| [1] | Ciacci, C., et al., Allergy prevalence in adult celiac disease. J Allergy ClinImmunol, 2004. 113(6): p. 1199-203. |
| |
| [2] | Ludvigsson, J.F., S.M. Montgomery, and A. Ekbom, Risk of pancreatitis in 14,000 individuals with celiac disease. ClinGastroenterolHepatol, 2007. 5(11): p. 1347-53. |
| |
| [3] | Sadr-Azodi, O., et al.. Patients with celiac disease have an increased risk for pancreatitis. ClinGastroenterolHepatol, 2012. 10(10): p. 1136-1142 e3. |
| |
| [4] | DiMagno, M.J. and E.P. DiMagno, Chronic pancreatitis. CurrOpinGastroenterol, 2013. 29(5): p. 531-6. |
| |
| [5] | Sziksz, E., et al., Coeliac Disease: From Triggering Factors to Treatment. International Journal of Celiac Disease, 2013. 1(1): p. 9-13. |
| |
| [6] | Schuppan, D., Current concepts of celiac disease pathogenesis. Gastroenterology, 2000. 119(1): p. 234-42. |
| |
| [7] | Romanos, J., et al., Analysis of HLA and non-HLA alleles can identify individuals at high risk for celiac disease. Gastroenterology, 2009. 137(3): p. 834-40, 840 e1-3. |
| |
| [8] | Trynka, G., et al., Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaBsignalling. Gut, 2009. 58(8): p. 1078-83. |
| |
| [9] | Susi, M., et al., Candidate gene region 15q26 and genetic susceptibility to coeliac disease in Finnish families.Scand J Gastroenterol, 2001. 36(4): p. 372-4. |
| |
| [10] | Latiano, A., et al., Analysis of candidate genes on chromosomes 5q and 19p in celiac disease. J PediatrGastroenterolNutr, 2007. 45(2): p. 180-6. |
| |
| [11] | Einarsdottir, E., et al., Multiple independent variants in 6q21-22 associated with susceptibility to celiac disease in the Dutch, Finnish and Hungarian populations. Eur J Hum Genet, 2011. 19(6): p. 682-6. |
| |
| [12] | Kaukinen, K., et al., HLA-DQ typing in the diagnosis of celiac disease. Am J Gastroenterol, 2002.97(3): p. 695-9. |
| |
| [13] | Al-Toma, A., et al., Human leukocyte antigen-DQ2 homozygosity and the development of refractory celiac disease and enteropathy-associated T-cell lymphoma. ClinGastroenterolHepatol, 2006. 4(3): p. 315-9. |
| |
| [14] | Pietzak, M.M., et al., Stratifying risk for celiac disease in a large at-risk United States population by using HLA alleles. ClinGastroenterolHepatol, 2009. 7(9): p. 966-71. |
| |
| [15] | Hunt, K.A., et al., Newly identified genetic risk variants for celiac disease related to the immune response. Nat Genet, 2008. 40(4): p. 395-402. |
| |
| [16] | Lennon, A.M., et al., The Early Detection of Pancreatic Cancer: What Will It Take to Diagnose and Treat Curable Pancreatic Neoplasia? Cancer Res, 2014. 74(13): p. 3381-3389. |
| |
| [17] | Porta, M., et al., Cigarette smoking and K-ras mutations in pancreas, lung and colorectal adenocarcinomas: etiopathogenic similarities, differences and paradoxes. Mutat Res, 2009. 682(2-3): p. 83-93. |
| |
| [18] | Hruban, R.H., A. Maitra, and M. Goggins, Update on pancreatic intraepithelial neoplasia. Int J ClinExpPathol, 2008. 1(4): p. 306-16. |
| |
| [19] | Quinlan, M.P., et al., Activated Kras, but not Hras or Nras, may initiate tumors of endodermal origin via stem cell expansion. Mol Cell Biol, 2008. 28(8): p. 2659-74. |
| |
| [20] | Allegra, C.J., et al., American Society of Clinical Oncology provisional clinical opinion: testing for KRAS gene mutations in patients with metastatic colorectal carcinoma to predict response to anti-epidermal growth factor receptor monoclonal antibody therapy. J ClinOncol, 2009. 27(12): p. 2091-6. |
| |
| [21] | Halilovic, E., et al., PIK3CA mutation uncouples tumor growth and cyclin D1 regulation from MEK/ERK and mutant KRAS signaling. Cancer Res, 2010. 70(17): p. 6804-14. |
| |
| [22] | Murphy, K.M., et al., Evaluation of candidate genes MAP2K4, MADH4, ACVR1B, and BRCA2 in familial pancreatic cancer: deleterious BRCA2 mutations in 17%. Cancer Res, 2002. 62(13): p. 3789-93. |
| |
| [23] | Hahn, S.A., et al., BRCA2 germline mutations in familial pancreatic carcinoma. J Natl Cancer Inst, 2003. 95(3): p. 214-21. |
| |
| [24] | Iqbal, J., et al., The incidence of pancreatic cancer in BRCA1 and BRCA2 mutation carriers. Br J Cancer, 2012. 107(12): p. 2005-9. |
| |
| [25] | Ferrone, C.R., et al., BRCA germline mutations in Jewish patients with pancreatic adenocarcinoma. J ClinOncol, 2009. 27(3): p. 433-8. |
| |
| [26] | Lal, G., et al., Inherited predisposition to pancreatic adenocarcinoma: role of family history and germ-line p16, BRCA1, and BRCA2 mutations. Cancer Res, 2000. 60(2): p. 409-16. |
| |
| [27] | Jones, S., et al., Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene. Science, 2009. 324(5924): p. 217. |
| |
| [28] | Tischkowitz, M.D., et al., Analysis of the gene coding for the BRCA2-interacting protein PALB2 in familial and sporadic pancreatic cancer. Gastroenterology, 2009. 137(3): p. 1183-6. |
| |
| [29] | Slater, E.P., et al., PALB2 mutations in European familial pancreatic cancer families.Clin Genet, 2010. 78(5): p. 490-4. |
| |
| [30] | Giardiello, F.M., et al., Very high risk of cancer in familial Peutz-Jeghers syndrome. Gastroenterology, 2000. 119(6): p. 1447-53. |
| |
| [31] | Rebours, V., et al., Risk of pancreatic adenocarcinoma in patients with hereditary pancreatitis: a national exhaustive series. Am J Gastroenterol, 2008.103(1): p. 111-9. |
| |
| [32] | Howes, N., et al., Clinical and genetic characteristics of hereditary pancreatitis in Europe. ClinGastroenterolHepatol, 2004. 2(3): p. 252-61. |
| |
| [33] | Vymetalkova, V.P., et al., Molecular characteristics of mismatch repair genes in sporadic colorectal tumors in Czech patients. BMC Med Genet, 2014. 15: p. 17. |
| |
| [34] | Vasen, H.F., et al., Risk of developing pancreatic cancer in families with familial atypical multiple mole melanoma associated with a specific 19 deletion of p16 (p16-Leiden).Int J Cancer, 2000. 87(6): p. 809-11. |
| |
| [35] | Lundin, K.E. and L.M. Sollid, Advances in coeliac disease. CurrOpinGastroenterol, 2014. 30(2): p. 154-62. |
| |