Decisions should be made following MDT discussion. The decision-making flowchart for the management of high-risk individuals for pancreatic cancer is shown in Figure 1.
Recommendations for lifestyle habits in the high-risk population for pancreatic cancer
Recommendation 25 (editorially clarified): Patients are advised to stop smoking, avoid excessive alcohol consumption, maintain a balanced diet and healthy body weight, and engage in regular physical activity. Smoking is associated with increased pancreatic cancer risk and earlier cancer onset in hereditary pancreatitis.101,151â153 Cohort evidence also supports the combined importance of smoking status, alcohol intake, body weight, physical activity, and diet as components of a healthy lifestyle.152 Avoiding tobacco and excessive alcohol consumption is also relevant to chronic pancreatitis prevention and management.67,68
Furthermore, obesity is another risk factor for the occurrence of pancreatic cancer. There is a significant positive correlation between increasing BMI and the occurrence of pancreatic cancer.154 In some multicenter caseâcontrol studies, researchers have identified dietary factors such as adequate consumption of fruits and vegetables, which are considered protective in reducing the occurrence of pancreatic cancer.155
Institutions for early pancreatic cancer screening
Recommendation 26: Surveillance for pancreatic cancer in the four high-risk populations that meet the screening criteria should be conducted at pancreatic specialty centers. (Certainty of evidence: C; Recommendation strength: Strong recommendation) Outcomes of pancreatic surgery are generally better at high-volume centers,156,157 but these studies do not establish a universal threshold of 20 pancreaticoduodenectomies per year for a surveillance center. A pancreatic specialty center should instead be defined by applicable national or regional standards and by access to multidisciplinary expertise, high-quality MRI/MRCP and EUS, pathology, pancreatic surgery, oncology, genetic counseling where indicated, and longitudinal follow-up. Shared-care arrangements may be used when appropriate.
Although the certainty of evidence was classified as low, the original consensus assigned a strong recommendation to this organizational measure. Because a recommendation-specific Evidence-to-Decision assessment was not reported, the strength rating should be interpreted as a consensus classification. Given challenges related to cost, accessibility, and geographic distribution within the Chinese healthcare system, a shared-care follow-up model may offer a feasible alternative. Subsequent surveillance can be alternated between local hospitals (e.g., for routine blood glucose monitoring and clinically indicated CA19-9 testing) and specialty centers (e.g., for MRI/EUS examinations), based on the patient's distance from the center, clinical findings, and preferences.
Potential harms and feasibility considerations
Although early screening for pancreatic cancer in high-risk populations offers potential survival benefits, it is essential to fully recognize the associated harms, including false positives, overdiagnosis, procedural risks, and psychological burden. During surveillance, misclassification of benign or low-risk lesions as suspicious is not uncommon and may lead to unnecessary surgical intervention. A meta-analysis focusing on high-risk individuals with familial pancreatic cancer revealed that over two-thirds of those who underwent surgery were ultimately confirmed by pathology to have non-malignant or low-grade lesions.158 Pancreatic surgery remains a high-risk procedure, with complications such as postoperative pancreatic fistula occurring in 5â22% of cases, delayed gastric emptying affecting up to 57% of patients, and post-pancreatectomy hemorrhage occurring in 3â13% of cases.159 The issue of overtreatment is especially prominent in patients with pancreatic cystic neoplasms. Some low-risk BD-IPMNs may never progress to invasive cancer throughout a patientâs lifetime, yet these patients are still subjected to repeated imaging surveillance or even surgical resection, leading to unnecessary physical harm and inefficient use of healthcare resources.160 In addition, long-term surveillance itself imposes persistent psychological anxiety and economic burden, particularly among young individuals carrying susceptibility genes, whose concerns about disease progression may negatively affect their quality of life.161
From a health system perspective, the feasibility of implementing large-scale screening programs is constrained by several factors. High-quality surveillance relies on specialized imaging modalities such as EUS and MRI, which require advanced infrastructure and operator expertise that are not uniformly available across different regions in China. This disparity in access may exacerbate existing inequalities in cancer outcomes. Additionally, the cumulative economic burden of repeated surveillance, combined with the potential for surveillance fatigue, may reduce long-term adherence. To optimize net benefit, screening strategies should incorporate robust risk stratification tools, establish clear criteria for discontinuing surveillance in stable low-risk lesions, and emphasize multidisciplinary decision-making to minimize unnecessary interventions while ensuring that high-risk individuals receive appropriate care.
Declarations
Acknowledgement
The authors gratefully acknowledge Prof. Helmut Friess from the Department of Surgery, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany, for his valuable support in the formulation of this consensus.
Expert Panel (in alphabetical order by surname)
Ningli Chai (The First Medical Center of Chinese PLA General Hospital); Youxiang Chen (The First Affiliated Hospital of Nanchang University); Zhen Ding (Union Hospital, Tongji Medical College, Huazhong University of Science and Technology); Yiqi Du (The First Affiliated Hospital of Naval Medical University); Zhizheng Ge (Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine); Jianyu Hao (Beijing Chaoyang Hospital, Capital Medical University); Jian He (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Senlin Hou (The Second Hospital of Hebei Medical University); Bing Hu (West China Hospital, Sichuan University); Bing Hu (The Third Affiliated Hospital of Naval Medical University); Yonghui Huang (Peking University Third Hospital); Ming Ji (Beijing Friendship Hospital, Capital Medical University); Huiqing Jiang (The Second Hospital of Hebei Medical University); Junmei Jiang (Shandong Provincial Hospital Affiliated to Shandong First Medical University); Kuirong Jiang (The First Affiliated Hospital of Nanjing Medical University); Qingwei Jiang (Peking Union Medical College Hospital); Yueping Jiang (The Affiliated Hospital of Qingdao University); Gang Jin (Changhai Hospital, Naval Medical University); Zhendong Jin (Changhai Hospital, Naval Medical University); Bo Kong (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Huikai Li (The First Medical Center of Chinese PLA General Hospital); Lianyong Li (Strategic Support Force Medical Center); Wen Li (Tianjin Union Medical Center); Xun Li (The First Hospital of Lanzhou University); Yanqing Li (Qilu Hospital of Shandong University); Enqiang Linghu (The First Medical Center of Chinese PLA General Hospital); Gaifang Liu (Hebei General Hospital); Jun Liu (Union Hospital, Tongji Medical College, Huazhong University of Science and Technology); Ying Lv (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Liang Mao (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Yanglin Pan (Xijing Hospital of Air Force Military Medical University); Guiyong Peng (The First Hospital Affiliated to Army Medical University); Shanyu Qin (The First Affiliated Hospital of Guangxi Medical University); Yudong Qiu (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Shanshan Shen (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Siyu Sun (Shengjing Hospital of China Medical University); Bangmao Wang (Tianjin Medical University General Hospital); Guiqi Wang (Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College); Lei Wang (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Yi Wang (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Mingxing Xia (The Third Affiliated Hospital of Naval Medical University); Guoqiang Xu (The First Affiliated Hospital, Zhejiang University School of Medicine); Hong Xu (The First Bethune Hospital of Jilin University); Chao Yan (Nanjing University); Aiming Yang (Peking Union Medical College Hospital); Honggang Yu (Renmin Hospital of Wuhan University); Shu Zhang (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Ruhua Zheng (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University); Fachao Zhi (Nanfang Hospital, Southern Medical University); Liang Zhong (Huashan Hospital, Fudan University); Pinghong Zhou (Zhongshan Hospital, Fudan University); Yin Zhu (The First Affiliated Hospital of Nanchang University); Xiaoping Zou (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University)
Writing Group
Shanshan Shen (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University), Hongzhen Li (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University), Yuanyuan Yu (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University), Xintong Zhang (Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University).
Translation disclaimer
Translated in full with permission from the Chinese Medical Association (CMA). Sole responsibility of the translation rests with the translator. This translation, Copyright © 2026 by the Chinese Medical Association (CMA). The original article was published as: ä¸å½è°è
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±è¯æè§ (2021, å京). Chin J Dig Endosc 2022;39(2):85â95. doi:10.3760/cma.j.cn321463-20211223-00768. The Chinese Medical Association takes no responsibility for the accuracy of the translation from the published Chinese original and is not liable for any errors which may occur. No responsibility is assumed, and responsibility is hereby disclaimed, by the Chinese Medical Association for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of methods, products, instructions or ideas presented in this translation. Independent verification of diagnosis and drug dosages should be made. Discussions, views, and recommendations as to medical procedures, choice of drugs and drug dosages are the responsibility of the authors.
Funding
The work was supported by the Sino-German Mobility Programme (M-0251).
Conflict of interest
All authors declare no conflicts of interest. Among the listed expert panel members, Yiqi Du serves as Editor-in-Chief of Cancer Screening and Prevention; Zhizheng Ge, Yanqing Li, Honggang Yu, and Fachao Zhi serve as Associate Editors; and Huiqing Jiang, Xun Li, and Yin Zhu serve as Editorial Board Members. They were not involved in the peer-review process, editorial handling, or decision-making for this article.
Authors’ contributions
Original Chinese consensus: SS, HL, YY, and XtZ served as the writing group, and the listed expert panel participated in voting and group discussion, as reported in the Chinese publication.6English secondary publication: LW and XpZ are listed as corresponding authors. The individuals who performed the English translation and selected narrative updates were not separately identified in the publication records available to the Editorial Office. These roles and responsibility for the translated and updated content should therefore be confirmed from documentary records before finalization of the correction. Members listed under Expert Panel are consensus participants/collaborators; listing does not by itself establish individual authorship of the English translation.