Skip to main content
Erschienen in: Current Treatment Options in Gastroenterology 4/2017

06.09.2017 | Pancreas (V Chandrasekhara, Section Editor)

Pancreatic Cancer Screening

verfasst von: Koushik K. Das, MD, Dayna Early, MD

Erschienen in: Current Treatment Options in Gastroenterology | Ausgabe 4/2017

Einloggen, um Zugang zu erhalten

Abstract

Purpose of Review

This review describes the rationale for pancreatic cancer screening, outlines groups that are at elevated risk for pancreatic cancer, and summarizes the relative risk in each setting. We also review the methods available for performing pancreatic cancer screening and the recommended screening intervals.

Recent Findings

Several genetic mutations have been identified that increase the risk for pancreatic cancer. Most are rare, however, and at-risk individuals are most often those with a strong family history of pancreatic cancer (with multiple family members affected) but no identifiable genetic mutation. Known genetic syndromes that increase the risk for pancreatic cancer include hereditary pancreatitis, familial atypical mole and multiple melanoma, Peutz-Jeghers syndrome, Lynch syndrome, BRCA mutations, and Li-Fraumeni syndrome. Genetic testing should be performed in conjunction with genetic counseling, and testing of an affected family member is preferred if possible.The goal of pancreatic cancer screening is to identify pancreatic cancer at an early, curable stage or, ideally, to identify precancerous lesions that can be resected to prevent the development of cancer. Imaging can be performed with either endoscopic ultrasound (EUS) or magnetic resonance cholangiopancreatography (MRCP). These techniques are generally considered to be complementary, although an advantage of EUS is that cysts or solid lesions can be sampled at the time of the procedure. Published results of small cohorts of high-risk patients in pancreatic cancer screening programs have demonstrated a high prevalence of small cystic lesions identified on EUS or MRCP, which often represent side-branch intraductal papillary mucinous neoplasms (IPMN).

Summary

Knowledge of conditions and syndromes that increase pancreatic cancer risk allows one to identify those patients that may benefit from pancreatic cancer screening. As we gather evidence from large, international, multicenter cohorts of patients at high-risk for pancreatic cancer who are undergoing screening and as our understanding of the genetic underpinnings of pancreatic cancer improve, recommendations on screening will continue to be refined.
Literatur
1.
Zurück zum Zitat Ma J, Jemal A. The rise and fall of cancer mortality in the USA: why does pancreatic cancer not follow the trend? Future Oncol. 2013;9:917–9.CrossRefPubMed Ma J, Jemal A. The rise and fall of cancer mortality in the USA: why does pancreatic cancer not follow the trend? Future Oncol. 2013;9:917–9.CrossRefPubMed
2.
Zurück zum Zitat Yeo CJ, Cameron JL. Prognostic factors in ductal pancreatic cancer. Langenbeck's Arch Surg. 1998;383:129–33.CrossRef Yeo CJ, Cameron JL. Prognostic factors in ductal pancreatic cancer. Langenbeck's Arch Surg. 1998;383:129–33.CrossRef
3.
Zurück zum Zitat Shimizu Y, Yasui K, Matsueda K, Yanagisawa A, Yamao K. Small carcinoma of the pancreas is curable: new computed tomography finding, pathological study and postoperative results from a single institute. J Gastroenterol Hepatol. 2005;20:1591–4.CrossRefPubMed Shimizu Y, Yasui K, Matsueda K, Yanagisawa A, Yamao K. Small carcinoma of the pancreas is curable: new computed tomography finding, pathological study and postoperative results from a single institute. J Gastroenterol Hepatol. 2005;20:1591–4.CrossRefPubMed
4.
Zurück zum Zitat Permuth-Wey J, Egan KM. Family history is a significant risk factor for pancreatic cancer: results from a systematic review and meta-analysis. Familial Cancer. 2009;8:109–17.CrossRefPubMed Permuth-Wey J, Egan KM. Family history is a significant risk factor for pancreatic cancer: results from a systematic review and meta-analysis. Familial Cancer. 2009;8:109–17.CrossRefPubMed
5.
Zurück zum Zitat •• Rustgi AK. Familial pancreatic cancer: genetic advances. Genes Dev. 2014;28:1–7. This article reviews the known genetic mutations associated with familial pancreatic cancer, associated cancer syndromes, and their underlying pathobiology.CrossRefPubMedPubMedCentral •• Rustgi AK. Familial pancreatic cancer: genetic advances. Genes Dev. 2014;28:1–7. This article reviews the known genetic mutations associated with familial pancreatic cancer, associated cancer syndromes, and their underlying pathobiology.CrossRefPubMedPubMedCentral
6.
Zurück zum Zitat Whitcomb DC, Shelton C, Brand RE. Genetics and genetic testing in pancreatic cancer. YGAST. 2015;149:1252-64. Whitcomb DC, Shelton C, Brand RE. Genetics and genetic testing in pancreatic cancer. YGAST. 2015;149:1252-64.
7.
Zurück zum Zitat •• Canto MI, Harinck F, Hruban RH, et al. International Cancer of the Pancreas Screening (CAPS) Consortium summit on the management of patients with increased risk for familial pancreatic cancer. Gut. 2013;62:339–47. This article summarizes the findings of the Cancer of the Pancreas Screening Consortium Summit (CAPS), with expert level recommendations for those patients who may benefit from pancreatic cancer screening and modalities and intervals to be considered.CrossRefPubMed •• Canto MI, Harinck F, Hruban RH, et al. International Cancer of the Pancreas Screening (CAPS) Consortium summit on the management of patients with increased risk for familial pancreatic cancer. Gut. 2013;62:339–47. This article summarizes the findings of the Cancer of the Pancreas Screening Consortium Summit (CAPS), with expert level recommendations for those patients who may benefit from pancreatic cancer screening and modalities and intervals to be considered.CrossRefPubMed
8.
Zurück zum Zitat Iodice S, Gandini S, Maisonneuve P, Lowenfels AB. Tobacco and the risk of pancreatic cancer: a review and meta-analysis. Langenbeck's Arch Surg. 2008;393:535–45.CrossRef Iodice S, Gandini S, Maisonneuve P, Lowenfels AB. Tobacco and the risk of pancreatic cancer: a review and meta-analysis. Langenbeck's Arch Surg. 2008;393:535–45.CrossRef
9.
Zurück zum Zitat Silverman DT, Dunn JA, Hoover RN, Schiffman M, Lillemoe KD, Schoenberg JB, et al. Cigarette smoking and pancreas cancer: a case-control study based on direct interviews. J Natl Cancer Inst. 1994;86:1510–6.CrossRefPubMed Silverman DT, Dunn JA, Hoover RN, Schiffman M, Lillemoe KD, Schoenberg JB, et al. Cigarette smoking and pancreas cancer: a case-control study based on direct interviews. J Natl Cancer Inst. 1994;86:1510–6.CrossRefPubMed
10.
Zurück zum Zitat Villeneuve PJ, Johnson KC, Mao Y, Hanley AJ, Canadian Cancer Registries Research Group. Environmental tobacco smoke and the risk of pancreatic cancer: findings from a Canadian population-based case-control study. Can J Public Health. 2004;95:32–7.PubMed Villeneuve PJ, Johnson KC, Mao Y, Hanley AJ, Canadian Cancer Registries Research Group. Environmental tobacco smoke and the risk of pancreatic cancer: findings from a Canadian population-based case-control study. Can J Public Health. 2004;95:32–7.PubMed
11.
Zurück zum Zitat Hoffmann D, Djordjevic MV, Fan J, Zang E, Glynn T, Connolly GN. Five leading U.S. commercial brands of moist snuff in 1994: assessment of carcinogenic N-nitrosamines. J Natl Cancer Inst. 1995;87:1862–9.CrossRefPubMed Hoffmann D, Djordjevic MV, Fan J, Zang E, Glynn T, Connolly GN. Five leading U.S. commercial brands of moist snuff in 1994: assessment of carcinogenic N-nitrosamines. J Natl Cancer Inst. 1995;87:1862–9.CrossRefPubMed
12.
13.
Zurück zum Zitat Lowenfels AB. Chronic pancreatitis, pancreatic cancer, alcohol, and smoking. YGAST. 1984;87:744–5. Lowenfels AB. Chronic pancreatitis, pancreatic cancer, alcohol, and smoking. YGAST. 1984;87:744–5.
14.
Zurück zum Zitat Lucenteforte E, La Vecchia C, Silverman D, et al. Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case-Control Consortium (PanC4). Ann Oncol. 2012;23:374–82.CrossRefPubMed Lucenteforte E, La Vecchia C, Silverman D, et al. Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case-Control Consortium (PanC4). Ann Oncol. 2012;23:374–82.CrossRefPubMed
15.
Zurück zum Zitat Karlson BM, Ekbom A, Josefsson S, McLaughlin JK, Fraumeni JF, Nyrén O. The risk of pancreatic cancer following pancreatitis: an association due to confounding? YGAST. 1997;113:587–92. Karlson BM, Ekbom A, Josefsson S, McLaughlin JK, Fraumeni JF, Nyrén O. The risk of pancreatic cancer following pancreatitis: an association due to confounding? YGAST. 1997;113:587–92.
16.
Zurück zum Zitat Esposito K, Chiodini P, Colao A, Lenzi A, Giugliano D. Metabolic syndrome and risk of cancer: a systematic review and meta-analysis. Diabetes Care. 2012;35:2402–11.CrossRefPubMedPubMedCentral Esposito K, Chiodini P, Colao A, Lenzi A, Giugliano D. Metabolic syndrome and risk of cancer: a systematic review and meta-analysis. Diabetes Care. 2012;35:2402–11.CrossRefPubMedPubMedCentral
17.
Zurück zum Zitat Michaud DS, Giovannucci E, Willett WC, Colditz GA, Stampfer MJ, Fuchs CS. Physical activity, obesity, height, and the risk of pancreatic cancer. JAMA. 2001;286:921–9.CrossRefPubMed Michaud DS, Giovannucci E, Willett WC, Colditz GA, Stampfer MJ, Fuchs CS. Physical activity, obesity, height, and the risk of pancreatic cancer. JAMA. 2001;286:921–9.CrossRefPubMed
19.
Zurück zum Zitat Everhart J, Wright D. Diabetes mellitus as a risk factor for pancreatic cancer. A meta-analysis. JAMA. 1995;273:1605–9.CrossRefPubMed Everhart J, Wright D. Diabetes mellitus as a risk factor for pancreatic cancer. A meta-analysis. JAMA. 1995;273:1605–9.CrossRefPubMed
20.
Zurück zum Zitat Gupta S, Vittinghoff E, Bertenthal D, Corley D, Shen H, Walter LC, et al. New-onset diabetes and pancreatic cancer. YJCGH. 2006;4:1366–72. quiz 1301 Gupta S, Vittinghoff E, Bertenthal D, Corley D, Shen H, Walter LC, et al. New-onset diabetes and pancreatic cancer. YJCGH. 2006;4:1366–72. quiz 1301
21.
Zurück zum Zitat Chari ST, Leibson CL, Rabe KG, Timmons LJ, Ransom J, de Andrade M, et al. Pancreatic cancer-associated diabetes mellitus: prevalence and temporal association with diagnosis of cancer. Gastroenterology. 2008;134:95–101.CrossRefPubMed Chari ST, Leibson CL, Rabe KG, Timmons LJ, Ransom J, de Andrade M, et al. Pancreatic cancer-associated diabetes mellitus: prevalence and temporal association with diagnosis of cancer. Gastroenterology. 2008;134:95–101.CrossRefPubMed
22.
Zurück zum Zitat Gangi S, Fletcher JG, Nathan MA, Christensen JA, Harmsen WS, Crownhart BS, et al. Time interval between abnormalities seen on CT and the clinical diagnosis of pancreatic cancer: retrospective review of CT scans obtained before diagnosis. Am J Roentgenol. 2004;182:897–903.CrossRef Gangi S, Fletcher JG, Nathan MA, Christensen JA, Harmsen WS, Crownhart BS, et al. Time interval between abnormalities seen on CT and the clinical diagnosis of pancreatic cancer: retrospective review of CT scans obtained before diagnosis. Am J Roentgenol. 2004;182:897–903.CrossRef
23.
Zurück zum Zitat Pannala R, Leirness JB, Bamlet WR, Basu A, Petersen GM, Chari ST. Prevalence and clinical profile of pancreatic cancer-associated diabetes mellitus. Gastroenterology. 2008;134:981–7.CrossRefPubMedPubMedCentral Pannala R, Leirness JB, Bamlet WR, Basu A, Petersen GM, Chari ST. Prevalence and clinical profile of pancreatic cancer-associated diabetes mellitus. Gastroenterology. 2008;134:981–7.CrossRefPubMedPubMedCentral
24.
Zurück zum Zitat Valerio A, Basso D, Brigato L, Ceolotto G, Baldo G, Tiengo A, et al. Glucose metabolic alterations in isolated and perfused rat hepatocytes induced by pancreatic cancer conditioned medium: a low molecular weight factor possibly involved. Biochem Biophys Res Commun. 1999;257:622–8.CrossRefPubMed Valerio A, Basso D, Brigato L, Ceolotto G, Baldo G, Tiengo A, et al. Glucose metabolic alterations in isolated and perfused rat hepatocytes induced by pancreatic cancer conditioned medium: a low molecular weight factor possibly involved. Biochem Biophys Res Commun. 1999;257:622–8.CrossRefPubMed
25.
Zurück zum Zitat Aggarwal G, Ramachandran V, Javeed N, et al. Adrenomedullin is up-regulated in patients with pancreatic cancer and causes insulin resistance in β cells and mice. Gastroenterology. 2012;143:1510–1517.e1.CrossRefPubMedPubMedCentral Aggarwal G, Ramachandran V, Javeed N, et al. Adrenomedullin is up-regulated in patients with pancreatic cancer and causes insulin resistance in β cells and mice. Gastroenterology. 2012;143:1510–1517.e1.CrossRefPubMedPubMedCentral
26.
Zurück zum Zitat Sekine N. Adrenomedullin inhibits insulin exocytosis via pertussis toxin-sensitive G protein-coupled mechanism. AJP: Endocrinol Metab. 2006;291:E9–E14. Sekine N. Adrenomedullin inhibits insulin exocytosis via pertussis toxin-sensitive G protein-coupled mechanism. AJP: Endocrinol Metab. 2006;291:E9–E14.
27.
Zurück zum Zitat Permert J, Larsson J, Westermark GT, Herrington MK, Christmanson L, Pour PM, et al. Islet amyloid polypeptide in patients with pancreatic cancer and diabetes. N Engl J Med. 1994;330:313–8.CrossRefPubMed Permert J, Larsson J, Westermark GT, Herrington MK, Christmanson L, Pour PM, et al. Islet amyloid polypeptide in patients with pancreatic cancer and diabetes. N Engl J Med. 1994;330:313–8.CrossRefPubMed
28.
Zurück zum Zitat Ding X, Flatt PR, Permert J, Adrian TE. Pancreatic cancer cells selectively stimulate islet β cells to secrete amylin. Gastroenterology. 1998;114:130–8.CrossRefPubMed Ding X, Flatt PR, Permert J, Adrian TE. Pancreatic cancer cells selectively stimulate islet β cells to secrete amylin. Gastroenterology. 1998;114:130–8.CrossRefPubMed
29.
Zurück zum Zitat Basso D, Greco E, Fogar P, et al. Pancreatic cancer-derived S-100A8 N-terminal peptide: a diabetes cause? Clin Chim Acta. 2006;372:120–8.CrossRefPubMed Basso D, Greco E, Fogar P, et al. Pancreatic cancer-derived S-100A8 N-terminal peptide: a diabetes cause? Clin Chim Acta. 2006;372:120–8.CrossRefPubMed
30.
Zurück zum Zitat •• Klein AP, Brune KA, Petersen GM, et al. Prospective risk of pancreatic cancer in familial pancreatic cancer kindreds. Cancer Res. 2004;64:2634–8. This article evaluates the relative risk of pancreatic cancer in FPC kindreds utilizing the SEER databaseCrossRefPubMed •• Klein AP, Brune KA, Petersen GM, et al. Prospective risk of pancreatic cancer in familial pancreatic cancer kindreds. Cancer Res. 2004;64:2634–8. This article evaluates the relative risk of pancreatic cancer in FPC kindreds utilizing the SEER databaseCrossRefPubMed
32.
Zurück zum Zitat Klein AP. Identifying people at a high risk of developing pancreatic cancer. Nat Rev Cancer. 2013;13:66–74.CrossRefPubMed Klein AP. Identifying people at a high risk of developing pancreatic cancer. Nat Rev Cancer. 2013;13:66–74.CrossRefPubMed
33.
Zurück zum Zitat Brune KA, Lau B, Palmisano E, Canto M, Goggins MG, Hruban RH, et al. Importance of age of onset in pancreatic cancer kindreds. J Natl Cancer Inst. 2010;102:119–26.CrossRefPubMedPubMedCentral Brune KA, Lau B, Palmisano E, Canto M, Goggins MG, Hruban RH, et al. Importance of age of onset in pancreatic cancer kindreds. J Natl Cancer Inst. 2010;102:119–26.CrossRefPubMedPubMedCentral
34.
Zurück zum Zitat Whitcomb DC, Gorry MC, Preston RA, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet. 1996;14:141–5.CrossRefPubMed Whitcomb DC, Gorry MC, Preston RA, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet. 1996;14:141–5.CrossRefPubMed
35.
Zurück zum Zitat Rosendahl J, Witt H, Szmola R, et al. Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis. Nat Publ Group. 2008;40:78–82. Rosendahl J, Witt H, Szmola R, et al. Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis. Nat Publ Group. 2008;40:78–82.
36.
Zurück zum Zitat Szabó A, Sahin-Tóth M. Increased activation of hereditary pancreatitis-associated human cationic trypsinogen mutants in presence of chymotrypsin C. J Biol Chem. 2012;287:20701–10.CrossRefPubMedPubMedCentral Szabó A, Sahin-Tóth M. Increased activation of hereditary pancreatitis-associated human cationic trypsinogen mutants in presence of chymotrypsin C. J Biol Chem. 2012;287:20701–10.CrossRefPubMedPubMedCentral
37.
Zurück zum Zitat Cohn JA, Friedman KJ, Noone PG, Knowles MR, Silverman LM, Jowell PS. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med. 1998;339:653–8.CrossRefPubMed Cohn JA, Friedman KJ, Noone PG, Knowles MR, Silverman LM, Jowell PS. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med. 1998;339:653–8.CrossRefPubMed
38.
Zurück zum Zitat Lowenfels AB, Maisonneuve P, DiMagno EP, Elitsur Y, Gates LK, Perrault J, et al. Hereditary pancreatitis and the risk of pancreatic cancer. International Hereditary Pancreatitis Study Group. J Natl Cancer Inst. 1997;89:442–6.CrossRefPubMed Lowenfels AB, Maisonneuve P, DiMagno EP, Elitsur Y, Gates LK, Perrault J, et al. Hereditary pancreatitis and the risk of pancreatic cancer. International Hereditary Pancreatitis Study Group. J Natl Cancer Inst. 1997;89:442–6.CrossRefPubMed
39.
Zurück zum Zitat Rebours V, Boutron-Ruault M-C, Jooste V, Bouvier A-M, Hammel P, Ruszniewski P, et al. Mortality rate and risk factors in patients with hereditary pancreatitis: uni- and multidimensional analyses. Am J Gastroenterol. 2009;104:2312–7.CrossRefPubMed Rebours V, Boutron-Ruault M-C, Jooste V, Bouvier A-M, Hammel P, Ruszniewski P, et al. Mortality rate and risk factors in patients with hereditary pancreatitis: uni- and multidimensional analyses. Am J Gastroenterol. 2009;104:2312–7.CrossRefPubMed
40.
Zurück zum Zitat Rebours V, Levy P, Mosnier JF, et al. Pathology analysis reveals that dysplastic pancreatic ductal lesions are frequent in patients with hereditary pancreatitis. Clin Gastroenterol Hepatol. 2010;8:206–12.CrossRefPubMed Rebours V, Levy P, Mosnier JF, et al. Pathology analysis reveals that dysplastic pancreatic ductal lesions are frequent in patients with hereditary pancreatitis. Clin Gastroenterol Hepatol. 2010;8:206–12.CrossRefPubMed
41.
Zurück zum Zitat Lowenfels AB, Maisonneuve P, Whitcomb DC, Lerch MM, DiMagno EP. Cigarette smoking as a risk factor for pancreatic cancer in patients with hereditary pancreatitis. JAMA. 2001;286:169–70.CrossRefPubMed Lowenfels AB, Maisonneuve P, Whitcomb DC, Lerch MM, DiMagno EP. Cigarette smoking as a risk factor for pancreatic cancer in patients with hereditary pancreatitis. JAMA. 2001;286:169–70.CrossRefPubMed
42.
Zurück zum Zitat Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, et al. Ras activity levels control the development of pancreatic diseases. Gastroenterology. 2009;137:1072–1082.e6.CrossRefPubMedPubMedCentral Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, et al. Ras activity levels control the development of pancreatic diseases. Gastroenterology. 2009;137:1072–1082.e6.CrossRefPubMedPubMedCentral
43.
Zurück zum Zitat Daniluk J, Liu Y, Deng D, Chu J, Huang H, Gaiser S, et al. An NF-κB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice. J Clin Invest. 2012;122:1519–28.CrossRefPubMedPubMedCentral Daniluk J, Liu Y, Deng D, Chu J, Huang H, Gaiser S, et al. An NF-κB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice. J Clin Invest. 2012;122:1519–28.CrossRefPubMedPubMedCentral
45.
Zurück zum Zitat Collins MA, Yan W, Sebolt-Leopold JS, Pasca di Magliano M. MAPK signaling is required for dedifferentiation of acinar cells and development of pancreatic intraepithelial neoplasia in mice. Gastroenterology. 2014;146:822–834.e7.CrossRefPubMed Collins MA, Yan W, Sebolt-Leopold JS, Pasca di Magliano M. MAPK signaling is required for dedifferentiation of acinar cells and development of pancreatic intraepithelial neoplasia in mice. Gastroenterology. 2014;146:822–834.e7.CrossRefPubMed
46.
Zurück zum Zitat Collins MA, Bednar F, Zhang Y, Brisset J-C, Galbán S, Galbán CJ, et al. Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice. J Clin Invest. 2012;122:639–53.CrossRefPubMedPubMedCentral Collins MA, Bednar F, Zhang Y, Brisset J-C, Galbán S, Galbán CJ, et al. Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice. J Clin Invest. 2012;122:639–53.CrossRefPubMedPubMedCentral
47.
Zurück zum Zitat Gruis NA, van der Velden PA, Sandkuijl LA, Prins DE, Weaver-Feldhaus J, Kamb A, et al. Homozygotes for CDKN2 (p16) germline mutation in Dutch familial melanoma kindreds. Nat Genet. 1995;10:351–3.CrossRefPubMed Gruis NA, van der Velden PA, Sandkuijl LA, Prins DE, Weaver-Feldhaus J, Kamb A, et al. Homozygotes for CDKN2 (p16) germline mutation in Dutch familial melanoma kindreds. Nat Genet. 1995;10:351–3.CrossRefPubMed
48.
Zurück zum Zitat Ranade K, Hussussian CJ, Sikorski RS, Varmus HE, Goldstein AM, Tucker MA, et al. Mutations associated with familial melanoma impair p16INK4 function. Nat Genet. 1995;10:114–6.CrossRefPubMed Ranade K, Hussussian CJ, Sikorski RS, Varmus HE, Goldstein AM, Tucker MA, et al. Mutations associated with familial melanoma impair p16INK4 function. Nat Genet. 1995;10:114–6.CrossRefPubMed
49.
Zurück zum Zitat Campbell PJ, Yachida S, Mudie LJ, et al. The patterns and dynamics of genomic instability in metastatic pancreatic cancer. Nature. 2010;467:1109–13.CrossRefPubMedPubMedCentral Campbell PJ, Yachida S, Mudie LJ, et al. The patterns and dynamics of genomic instability in metastatic pancreatic cancer. Nature. 2010;467:1109–13.CrossRefPubMedPubMedCentral
50.
51.
Zurück zum Zitat Sato N, Rosty C, Jansen M, Fukushima N, Ueki T, Yeo CJ, et al. STK11/LKB1 Peutz-Jeghers gene inactivation in intraductal papillary-mucinous neoplasms of the pancreas. Am J Pathol. 2001;159:2017–22.CrossRefPubMedPubMedCentral Sato N, Rosty C, Jansen M, Fukushima N, Ueki T, Yeo CJ, et al. STK11/LKB1 Peutz-Jeghers gene inactivation in intraductal papillary-mucinous neoplasms of the pancreas. Am J Pathol. 2001;159:2017–22.CrossRefPubMedPubMedCentral
52.
Zurück zum Zitat Korsse SE, Harinck F, van Lier MGF, et al. Pancreatic cancer risk in Peutz-Jeghers syndrome patients: a large cohort study and implications for surveillance. J Med Genet. 2013;50:59–64.CrossRefPubMed Korsse SE, Harinck F, van Lier MGF, et al. Pancreatic cancer risk in Peutz-Jeghers syndrome patients: a large cohort study and implications for surveillance. J Med Genet. 2013;50:59–64.CrossRefPubMed
53.
Zurück zum Zitat Giardiello FM, Brensinger JD, Tersmette AC, Goodman SN, Petersen GM, Booker SV, et al. Very high risk of cancer in familial Peutz–Jeghers syndrome. Gastroenterology. 2000;119:1447–53.CrossRefPubMed Giardiello FM, Brensinger JD, Tersmette AC, Goodman SN, Petersen GM, Booker SV, et al. Very high risk of cancer in familial Peutz–Jeghers syndrome. Gastroenterology. 2000;119:1447–53.CrossRefPubMed
54.
Zurück zum Zitat Giardiello FM, Offerhaus GJ, Lee DH, Krush AJ, Tersmette AC, Booker SV, et al. Increased risk of thyroid and pancreatic carcinoma in familial adenomatous polyposis. Gut. 1993;34:1394–6.CrossRefPubMedPubMedCentral Giardiello FM, Offerhaus GJ, Lee DH, Krush AJ, Tersmette AC, Booker SV, et al. Increased risk of thyroid and pancreatic carcinoma in familial adenomatous polyposis. Gut. 1993;34:1394–6.CrossRefPubMedPubMedCentral
55.
Zurück zum Zitat Galiatsatos P, Foulkes WD. Familial adenomatous polyposis. Am J Gastroenterol. 2006;101:385–98.CrossRefPubMed Galiatsatos P, Foulkes WD. Familial adenomatous polyposis. Am J Gastroenterol. 2006;101:385–98.CrossRefPubMed
56.
Zurück zum Zitat •• Syngal S, Brand RE, Church JM, Giardiello FM, Hampel HL, Burt RW. ACG clinical guideline: genetic testing and management of hereditary gastrointestinal cancer syndromes. Am J Gastroenterol. 2015;110:223–62. American College of Gastroenterology Guidelines on the testing and management of gastrointestinal cancer syndromes, including familial pancreatic cancerCrossRefPubMedPubMedCentral •• Syngal S, Brand RE, Church JM, Giardiello FM, Hampel HL, Burt RW. ACG clinical guideline: genetic testing and management of hereditary gastrointestinal cancer syndromes. Am J Gastroenterol. 2015;110:223–62. American College of Gastroenterology Guidelines on the testing and management of gastrointestinal cancer syndromes, including familial pancreatic cancerCrossRefPubMedPubMedCentral
57.
Zurück zum Zitat Kastrinos F, Mukherjee B, Tayob N, Wang F, Sparr J, Raymond VM, et al. Risk of pancreatic cancer in families with lynch syndrome. JAMA. 2009;302:1790–5.CrossRefPubMedPubMedCentral Kastrinos F, Mukherjee B, Tayob N, Wang F, Sparr J, Raymond VM, et al. Risk of pancreatic cancer in families with lynch syndrome. JAMA. 2009;302:1790–5.CrossRefPubMedPubMedCentral
58.
Zurück zum Zitat Goldgar DE. Analysis of familial breast cancer in genetic analysis workshop 9: summary of findings. Genet Epidemiol. 1995;12:833–6.CrossRefPubMed Goldgar DE. Analysis of familial breast cancer in genetic analysis workshop 9: summary of findings. Genet Epidemiol. 1995;12:833–6.CrossRefPubMed
59.
Zurück zum Zitat Ferrone CR, Levine DA, Tang LH, Allen PJ, Jarnagin W, Brennan MF, et al. BRCA germline mutations in Jewish patients with pancreatic adenocarcinoma. J Clin Oncol. 2008;27:433–8.CrossRefPubMed Ferrone CR, Levine DA, Tang LH, Allen PJ, Jarnagin W, Brennan MF, et al. BRCA germline mutations in Jewish patients with pancreatic adenocarcinoma. J Clin Oncol. 2008;27:433–8.CrossRefPubMed
60.
Zurück zum Zitat Mocci E, Milne RL, Mendez-Villamil EY, et al. Risk of pancreatic cancer in breast cancer families from the breast cancer family registry. Cancer Epidemiol Biomark Prev. 2013;22:803–11.CrossRef Mocci E, Milne RL, Mendez-Villamil EY, et al. Risk of pancreatic cancer in breast cancer families from the breast cancer family registry. Cancer Epidemiol Biomark Prev. 2013;22:803–11.CrossRef
61.
Zurück zum Zitat Breast Cancer Linkage Consortium T. Cancer risks in BRCA2 mutation carriers. J Natl Cancer Inst. 1999;91:1310–6.CrossRef Breast Cancer Linkage Consortium T. Cancer risks in BRCA2 mutation carriers. J Natl Cancer Inst. 1999;91:1310–6.CrossRef
62.
Zurück zum Zitat Ozçelik H, Schmocker B, Di Nicola N, et al. Germline BRCA2 6174delT mutations in Ashkenazi Jewish pancreatic cancer patients. Nat Genet. 1997;16:17–8.CrossRefPubMed Ozçelik H, Schmocker B, Di Nicola N, et al. Germline BRCA2 6174delT mutations in Ashkenazi Jewish pancreatic cancer patients. Nat Genet. 1997;16:17–8.CrossRefPubMed
63.
Zurück zum Zitat Thompson D, Easton DF, Breast Cancer Linkage Consortium. Cancer incidence in BRCA1 mutation carriers. J Natl Cancer Inst. 2002;94:1358–65.CrossRefPubMed Thompson D, Easton DF, Breast Cancer Linkage Consortium. Cancer incidence in BRCA1 mutation carriers. J Natl Cancer Inst. 2002;94:1358–65.CrossRefPubMed
64.
65.
Zurück zum Zitat Brose MS, Rebbeck TR, Calzone KA, Stopfer JE, Nathanson KL, Weber BL. Cancer risk estimates for BRCA1 mutation carriers identified in a risk evaluation program. J Natl Cancer Inst. 2002;94:1365–72.CrossRefPubMed Brose MS, Rebbeck TR, Calzone KA, Stopfer JE, Nathanson KL, Weber BL. Cancer risk estimates for BRCA1 mutation carriers identified in a risk evaluation program. J Natl Cancer Inst. 2002;94:1365–72.CrossRefPubMed
66.
Zurück zum Zitat Roberts NJ, Jiao Y, Yu J, et al. ATM mutations in patients with hereditary pancreatic cancer. Cancer Discovery. 2012;2:41–6.CrossRefPubMed Roberts NJ, Jiao Y, Yu J, et al. ATM mutations in patients with hereditary pancreatic cancer. Cancer Discovery. 2012;2:41–6.CrossRefPubMed
67.
Zurück zum Zitat Geoffroy-Perez B, Janin N, Ossian K, et al. Cancer risk in heterozygotes for ataxia-telangiectasia. Int J Cancer. 2001;93:288–93.CrossRefPubMed Geoffroy-Perez B, Janin N, Ossian K, et al. Cancer risk in heterozygotes for ataxia-telangiectasia. Int J Cancer. 2001;93:288–93.CrossRefPubMed
68.
69.
70.
Zurück zum Zitat Fernandes PH, Saam J, Peterson J, Hughes E, Kaldate R, Cummings S, et al. Comprehensive sequencing of PALB2 in patients with breast cancer suggests PALB2 mutations explain a subset of hereditary breast cancer. Cancer. 2014;120:963–7.CrossRefPubMed Fernandes PH, Saam J, Peterson J, Hughes E, Kaldate R, Cummings S, et al. Comprehensive sequencing of PALB2 in patients with breast cancer suggests PALB2 mutations explain a subset of hereditary breast cancer. Cancer. 2014;120:963–7.CrossRefPubMed
71.
Zurück zum Zitat Ruijs MWG, Verhoef S, Rookus MA, et al. TP53 germline mutation testing in 180 families suspected of Li-Fraumeni syndrome: mutation detection rate and relative frequency of cancers in different familial phenotypes. J Med Genet. 2010;47:421–8.CrossRefPubMed Ruijs MWG, Verhoef S, Rookus MA, et al. TP53 germline mutation testing in 180 families suspected of Li-Fraumeni syndrome: mutation detection rate and relative frequency of cancers in different familial phenotypes. J Med Genet. 2010;47:421–8.CrossRefPubMed
72.
Zurück zum Zitat Pogue-Geile KL, Chen R, Bronner MP, et al. Palladin mutation causes familial pancreatic cancer and suggests a new cancer mechanism. PLoS Med. 2006;3:e516–3.CrossRefPubMedPubMedCentral Pogue-Geile KL, Chen R, Bronner MP, et al. Palladin mutation causes familial pancreatic cancer and suggests a new cancer mechanism. PLoS Med. 2006;3:e516–3.CrossRefPubMedPubMedCentral
73.
Zurück zum Zitat Grant RC, Selander I, Connor AA, Selvarajah S, Borgida A, Briollais L, et al. Prevalence of germline mutations in cancer predisposition genes in patients with pancreatic cancer. YGAST. 2015;148:556–64. Grant RC, Selander I, Connor AA, Selvarajah S, Borgida A, Briollais L, et al. Prevalence of germline mutations in cancer predisposition genes in patients with pancreatic cancer. YGAST. 2015;148:556–64.
75.
Zurück zum Zitat Lowery MA, Kelsen DP, Stadler ZK, et al. An emerging entity: pancreatic adenocarcinoma associated with a known BRCA mutation: clinical descriptors, treatment implications, and future directions. Oncologist. 2011;16:1397–402.CrossRefPubMedPubMedCentral Lowery MA, Kelsen DP, Stadler ZK, et al. An emerging entity: pancreatic adenocarcinoma associated with a known BRCA mutation: clinical descriptors, treatment implications, and future directions. Oncologist. 2011;16:1397–402.CrossRefPubMedPubMedCentral
76.
Zurück zum Zitat Dewitt J, Devereaux BM, Lehman GA, Sherman S, Imperiale TF. Comparison of endoscopic ultrasound and computed tomography for the preoperative evaluation of pancreatic cancer: a systematic review. YJCGH. 2006;4:717–25. Dewitt J, Devereaux BM, Lehman GA, Sherman S, Imperiale TF. Comparison of endoscopic ultrasound and computed tomography for the preoperative evaluation of pancreatic cancer: a systematic review. YJCGH. 2006;4:717–25.
77.
Zurück zum Zitat •• Canto MI, Hruban RH, Fishman EK, et al. Frequent detection of pancreatic lesions in asymptomatic high-risk individuals. Gastroenterology. 2012;142:796–804. quiz e14–5. Prospective report of a high rate of detection of small cystic lesions of the pancreas as well as preneoplastic lesions of the pancreas in a screening program of high-risk patients with EUS and MRICrossRefPubMedPubMedCentral •• Canto MI, Hruban RH, Fishman EK, et al. Frequent detection of pancreatic lesions in asymptomatic high-risk individuals. Gastroenterology. 2012;142:796–804. quiz e14–5. Prospective report of a high rate of detection of small cystic lesions of the pancreas as well as preneoplastic lesions of the pancreas in a screening program of high-risk patients with EUS and MRICrossRefPubMedPubMedCentral
78.
Zurück zum Zitat Shin EJ, Topazian M, Goggins MG, Syngal S, Saltzman JR, Lee JH, et al. Linear-array EUS improves detection of pancreatic lesions in high-risk individuals: a randomized tandem study. Gastrointest Endosc. 2015;82:812–8.CrossRefPubMedPubMedCentral Shin EJ, Topazian M, Goggins MG, Syngal S, Saltzman JR, Lee JH, et al. Linear-array EUS improves detection of pancreatic lesions in high-risk individuals: a randomized tandem study. Gastrointest Endosc. 2015;82:812–8.CrossRefPubMedPubMedCentral
79.
Zurück zum Zitat Shi C, Klein AP, Goggins M, Maitra A, Canto M, Ali S, et al. Increased prevalence of precursor lesions in familial pancreatic cancer patients. Clin Cancer Res. 2009;15:7737–43.CrossRefPubMedPubMedCentral Shi C, Klein AP, Goggins M, Maitra A, Canto M, Ali S, et al. Increased prevalence of precursor lesions in familial pancreatic cancer patients. Clin Cancer Res. 2009;15:7737–43.CrossRefPubMedPubMedCentral
80.
Zurück zum Zitat Brune K, Abe T, Canto M, et al. Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer. Am J Surg Pathol. 2006;30:1067–76.PubMedPubMedCentral Brune K, Abe T, Canto M, et al. Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer. Am J Surg Pathol. 2006;30:1067–76.PubMedPubMedCentral
81.
Zurück zum Zitat Hruban RH, Goggins M, Parsons J, Kern SE. Progression model for pancreatic cancer. Clin Cancer Res. 2000;6:2969–72.PubMed Hruban RH, Goggins M, Parsons J, Kern SE. Progression model for pancreatic cancer. Clin Cancer Res. 2000;6:2969–72.PubMed
82.
Zurück zum Zitat Hruban RH, Takaori K, Klimstra DS, et al. An illustrated consensus on the classification of pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms. Am J Surg Pathol. 2004;28:977–87.CrossRefPubMed Hruban RH, Takaori K, Klimstra DS, et al. An illustrated consensus on the classification of pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms. Am J Surg Pathol. 2004;28:977–87.CrossRefPubMed
83.
Zurück zum Zitat Maitra A. Multicomponent analysis of the pancreatic adenocarcinoma progression model using a pancreatic intraepithelial neoplasia tissue microarray. Mod Pathol. 2003;16:902–12.CrossRefPubMed Maitra A. Multicomponent analysis of the pancreatic adenocarcinoma progression model using a pancreatic intraepithelial neoplasia tissue microarray. Mod Pathol. 2003;16:902–12.CrossRefPubMed
84.
Zurück zum Zitat Bartsch DK, Dietzel K, Bargello M, Matthaei E, Kloeppel G, Esposito I, et al. Multiple small “imaging” branch-duct type intraductal papillary mucinous neoplasms (IPMNs) in familial pancreatic cancer: indicator for concomitant high grade pancreatic intraepithelial neoplasia? Familial Cancer. 2012;12:89–96.CrossRef Bartsch DK, Dietzel K, Bargello M, Matthaei E, Kloeppel G, Esposito I, et al. Multiple small “imaging” branch-duct type intraductal papillary mucinous neoplasms (IPMNs) in familial pancreatic cancer: indicator for concomitant high grade pancreatic intraepithelial neoplasia? Familial Cancer. 2012;12:89–96.CrossRef
85.
Zurück zum Zitat Hruban RH, Pitman MB, Klimstra DS. Tumors of the pancreas. Amer Registry of Pathology; 2007. Hruban RH, Pitman MB, Klimstra DS. Tumors of the pancreas. Amer Registry of Pathology; 2007.
86.
Zurück zum Zitat Crippa S, del Castillo CF, Salvia R, et al. Mucin-producing neoplasms of the pancreas: an analysis of distinguishing clinical and epidemiologic characteristics. YJCGH. 2010;8:213–219.e4. Crippa S, del Castillo CF, Salvia R, et al. Mucin-producing neoplasms of the pancreas: an analysis of distinguishing clinical and epidemiologic characteristics. YJCGH. 2010;8:213–219.e4.
87.
Zurück zum Zitat Laffan TA, Horton KM, Klein AP, Berlanstein B, Siegelman SS, Kawamoto S, et al. Prevalence of unsuspected pancreatic cysts on MDCT. Am J Roentgenol. 2008;191:802–7.CrossRef Laffan TA, Horton KM, Klein AP, Berlanstein B, Siegelman SS, Kawamoto S, et al. Prevalence of unsuspected pancreatic cysts on MDCT. Am J Roentgenol. 2008;191:802–7.CrossRef
88.
Zurück zum Zitat •• Harinck F, Konings ICAW, Kluijt I, et al. A multicentre comparative prospective blinded analysis of EUS and MRI for screening of pancreatic cancer in high-risk individuals. Gut. 2016;65:1505–13. Prospective report on the results of MRI and EUS screening for pancreatic cancer in a multi-center Dutch cohort of high-risk patientsCrossRefPubMed •• Harinck F, Konings ICAW, Kluijt I, et al. A multicentre comparative prospective blinded analysis of EUS and MRI for screening of pancreatic cancer in high-risk individuals. Gut. 2016;65:1505–13. Prospective report on the results of MRI and EUS screening for pancreatic cancer in a multi-center Dutch cohort of high-risk patientsCrossRefPubMed
89.
Zurück zum Zitat Kinde I, Wu J, Papadopoulos N, Kinzler KW, Vogelstein B. Detection and quantification of rare mutations with massively parallel sequencing. Proc Natl Acad Sci U S A. 2011;108:9530–5.CrossRefPubMedPubMedCentral Kinde I, Wu J, Papadopoulos N, Kinzler KW, Vogelstein B. Detection and quantification of rare mutations with massively parallel sequencing. Proc Natl Acad Sci U S A. 2011;108:9530–5.CrossRefPubMedPubMedCentral
90.
Zurück zum Zitat Wu J, Matthaei H, Maitra A, et al. Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development. Sci Transl Med. 2011;3:92ra66.CrossRefPubMedPubMedCentral Wu J, Matthaei H, Maitra A, et al. Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development. Sci Transl Med. 2011;3:92ra66.CrossRefPubMedPubMedCentral
91.
Zurück zum Zitat Dal Molin M, Matthaei H, Wu J, et al. Clinicopathological correlates of activating GNAS mutations in intraductal papillary mucinous neoplasm (IPMN) of the pancreas. Ann Surg Oncol. 2013;20:3802–8.CrossRef Dal Molin M, Matthaei H, Wu J, et al. Clinicopathological correlates of activating GNAS mutations in intraductal papillary mucinous neoplasm (IPMN) of the pancreas. Ann Surg Oncol. 2013;20:3802–8.CrossRef
92.
Zurück zum Zitat Kanda M, Knight S, Topazian M, et al. Mutant GNAS detected in duodenal collections of secretin-stimulated pancreatic juice indicates the presence or emergence of pancreatic cysts. Gut. 2013;62:1024–33.CrossRefPubMed Kanda M, Knight S, Topazian M, et al. Mutant GNAS detected in duodenal collections of secretin-stimulated pancreatic juice indicates the presence or emergence of pancreatic cysts. Gut. 2013;62:1024–33.CrossRefPubMed
94.
Zurück zum Zitat Hingorani SR, Wang L, Multani AS, Combs C, Deramaudt TB, Hruban RH, et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell. 2005;7:469–83.CrossRefPubMed Hingorani SR, Wang L, Multani AS, Combs C, Deramaudt TB, Hruban RH, et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell. 2005;7:469–83.CrossRefPubMed
95.
Zurück zum Zitat Kanda M, Sadakari Y, Borges M, et al. Mutant TP53 in duodenal samples of pancreatic juice from patients with pancreatic cancer or high-grade dysplasia. Clin Gastroenterol Hepatol. 2013;11:719–30.e5.CrossRefPubMed Kanda M, Sadakari Y, Borges M, et al. Mutant TP53 in duodenal samples of pancreatic juice from patients with pancreatic cancer or high-grade dysplasia. Clin Gastroenterol Hepatol. 2013;11:719–30.e5.CrossRefPubMed
96.
Zurück zum Zitat Springer S, Wang Y, Dal Molin M, et al. A combination of molecular markers and clinical features improve the classification of pancreatic cysts. Gastroenterology. 2015;149:1501–10.CrossRefPubMedPubMedCentral Springer S, Wang Y, Dal Molin M, et al. A combination of molecular markers and clinical features improve the classification of pancreatic cysts. Gastroenterology. 2015;149:1501–10.CrossRefPubMedPubMedCentral
Metadaten
Titel
Pancreatic Cancer Screening
verfasst von
Koushik K. Das, MD
Dayna Early, MD
Publikationsdatum
06.09.2017
Verlag
Springer US
Erschienen in
Current Treatment Options in Gastroenterology / Ausgabe 4/2017
Print ISSN: 1092-8472
Elektronische ISSN: 1534-309X
DOI
https://doi.org/10.1007/s11938-017-0149-8

Weitere Artikel der Ausgabe 4/2017

Current Treatment Options in Gastroenterology 4/2017 Zur Ausgabe

Pancreas (V Chandrasekhara, Section Editor)

Recent Advances in Pancreatic Cancer Surgery

Motility (H Parkman and R Schey, Section Editors)

Diabetes and the Small Intestine

Stomach (DA Johnson, Section Editor)

Endoscopic Treatments for Obesity

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.