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1. Type 1 Autoimmune Pancreatitis in Europe: Clinical Profile and Response to Treatment

Author

Drewes, A. Mohr, Haas, S.L., Hoyer, B.F., Hampe, J., Hinrichs, C. Noreen, Lerch, M.M., Aghdassi, A.A., Grote, T., Heuser, D.J., Ignatavicius, P., Malecka-Panas, E., Domínguez-Muñoz, J.E., López-Serrano, A., Auriemma, F., Oracz, G., Duman, D., Gubergrits, N., Overbeek, Kasper A., Poulsen, Jakob L., Lanzillotta, Marco, Vinge-Holmquist, Olof, Macinga, Peter, Demirci, A. Fatih, Sindhunata, Daniko P., Backhus, Johanna, Algül, Hana, Buijs, Jorie, Levy, Philippe, Kiriukova, Mariia, Goni, Elisabetta, Hollenbach, Marcus, Miksch, Rainer C., Kunovsky, Lumir, Vujasinovic, Miroslav, Nikolic, Sara, Dickerson, Luke, Hirth, Michael, Neurath, Markus F., Zumblick, Malte, Vila, Josephine, Jalal, Mustafa, Beyer, Georg, Frost, Fabian, Carrara, Silvia, Kala, Zdenek, Jabandziev, Petr, Sisman, Gurhan, Akyuz, Filiz, Capurso, Gabriele, Falconi, Massimo, Arlt, Alexander, Vleggaar, Frank P., Barresi, Luca, Greenhalf, Bill, Czakó, László, Hegyi, Peter, Hopper, Andrew, Nayar, Manu K., Gress, Thomas M., Vitali, Francesco, Schneider, Alexander, Halloran, Chris M., Trna, Jan, Okhlobystin, Alexey V., Dagna, Lorenzo, Cahen, Djuna L., Bordin, Dmitry, Rebours, Vinciane, Mayerle, Julia, Kahraman, Alisan, Rasch, Sebastian, Culver, Emma, Kleger, Alexander, Martínez-Moneo, Emma, Røkke, Ola, Hucl, Tomas, Olesen, Søren S., Bruno, Marco J., Della-Torre, Emanuel, Beuers, Ulrich, Löhr, J.-Matthias, and Rosendahl, Jonas

Published
2024
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2. PITX2 as a Sensitive and Specific Marker of Midgut Neuroendocrine Tumors: Results from a Cohort of 1157 Primary Neuroendocrine Neoplasms

Author

Grass, Albert, Kasajima, Atsuko, Foersch, Sebastian, Kriegsmann, Mark, Brobeil, Alexander, Schmitt, Maxime, Wagner, Daniel, Poppinga, Jelte, Wiese, Dominik, Maurer, Elisabeth, Kirschbaum, Andreas, Muley, Thomas, Winter, Hauke, Rinke, Anja, Gress, Thomas M., Kremer, Markus, Evert, Matthias, Märkl, Bruno, Quaas, Alexander, Eckstein, Markus, Tschurtschenthaler, Markus, Klöppel, Günter, Denkert, Carsten, Bartsch, Detlef K., and Jesinghaus, Moritz

Published
2024
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3. DYRK1B blockade promotes tumoricidal macrophage activity in pancreatic cancer.

Author

Brichkina, Anna, Ems, Miriam, Suezov, Roman, Singh, Rajeev, Lutz, Veronika, Picard, Felix S. R., Nist, Andrea, Stiewe, Thorsten, Graumann, Johannes, Daude, Michael, Diederich, Wibke E., Finkernagel, Florian, Ho-Ryun Chung, Bartsch, Detlef K., Roth, Katrin, Keber, Corinna, Denkert, Carsten, Huber, Magdalena, Gress, Thomas M., and Lauth, Matthias

Subjects
MOLECULAR biology, TRANSFORMING growth factors-beta, CANCER cell physiology, LIFE sciences, CELL receptors, PANCREATIC intraepithelial neoplasia, PANCREATIC tumors
Published
2024
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4. Timeline of Development of Pancreatic Cancer and Implications for Successful Early Detection in High-Risk Individuals

Author

Overbeek, Kasper A., Goggins, Michael G., Dbouk, Mohamad, Levink, Iris J.M., Koopmann, Brechtje D.M., Chuidian, Miguel, Konings, Ingrid C.A.W., Paiella, Salvatore, Earl, Julie, Fockens, Paul, Gress, Thomas M., Ausems, Margreet G.E.M., Poley, Jan-Werner, Thosani, Nirav C., Half, Elizabeth, Lachter, Jesse, Stoffel, Elena M., Kwon, Richard S., Stoita, Alina, Kastrinos, Fay, Lucas, Aimee L., Syngal, Sapna, Brand, Randall E., Chak, Amitabh, Carrato, Alfredo, Vleggaar, Frank P., Bartsch, Detlef K., van Hooft, Jeanin E., Cahen, Djuna L., Canto, Marcia Irene, and Bruno, Marco J.

Published
2022
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5. International consensus guidelines on interventional endoscopy in chronic pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club

Author

Kitano, Masayuki, Gress, Thomas M., Garg, Pramod K., Itoi, Takao, Irisawa, Atsushi, Isayama, Hiroyuki, Kanno, Atsushi, Takase, Kei, Levy, Michael, Yasuda, Ichiro, Lévy, Phillipe, Isaji, Shuiji, Fernandez-Del Castillo, Carlos, Drewes, Asbjørn M., Sheel, Andrea R.G., Neoptolemos, John P., Shimosegawa, Tooru, Boermeester, Marja, Wilcox, C. Mel, and Whitcomb, David C.

Published
2020
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9. Endoscopic retrograde cholangiopancreatography‐obtained bile culture in acute cholangitis: retrospective analysis of bile cultures and risk factors in a tertiary care center.

Author

Stathopoulos, Petros, Lerner, Paulina, Astheimer, Philipp, Breitling, Lutz P., Zumblick, Malte, Pararas, Michael, Lohoff, Michael, Gress, Thomas M., and Denzer, Ulrike W.

Subjects
CHOLANGITIS, ENDOSCOPIC retrograde cholangiopancreatography, TERTIARY care, MULTIDRUG resistance, VANCOMYCIN resistance, ENTEROCOCCUS faecalis
Abstract

Background: Collection of bile aspirate during endoscopic retrograde cholangiopancreatography (ERCP) is essential to identify pathogens responsible for acute cholangitis. Limited data are available on the risk factors for the presence of multidrug‐resistant organisms (MDRO) in bile. Methods: We conducted this retrospective, single‐center study to assess the prevalence and susceptibility rates of bacteria in bile cultures, and the risk factors for the presence of pathogens, MDRO, and fungi in bile. All consecutive patients who underwent biliary drainage for acute cholangitis from January 2017 to December 2019 were included. Results: 443/1610 ERCPs were performed for acute cholangitis. Bile culture was collected in 91.4% (405/443), of which 86.7% were positive. Most common isolates were Enterococcus faecalis (37.6%) and Escherichia coli (32.8%). Vancomycin resistance was found in 9.9% of Enterococcus species (spp.); extended‐spectrum beta‐lactamases (ESBL) and carbapenemases in 11.2% and 0.9% of Enterobacteriaceae, respectively. The empiric antimicrobial therapy was changed in 26.4% (n = 107) of cases, with a clinical response in 90.7%. In multivariate analysis, biliary stenting was an independent risk factor for positive bile culture (odds ratio [OR] 9.43; P < 0.01). Independent risk factors for MDRO in bile were patient age>60 years (OR 2.51; P = 0.03), previous sphincterotomy (OR 2.57; P = 0.02), and biliary stenting (OR 2.80; P < 0.01). Previous sphincterotomy was the only risk factor for isolation of fungi in bile (OR 1.61; P = 0.04). Conclusions: Our study showed an increasing prevalence of Enterococcus spp. and MDRO. Bile cultures should be routinely collected in cholangitis and in patients with repeated ERCPs to allow more efficient antimicrobial treatment. [ABSTRACT FROM AUTHOR]

Published
2024
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15. High expression of insulinoma‐associated protein 1 (INSM1) distinguishes colorectal mixed and pure neuroendocrine carcinomas from conventional adenocarcinomas with diffuse expression of synaptophysin.

Author

Litmeyer, Anne‐Sophie, Konukiewitz, Björn, Kasajima, Atsuko, Foersch, Sebastian, Schicktanz, Felix, Schmitt, Maxime, Kellers, Franziska, Grass, Albert, Jank, Paul, Lehman, Bettina, Gress, Thomas M, Rinke, Anja, Bartsch, Detlef K, Denkert, Carsten, Weichert, Wilko, Klöppel, Günter, and Jesinghaus, Moritz

Subjects
NEUROENDOCRINE tumors, SYNAPTOPHYSIN, PROTEIN expression, ADENOCARCINOMA, OVERALL survival, COLORECTAL cancer
Abstract

Complementary to synaptophysin and chromogranin A, insulinoma‐associated protein 1 (INSM1) has emerged as a sensitive marker for the diagnosis of neuroendocrine neoplasms. Since there are no comparative data regarding INSM1 expression in conventional colorectal adenocarcinomas (CRCs) and colorectal mixed adenoneuroendocrine carcinomas/neuroendocrine carcinomas (MANECs/NECs), we examined INSM1 in a large cohort of conventional CRCs and MANECs/NECs. In conventional CRC, we put a special focus on conventional CRC with diffuse expression of synaptophysin, which carry the risk of being misinterpreted as a MANEC or a NEC. We investigated INSM1 according to the immunoreactive score in our main cohort of 1,033 conventional CRCs and 21 MANECs/NECs in comparison to the expression of synaptophysin and chromogranin A and correlated the results with clinicopathological parameters and patient survival. All MANECs/NECs expressed INSM1, usually showing high or moderate expression (57% high, 34% moderate, and 9% low), which distinguished them from conventional CRCs, which were usually INSM1 negative or low, even if they diffusely expressed synaptophysin. High expression of INSM1 was not observed in conventional CRCs. Chromogranin A was negative/low in most conventional CRCs (99%), but also in most MANECs/NECs (66%). Comparable results were observed in our independent validation cohorts of conventional CRC (n = 274) and MANEC/NEC (n = 19). Similar to synaptophysin, INSM1 expression had no prognostic relevance in conventional CRCs, while true MANEC/NEC showed a highly impaired survival in univariate and multivariate analyses (e.g. disease‐specific survival: p < 0.001). MANECs/NECs are a highly aggressive variant of colorectal cancer, which must be reliably identified. High expression of INSM1 distinguishes MANEC/NEC from conventional CRCs with diffuse expression of the standard neuroendocrine marker synaptophysin, which do not share the same dismal prognosis. Therefore, high INSM1 expression is a highly specific/sensitive marker that is supportive for the diagnosis of true colorectal MANEC/NEC. [ABSTRACT FROM AUTHOR]

Published
2023
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20. A systems biology approach to define mechanisms, phenotypes, and drivers in PanNETs with a personalized perspective.

Author

Werle, Silke D., Ikonomi, Nensi, Lausser, Ludwig, Kestler, Annika M. T. U., Weidner, Felix M., Schwab, Julian D., Maier, Julia, Buchholz, Malte, Gress, Thomas M., Kestler, Angelika M. R., and Kestler, Hans A.

Subjects
SYSTEMS biology, PHENOTYPES, TUBEROUS sclerosis, PANCREATIC tumors, NEUROENDOCRINE tumors, DEVELOPED countries
Abstract

Pancreatic neuroendocrine tumors (PanNETs) are a rare tumor entity with largely unpredictable progression and increasing incidence in developed countries. Molecular pathways involved in PanNETs development are still not elucidated, and specific biomarkers are missing. Moreover, the heterogeneity of PanNETs makes their treatment challenging and most approved targeted therapeutic options for PanNETs lack objective responses. Here, we applied a systems biology approach integrating dynamic modeling strategies, foreign classifier tailored approaches, and patient expression profiles to predict PanNETs progression as well as resistance mechanisms to clinically approved treatments such as the mammalian target of rapamycin complex 1 (mTORC1) inhibitors. We set up a model able to represent frequently reported PanNETs drivers in patient cohorts, such as Menin-1 (MEN1), Death domain associated protein (DAXX), Tuberous Sclerosis (TSC), as well as wild-type tumors. Model-based simulations suggested drivers of cancer progression as both first and second hits after MEN1 loss. In addition, we could predict the benefit of mTORC1 inhibitors on differentially mutated cohorts and hypothesize resistance mechanisms. Our approach sheds light on a more personalized prediction and treatment of PanNET mutant phenotypes. [ABSTRACT FROM AUTHOR]

Published
2023
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21. Dissecting the role of toll‐like receptor 7 in pancreatic cancer.

Author

Stark, Maren, Nicolai, Marina, Tatura, Marina, Keber, Corinna U., Kaufmann, Andreas, Chung, Ho‐Ryun, Slater, Emily P., Heeschen, Christopher, Lawlor, Rita T., Scarpa, Aldo, Bartsch, Detlef K., Gress, Thomas M., Bauer, Stefan, and Buchholz, Malte

Subjects
TOLL-like receptors, PANCREATIC cancer, PANCREATIC duct, STROMAL cells, OVERALL survival, PANCREATIC tumors
Abstract

Background: Toll‐like receptors (TLRs) are gaining attention for their potential to influence tumor biology both on the level of the tumor cells as well as on the level of the surrounding inflammatory stroma. Previous studies resulted in partly conflicting data on the expression of TLR7 in healthy and neoplastic pancreatic tissues as well as its role in pancreatic tumor biology. Methods: We used qRT‐PCR and immunohistochemistry to asses TLR7 expression in primary patient material and cell lines. Cell viability was analyzed by MTT assay upon incubation with TLR7 agonist/antagonist. Mouse models were used to investigate the role of TLR7 in vivo. Results: TLR7 is overexpressed in more than 50% of primary human pancreatic ductal adenocarcinoma (PDAC). High TLR7 expression was associated with shorter patient survival, and TLR7 inhibition in cell lines reduced viability in a dose‐dependent manner. In contrast, global TLR7 deficiency did not alter survival or overall histopathological tumor features in genetic mouse models of PDAC. Conclusions: TLR7 may have opposing functions in tumor versus stroma cells. Further work is required to more precisely dissect the roles of TLR7 and its ligands in different populations of epithelial and stromal cells and to understand their relative contributions to tumor progression. [ABSTRACT FROM AUTHOR]

Published
2023
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27. IL18 Receptor Signaling Inhibits Intratumoral CD8 + T-Cell Migration in a Murine Pancreatic Cancer Model.

Author

Nasiri, Elena, Student, Malte, Roth, Katrin, Siti Utami, Nadya, Huber, Magdalena, Buchholz, Malte, Gress, Thomas M., and Bauer, Christian

Subjects
CELL culture, PANCREATIC cancer, CD8 antigen, T-cell exhaustion, PANCREATIC duct, T cells
Abstract

In pancreatic ductal adenocarcinoma (PDAC), the infiltration of CD8+ cytotoxic T cells (CTLs) is an important factor in determining prognosis. The migration pattern and interaction behavior of intratumoral CTLs are pivotal to tumor rejection. NLRP3-dependent proinflammatory cytokines IL-1β and IL-18 play a prominent role for CTL induction and differentiation. Here, we investigate the effects of T-cellular IL-1R and IL-18R signaling for intratumoral T-cell motility. Murine adenocarcinoma cell line Panc02 was stably transfected with ovalbumin (OVA) and fluorophore H2B-Cerulean to generate PancOVA H2B-Cerulean tumor cells. Dorsal skinfold chambers (DSFC) were installed on wild-type mice, and PancOVA H2B-Cerulean tumor cells were implanted into the chambers. PancOVA spheroids were formed using the Corning® Matrigel®-based 3D cell culture technique. CTLs were generated from OT-1 mice, Il1r−/− OT-1 mice, or Il18r−/− OT-1 mice and were marked with fluorophores. This was followed by the adoptive transfer of CTLs into tumor-bearing mice or the application into tumor spheroids. After visualization with multiphoton microscopy (MPM), Imaris software was used to perform T-cell tracking. Imaris analysis indicates a significantly higher accumulation of Il18r−/− CTLs in PancOVA tumors and a significant reduction in tumor volume compared to wild-type CTLs. Il18r−/− CTLs covered a longer distance (track displacement length) in comparison to wild-type (WT) CTLs, and had a higher average speed (mean track speed). The analysis of instantaneous velocity suggests a higher percentage of arrested tracks (arrests: <4 μm/min) for Il18r−/− CTLs. Our data indicate the contribution of IL-18R signaling to T-cell effector strength, warranting further investigation on phenomena such as intratumoral T-cell exhaustion. [ABSTRACT FROM AUTHOR]

Published
2023
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36. High rate of Ki‐67 increase in entero‐pancreatic NET relapses after surgery with curative intent.

Author

Merola, Elettra, Perren, Aurel, Rinke, Anja, Zerbi, Alessandro, McNamara, Mairéad G., Arsenic, Ruza, Fazio, Nicola, de Herder, Wouter, Valle, Juan W., Gress, Thomas M., Wiedenmann, Bertram, Pascher, Andreas, and Pavel, Marianne E.

Subjects
KI-67 antigen, PANCREATIC surgery, NEUROENDOCRINE tumors, TUMOR grading, DISEASE relapse, SURGERY, PANCREATIC tumors
Abstract

Neuroendocrine neoplasms (NENs) present with advanced disease at diagnosis in up to 28% of cases, precluding the possibility of curative‐intent surgery. Histopathological heterogeneity of this disease can be observed inter‐individually as well as intra‐individually during disease course. The present study aimed to assess the frequency of Ki‐67 change after radical surgery, in a series of patients with radically resected entero‐pancreatic neuroendocrine tumors (EP‐NETs). We present the analysis of a multicenter, retrospective, series of EP‐NETs G1–G2 recurring after radical resection and with histological re‐evaluation at disease recurrence (DR). The primary endpoint was the description of Ki‐67 change at DR compared to time of surgery. The secondary endpoint was assessment of recurrence‐free survival (RFS) rates. In total, 47 patients had a second histological evaluation and could be included in the present study. Median Ki‐67 at surgery was 3% (range 1–15%) but, at DR, a significant increase in the value was observed (7%, range 1–30%; p <.01) and involved 66.0% of cases, with a corresponding increase in tumor grading in 34.0% (p =.05). Median RFS of the overall population was 40 months, and was worse when Ki‐67 increased at DR vs. stable Ki‐67 value (36 vs. 61 months, respectively; p =.02). In conclusion, in more than half of the cases with relapse after radical surgery, a higher proliferative index with a potentially more aggressive potential was observed. Therefore, histological reassessment should be considered on DR because tailored therapeutic strategies may be required for these patients. [ABSTRACT FROM AUTHOR]

Published
2022
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37. Microbial short-chain fatty acids modulate CD8$^\text{+}$ T cell responses and improve adoptive immunotherapy for cancer

Author

Luu, Maik, Riester, Zeno, Baldrich, Adrian, Reichardt, Nicole, Yuille, Samantha, Busetti, Alessandro, Klein, Matthias, Wempe, Anne, Leister, Hanna, Raifer, Hartmann, Picard, Felix, Muhammad, Khalid, Ohl, Kim, Romero, Rossana, Fischer, Florence, Bauer, Christian A., Huber, Magdalena, Gress, Thomas M., Lauth, Matthias, Danhof, Sophia, Bopp, Tobias, Nerreter, Thomas, Mulder, Imke E., Steinhoff, Ulrich, Hudecek, Michael, and Visekruna, Alexander

Subjects
Megasphaera, Science, CD8-Positive T-Lymphocytes, Receptor Tyrosine Kinase-like Orphan Receptors, Immunotherapy, Adoptive, Article, Receptors, G-Protein-Coupled, Interferon-gamma, Mice, Cell Line, Tumor, Neoplasms, Animals, Immunologic Factors, Melanoma, Tumor Necrosis Factor-alpha, Microbiota, Interleukin-2 Receptor alpha Subunit, Fatty Acids, Volatile, Peptide Fragments, Mice, Inbred C57BL, Butyrates, Tumour immunology, Cytokines, Female, Immunotherapy, ddc:500, T-Lymphocytes, Cytotoxic
Abstract

Emerging data demonstrate that the activity of immune cells can be modulated by microbial molecules. Here, we show that the short-chain fatty acids (SCFAs) pentanoate and butyrate enhance the anti-tumor activity of cytotoxic T lymphocytes (CTLs) and chimeric antigen receptor (CAR) T cells through metabolic and epigenetic reprograming. We show that in vitro treatment of CTLs and CAR T cells with pentanoate and butyrate increases the function of mTOR as a central cellular metabolic sensor, and inhibits class I histone deacetylase activity. This reprogramming results in elevated production of effector molecules such as CD25, IFN-γ and TNF-α, and significantly enhances the anti-tumor activity of antigen-specific CTLs and ROR1-targeting CAR T cells in syngeneic murine melanoma and pancreatic cancer models. Our data shed light onto microbial molecules that may be used for enhancing cellular anti-tumor immunity. Collectively, we identify pentanoate and butyrate as two SCFAs with therapeutic utility in the context of cellular cancer immunotherapy., The activity of immune cells can be regulated by the microbiome. Here, the authors show that the fatty acids pentanoate and butyrate—normally released by the microbiome—increase the anti-tumour activity of cytotoxic T lymphocytes and chimeric antigen receptor T cells through metabolic and epigenetic reprogramming.

Published
2021
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43. The Immune Microenvironment in Pancreatic Cancer

Author

Huber, Magdalena, Brehm, Corinna U., Gress, Thomas M., Buchholz, Malte, Alashkar Alhamwe, Bilal, Pogge von Strandmann, Elke, Slater, Emily P., Bartsch, Jörg W., Bauer, Christian, and Lauth, Matthias

Subjects
natural killer cells, T-cells, pancreatic cancer, tumor stroma, Review, Adenocarcinoma, macrophages, lcsh:Chemistry, neutrophils, lcsh:Biology (General), lcsh:QD1-999, Tumor Microenvironment, Humans, Immunotherapy, cancer-associated fibroblasts, lcsh:QH301-705.5, Carcinoma, Pancreatic Ductal
Abstract

The biology of solid tumors is strongly determined by the interactions of cancer cells with their surrounding microenvironment. In this regard, pancreatic cancer (pancreatic ductal adenocarcinoma, PDAC) represents a paradigmatic example for the multitude of possible tumor-stroma interactions. PDAC has proven particularly refractory to novel immunotherapies, which is a fact that is mediated by a unique assemblage of various immune cells creating a strongly immunosuppressive environment in which this cancer type thrives. In this review, we outline currently available knowledge on the cross-talk between tumor cells and the cellular immune microenvironment, highlighting the physiological and pathological cellular interactions, as well as the resulting therapeutic approaches derived thereof. Hopefully a better understanding of the complex tumor-stroma interactions will one day lead to a significant advancement in patient care.

Published
2020

44. Pancreatic Cancer Risk in Relation to Lifetime Smoking Patterns, Tobacco Type, and Dose-Response Relationships

Author

Molina-Montes, Esther, Van Hoogstraten, Lisa, Gomez-Rubio, Paulina, Lohr, Matthias, Sharp, Linda, Molero, Xavier, Marquez, Mirari, Michalski, Christoph W, Farre, Antoni, Perea, Jose, O'Rorke, Michael, Greenhalf, William, Ilzarbe, Lucas, Tardon, Adonina, Gress, Thomas M, Barbera, Victor M, Crnogorac-Jurcevic, Tatjana, Munoz-Bellvis, Luis, Dominguez-Munoz, Enrique, Balsells, Joaquim, Costello, Eithne, Iglesias, Mar, Kleeff, Jorg, Kong, Bo, Mora, Josefina, O'Driscoll, Damian, Poves, Ignasi, Scarpa, Aldo, Yu, Jingru, Ye, Weimin, Hidalgo, Manuel, Carrato, Alfredo, Lawlor, Rita, Real, Francisco X, Malats, Nuria, and Investigators, PanGenEu Study

Subjects
Male, 0301 basic medicine, Time Factors, Epidemiology, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Logistic regression, Tobacco smoke, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Diabetes mellitus, Diabetes Mellitus, Odds Ratio, Tobacco Smoking, medicine, Humans, Family history, Risk factor, Medical History Taking, Aged, Chronic Pancreatitis, Smokers, Hepatology, business.industry, Pancreatic Neoplasm, Cancer Risk, Chronic Pancreatitis, Pancreatic Neoplasm, Gastroenterology, Case-control study, Non-Smokers, Odds ratio, Middle Aged, medicine.disease, Cancer Risk, Europe, Pancreatic Neoplasms, 030104 developmental biology, Oncology, Case-Control Studies, 030220 oncology & carcinogenesis, Smoking cessation, Female, Tobacco Smoke Pollution, business, Demography
Abstract

Background: Despite smoking being a well-established risk factor for pancreatic cancer, there is a need to further characterize pancreatic cancer risk according to lifespan smoking patterns and other smoking features, such as tobacco type. Our aim was to deeply investigate them within a large European case–control study. Methods: Tobacco smoking habits and other relevant information were obtained from 2,009 cases and 1,532 controls recruited in the PanGenEU study using standardized tools. Multivariate logistic regression analysis was performed to evaluate pancreatic cancer risk by smoking characteristics and interactions with other pancreatic cancer risk factors. Fractional polynomials and restricted cubic splines were used to test for nonlinearity of the dose–response relationships and to analyze their shape. Results: Relative to never-smokers, current smokers [OR = 1.72; 95% confidence interval (95% CI), 1.39–2.12], those inhaling into the throat (OR = 1.48; 95% CI, 1.11–1.99) or chest (OR = 1.33; 95% CI, 1.12–1.58), and those using nonfiltered cigarettes (OR = 1.69; 95% CI, 1.10–2.61), were all at an increased pancreatic cancer risk. Pancreatic cancer risk was highest in current black tobacco smokers (OR = 2.09; 95% CI, 1.31–3.41), followed by blond tobacco smokers (OR = 1.43; 95% CI, 1.01–2.04). Childhood exposure to tobacco smoke relative to parental smoking was also associated with increased pancreatic cancer risk (OR = 1.24; 95% CI, 1.03–1.49). Dose–response relationships for smoking duration, intensity, cumulative dose, and smoking cessation were nonlinear and showed different shapes by tobacco type. Effect modification by family history of pancreatic cancer and diabetes was likely. Conclusions: This study reveals differences in pancreatic cancer risk by tobacco type and other habit characteristics, as well as nonlinear risk associations. Impact: This characterization of smoking-related pancreatic cancer risk profiles may help in defining pancreatic cancer high-risk populations.

Published
2020

45. Keratin 8 sequence variants in patients with pancreatitis and pancreatic cancer

Author

Treiber, Matthias, Schulz, Hans-Ulrich, Landt, Olfert, Drenth, Joost PH, Castellani, Carlo, Real, Francisco X., Akar, Nejat, Ammann, Rudolf W., Bargetzi, Mario, Bhatia, Eesh, Demaine, Andrew Glenn, Battagia, Cinzia, Kingsnorth, Andrew, O’Reilly, Derek, Truninger, Kaspar, Koudova, Monika, Spicak, Julius, Cerny, Milos, Menzel, Hans-Jürgen, Moral, Pedro, Pignatti, Pier Franco, Romanelli, Maria Grazia, Rickards, Olga, De Stefano, Gian Franco, Zarnescu, Narcis Octavian, Choudhuri, Gourdas, Sikora, Sadiq S., Jansen, Jan B. M. J., Weiss, Frank Ulrich, Pietschmann, Matthias, Teich, Niels, Gress, Thomas M., Ockenga, Johann, Schmidt, Hartmut, Kage, Andreas, Halangk, Juliane, Rosendahl, Jonas, Groneberg, David Alexander, Nickel, Renate, and Witt, Heiko

Published
2006
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49. Long-term outcomes of autoimmune pancreatitis: a multicentre, international analysis

Author

Hart, Phil A, Kamisawa, Terumi, Brugge, William R, Chung, Jae Bock, Culver, Emma L, Czakó, László, Frulloni, Luca, Go, Vay Liang W, Gress, Thomas M, Kim, Myung-Hwan, Kawa, Shigeyuki, Lee, Kyu Taek, Lerch, Markus M, Liao, Wei-Chih, Löhr, Matthias, Okazaki, Kazuichi, Ryu, Ji Kon, Schleinitz, Nicolas, Shimizu, Kyoko, Shimosegawa, Tooru, Soetikno, Roy, Webster, George, Yadav, Dhiraj, Zen, Yoh, and Chari, Suresh T

Published
2013
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