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Journal articles on the topic 'Pancreatic Ductal'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Wachsmann, Megan B., Laurentiu M. Pop, and Ellen S. Vitetta. "Pancreatic Ductal Adenocarcinoma." Journal of Investigative Medicine 60, no. 4 (April 1, 2012): 643–63. http://dx.doi.org/10.2310/jim.0b013e31824a4d79.

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2

Habib, Joseph R., Lingdi Yin, and Jun Yu. "Pancreatic ductal adenocarcinoma." Journal of Pancreatology 2, no. 3 (September 2019): 72–75. http://dx.doi.org/10.1097/jp9.0000000000000021.

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3

Konstantinidis, Ioannis T., Andrew L. Warshaw, Jill N. Allen, Lawrence S. Blaszkowsky, Carlos Fernandez-del Castillo, Vikram Deshpande, Theodore S. Hong, et al. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 257, no. 4 (April 2013): 731–36. http://dx.doi.org/10.1097/sla.0b013e318263da2f.

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4

Erickson, Lori A. "Pancreatic Ductal Adenocarcinoma." Mayo Clinic Proceedings 92, no. 9 (September 2017): 1461–62. http://dx.doi.org/10.1016/j.mayocp.2017.07.002.

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5

Longnecker, Daniel S. "Pancreatic Ductal Adenocarcinoma." American Journal of Pathology 189, no. 1 (January 2019): 6–8. http://dx.doi.org/10.1016/j.ajpath.2018.10.006.

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6

Crippa, Stefano, Stefano Partelli, and Massimo Falconi. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 266, no. 6 (December 2017): e108-e109. http://dx.doi.org/10.1097/sla.0000000000001921.

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7

Strobel, Oliver, and Markus W. Büchler. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 266, no. 6 (December 2017): e109-e110. http://dx.doi.org/10.1097/sla.0000000000001927.

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8

Izumi, Motoyoshi, Koichi Suda, Akira Torii, and Eisuke Inadama. "Pancreatic ductal myofibroblasts." Virchows Archiv 438, no. 5 (February 8, 2001): 442–50. http://dx.doi.org/10.1007/s004280000359.

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9

Chen, Yan, Huiyun Zhu, Yuqiong Wang, Yingxiao Song, Pingping Zhang, Zhijie Wang, Jun Gao, Zhaoshen Li, and Yiqi Du. "MicroRNA-132 Plays an Independent Prognostic Role in Pancreatic Ductal Adenocarcinoma and Acts as a Tumor Suppressor." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381882431. http://dx.doi.org/10.1177/1533033818824314.

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The role of microRNA-132 in human pancreatic ductal adenocarcinomas is still ambiguous. We explored the association between microRNA-132 and pancreatic ductal adenocarcinoma prognosis. The expression of microRNA-132 in 50 pancreatic ductal adenocarcinoma tissue samples and pancreatic ductal adenocarcinoma cell lines was examined, and the association between its expression and pancreatic ductal adenocarcinoma prognosis was assessed. Functional analysis and factors downstream of microRNA-132 were investigated. Kaplan-Meier survival curves showed that high expression of microRNA-132 was a significant prognostic factor for 1-year survival of patients with pancreatic ductal adenocarcinoma ( P = .028). Multivariate analysis for overall survival indicated that high expression of microRNA-132 was an independent prognostic factor for patients with pancreatic ductal adenocarcinoma ( P = .044). Low expression of microRNA-132 was associated with poor prognosis in pancreatic ductal adenocarcinoma. Ectopic expression of microRNA-132 significantly inhibited proliferation and promoted apoptosis of 2 pancreatic ductal adenocarcinoma cell lines. Bioinformatic analysis revealed that microRNA-132 may exert its effects on pancreatic ductal adenocarcinoma through downregulating mitogen-activated protein kinase 3 and nuclear transcription factor Y subunit α. The results of this study further our understanding of the relationship between microRNA-132 and pancreatic ductal adenocarcinoma by showing that microRNA-132 might inhibit the progression of pancreatic ductal adenocarcinoma by regulating mitogen-activated protein kinase and nuclear transcription factor Y subunit alpha.

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10

Al-Hawary, Mahmoud M., and Isaac R. Francis. "Pancreatic ductal adenocarcinoma staging." Cancer Imaging 13, no. 3 (2013): 360–64. http://dx.doi.org/10.1102/1470-7330.2013.9020.

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11

Diaz, Kelly E., and Aimee L. Lucas. "Familial Pancreatic Ductal Adenocarcinoma." American Journal of Pathology 189, no. 1 (January 2019): 36–43. http://dx.doi.org/10.1016/j.ajpath.2018.06.026.

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12

Tamiolakis, Demetrio, Constantine Simopoulos, Athanasia Kotini, Ioannis Venizelos, Theodoros Jivannakis, and Nikolaos Papadopoulos. "Pancreatic-Polypeptide in the Human Pancreas: Expression and Quantitative Variation During Development and in Ductal Adenocarcinoma." Acta Medica (Hradec Kralove, Czech Republic) 46, no. 1 (2003): 9–14. http://dx.doi.org/10.14712/18059694.2019.2.

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Aim: To determine the immunoreactivity of pancreatic-polypeptide (PP) during the development of the human fetal pancreas and ductal pancreatic adenocarcinoma, given that, PP positive cells were demonstrated either into its embryonic anlage or into pancreatic cancer. Methods: Tissue sections from 15 pancreatic fetal specimens, and equal number of ductal adenocarcinoma specimens, were assessed. Results: The density of positive cells in the primitive exocrine ductal epithelium and endocrine epithelium was significantly higher than the relevant density in the neoplastic pancreatic tissue of mixed (ductal – endocrine) and pure ductal type (p1=0.001, p2<0.0005, p3 =0.046 and p4<0.0005 respectively). The above values were estimated during the 10th to 12th week. There was no significant difference in the density of positive cells in the mantle zone of the islets from the 13th to the 24th week, and the neoplastic tissue of mixed (p5=0.11) and pure ductal type (p6=0.23). Conclusion: The immunostaining for PP identifies a subgroup of pancreatic ductal adenocarcinomas with a neuroendocrine component, initially considered as pure ductal tumors, and mixed ductal and neuroendocrine tumors. This pattern of expression in neoplasms recapitulates the normal pattern during the embryonal development of the organ, raising the question of therapeutic efficacy of PP and analogues as potential adjuvant treatment of pancreatic cancer.

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13

Wang, Zhonglan, Xiao Chen, Jianhua Wang, Wenjing Cui, Shuai Ren, and Zhongqiu Wang. "Differentiating hypovascular pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinoma based on CT texture analysis." Acta Radiologica 61, no. 5 (September 14, 2019): 595–604. http://dx.doi.org/10.1177/0284185119875023.

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Background Hypovascular pancreatic neuroendocrine tumor is usually misdiagnosed as pancreatic ductal adenocarcinoma. Purpose To investigate the value of texture analysis in differentiating hypovascular pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinoma on contrast-enhanced computed tomography (CT) images. Material and Methods Twenty-one patients with hypovascular pancreatic neuroendocrine tumors and 63 patients with pancreatic ductal adenocarcinomas were included in this study. All patients underwent preoperative unenhanced and dynamic contrast-enhanced CT examinations. Two radiologists independently and manually contoured the region of interest of each lesion using texture analysis software on pancreatic parenchymal and portal phase CT images. Multivariate logistic regression analysis was performed to identify significant features to differentiate hypovascular pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinomas. Receiver operating characteristic curve analysis was performed to ascertain diagnostic ability. Results The following CT texture features were obtained to differentiate hypovascular pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinomas: RMS (root mean square) (odds ratio [OR] = 0.50, P<0.001), Quantile50 (OR = 1.83, P<0.001), and sumAverage (OR = 0.92, P=0.007) in parenchymal images and “contrast” in portal phase images (OR = 6.08, P<0.001). The areas under the curves were 0.76 for RMS (sensitivity = 0.75, specificity = 0.67), 0.73 for Quantile50 (sensitivity = 0.60, specificity = 0.77), 0.70 for sumAverage (sensitivity = 0.65, specificity = 0.82), 0.85 for the combined texture features (sensitivity = 0.77, specificity = 0.85). Conclusion CT texture analysis may be helpful to differentiate hypovascular pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinomas. The three combined texture features showed acceptable diagnostic performance.

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Sun, Hongzhi, Bo Zhang, and Haijun Li. "The Roles of Frequently Mutated Genes of Pancreatic Cancer in Regulation of Tumor Microenvironment." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382092096. http://dx.doi.org/10.1177/1533033820920969.

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Pancreatic ductal adenocarcinoma has extremely high malignancy and patients with pancreatic ductal adenocarcinoma have dismal prognosis. The failure of pancreatic ductal adenocarcinoma treatment is largely due to the tumor microenvironment, which is featured by ample stromal cells and complicated extracellular matrix. Recent genomic analysis revealed that pancreatic ductal adenocarcinoma harbors frequently mutated genes including KRAS, TP53, CDKN2A, and SMAD4, which can widely alter cellular processes and behaviors. As shown by accumulating studies, these mutant genes may also change tumor microenvironment, which in turn affects pancreatic ductal adenocarcinoma progression. In this review, we summarize the role of such genetic mutations in tumor microenvironment regulation and potential mechanisms.

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15

Shrikhande, Shailesh V., Jörg Kleeff, Carolin Reiser, Jürgen Weitz, Ulf Hinz, Irene Esposito, Jan Schmidt, Helmut Friess, and Markus W. Büchler. "Pancreatic Resection for M1 Pancreatic Ductal Adenocarcinoma." Annals of Surgical Oncology 14, no. 1 (October 25, 2006): 118–27. http://dx.doi.org/10.1245/s10434-006-9131-8.

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16

Molnár, Réka, Brigitta Molnár, Júlia Fanczal, Tamara Madácsy, Zoltán Rakonczay, Péter Hegyi, and József Maléth. "Pancreatic ductal organoid cultures are suitable model to study pancreatic ductal ion secretion." Pancreatology 18, no. 4 (June 2018): S124. http://dx.doi.org/10.1016/j.pan.2018.05.334.

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Molnár, Réka, Laith Alsardi, Júlia Fanczal, Tamara Madácsy, József Maléth, and Péter Hegyi. "Pancreatic ductal organoid cultures are suitable model to study pancreatic ductal ion secretion." Pancreatology 17, no. 3 (July 2017): S45. http://dx.doi.org/10.1016/j.pan.2017.05.141.

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18

Yamaguchi, Koji, Shuichi Kanemitsu, Takashi Hatori, Hiroyuki Maguchi, Yasuhiro Shimizu, Minoru Tada, Toshio Nakagohri, et al. "Pancreatic Ductal Adenocarcinoma Derived From IPMN and Pancreatic Ductal Adenocarcinoma Concomitant With IPMN." Pancreas 40, no. 4 (May 2011): 571–80. http://dx.doi.org/10.1097/mpa.0b013e318215010c.

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19

Rayn, V. U., M. A. Persidskiy, E. V. Malakhova, I. V. Anuchina, A. A. Khalikova, Ya E. Timofeeva, and L. V. Bereshkeeva. "Precursors of pancreatic cancer in background of chronic opisthorchiasis." Medical Science And Education Of Ural 22, no. 1 (March 31, 2021): 118–21. http://dx.doi.org/10.36361/1814-8999-2021-22-1-118-121.

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Aim. To establish the association between pancreatic cancer precursor lesions and chronic opisthorchiasis. Materials and methods. A single center case-control study was conducted at a low-volume pancreatic surgery center in Khanty-Mansiysk. We retrospectively collected morphological data from 47 pancreatoduodenectomies performed for pancreatic ductal adenocarcinoma. The study group included 23 cases of pancreatic ductal adenocarcinoma with concomitant chronic Opisthorchis felineus invasion which were compared to 24 controls consisting of “pure” cancer. Qualitative analysis was performed using χ2 Pearson criterion. Exact Fisher test was used for small samples. Time to progression and overall survival rates were calculated using Kaplan-Meier survival analysis. Data were collected and analyzed in Statistica 7.0. Results. PanINs were seen in 41,7% pancreata resected for ductal adenocarcinoma of the head and in 95,7% cases of pancreatic cancer in background of chronic opisthorchiasis (р = 0,000; 95% CI 3,5-268). PanIN high grade were observed only in opisthorchiasis group. In mixed pathology invasive cancer component tended to be more dedifferentiated and advanced when compared to pure cancer group (p = 0,029). Median disease free survival was 9 mo. in both groups and overall survival was 13 mo. in non-opisthorchiasis group and 15,3 mo. in opisthorchiasis group (р = 0,437). Conclusion. Chronic opisthorchiasis is associated with pancreatic intraepithelial neoplasia. Pancreatic ductal adenocarcinoma in background of opisthorchiasis with preneoplastic lesions tend to be more advanced in stage and poorly differentiated. Disease free and overall survival have no statistically significant differences in patients with and without Opisthorchis felineus invasion.

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20

Wei, Honglong, Zongzhen Xu, Feng Liu, Fuhai Wang, Xin Wang, Xueying Sun, and Jie Li. "Hypoxia induces oncogene yes-associated protein 1 nuclear translocation to promote pancreatic ductal adenocarcinoma invasion via epithelial–mesenchymal transition." Tumor Biology 39, no. 5 (May 2017): 101042831769168. http://dx.doi.org/10.1177/1010428317691684.

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Pancreatic ductal adenocarcinoma is one of the most lethal cancers. The Hippo pathway is involved in tumorigenesis and remodeling of tumor microenvironments. Hypoxia exists in the microenvironment of solid tumors, including pancreatic ductal adenocarcinoma and plays a vital role in tumor progression and metastasis. However, it remains unclear how hypoxia interacts with the Hippo pathway to regulate these events. In this study, expressions of yes-associated protein 1 and hypoxia-inducible factor-1α were found to be elevated in pancreatic ductal adenocarcinoma samples compared with those in matched adjacent non-tumor samples. Moreover, hypoxia-inducible factor-1α expression was positively correlated with yes-associated protein 1 level in pancreatic ductal adenocarcinoma tissues. The higher expression of nuclear yes-associated protein 1 was associated with poor histological grade and prognosis for pancreatic ductal adenocarcinoma patients. In vitro, yes-associated protein 1 was highly expressed in pancreatic ductal adenocarcinoma cells. Depletion of yes-associated protein 1 inhibited the invasion of pancreatic ductal adenocarcinoma cells via downregulation of Vimentin, matrix metalloproteinase-2, and matrix metalloproteinase-13, and upregulation of E-cadherin. In addition, hypoxia promoted the invasion of pancreatic ductal adenocarcinoma cells via regulating the targeted genes. Hypoxia also deactivated the Hippo pathway and induced yes-associated protein 1 nuclear translocation. Furthermore, depletion of yes-associated protein 1 or hypoxia-inducible factor-1α suppressed the invasion of pancreatic ductal adenocarcinoma cells under hypoxia. Mechanism studies showed that nuclear yes-associated protein 1 interacted with hypoxia-inducible factor-1α and activated Snail transcription to participate in epithelial–mesenchymal transition–mediated and matrix metalloproteinase–mediated remodeling of tumor microenvironments. Collectively, yes-associated protein 1 is an independent prognostic predictor that interacts with hypoxia-inducible factor-1α to enhance the invasion of pancreatic cancer cells and remodeling of tumor microenvironments. Therefore, yes-associated protein 1 may serve as a novel promising target to enhance therapeutic effects for treating pancreatic cancer.

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21

González-Boja, Iranzu, Antonio Viúdez, Saioa Goñi, Enrique Santamaria, Estefania Carrasco-García, Jairo Pérez-Sanz, Irene Hernández-García, et al. "Omics Approaches in Pancreatic Adenocarcinoma." Cancers 11, no. 8 (July 25, 2019): 1052. http://dx.doi.org/10.3390/cancers11081052.

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Pancreatic ductal adenocarcinoma, which represents 80% of pancreatic cancers, is mainly diagnosed when treatment with curative intent is not possible. Consequently, the overall five-year survival rate is extremely dismal—around 5% to 7%. In addition, pancreatic cancer is expected to become the second leading cause of cancer-related death by 2030. Therefore, advances in screening, prevention and treatment are urgently needed. Fortunately, a wide range of approaches could help shed light in this area. Beyond the use of cytological or histological samples focusing in diagnosis, a plethora of new approaches are currently being used for a deeper characterization of pancreatic ductal adenocarcinoma, including genetic, epigenetic, and/or proteo-transcriptomic techniques. Accordingly, the development of new analytical technologies using body fluids (blood, bile, urine, etc.) to analyze tumor derived molecules has become a priority in pancreatic ductal adenocarcinoma due to the hard accessibility to tumor samples. These types of technologies will lead us to improve the outcome of pancreatic ductal adenocarcinoma patients.

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22

Satoi, Sohei. "Surgical Treatment of Pancreatic Ductal Adenocarcinoma." Cancers 13, no. 16 (August 10, 2021): 4015. http://dx.doi.org/10.3390/cancers13164015.

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This special issue, “Surgical Treatment of Pancreatic Ductal Adenocarcinoma” contains 13 articles (five original articles, five reviews, and three systematic reviews/meta-analyses) authored by international leaders and surgeons who treat patients with pancreatic ductal adenocarcinoma (PDAC) [...]

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23

Hartl, Leonie, JanWillem Duitman, Hella L. Aberson, Kan Chen, Frederike Dijk, Joris J. T. H. Roelofs, Mark P. G. Dings, et al. "CCAAT/Enhancer-Binding Protein Delta (C/EBPδ): A Previously Unrecognized Tumor Suppressor that Limits the Oncogenic Potential of Pancreatic Ductal Adenocarcinoma Cells." Cancers 12, no. 9 (September 7, 2020): 2546. http://dx.doi.org/10.3390/cancers12092546.

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CCAAT/enhancer-binding protein δ (C/EBPδ) is a transcription factor involved in growth arrest and differentiation, which has consequently been suggested to harbor tumor suppressive activities. However, C/EBPδ over-expression correlates with poor prognosis in glioblastoma and promotes genomic instability in cervical cancer, hinting at an oncogenic role of C/EBPδ in these contexts. Here, we explore the role of C/EBPδ in pancreatic cancer. We determined C/EBPδ expression in biopsies from pancreatic cancer patients using public gene-expression datasets and in-house tissue microarrays. We found that C/EBPδ is highly expressed in healthy pancreatic ductal cells but lost in pancreatic ductal adenocarcinoma. Furthermore, loss of C/EBPδ correlated with increased lymph node involvement and shorter overall survival in pancreatic ductal adenocarcinoma patients. In accordance with this, in vitro experiments showed reduced clonogenic capacity and proliferation of pancreatic ductal adenocarcinoma cells following C/EBPδ re-expression, concurrent with decreased sphere formation capacity in soft agar assays. We thus report a previously unrecognized but important tumor suppressor role of C/EBPδ in pancreatic ductal adenocarcinoma. This is of particular interest since only few tumor suppressors have been identified in the context of pancreatic cancer. Moreover, our findings suggest that restoration of C/EBPδ activity could hold therapeutic value in pancreatic ductal adenocarcinoma, although the latter claim needs to be substantiated in future studies.

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Seppänen, H., A. Juuti, H. Mustonen, C. Haapamäki, S. Nordling, M. Carpelan-Holmström, J. Sirén, J. Luettges, C. Haglund, and T. Kiviluoto. "The Results of Pancreatic Resections and Long-Term Survival for Pancreatic Ductal Adenocarcinoma: A Single-Institution Experience." Scandinavian Journal of Surgery 106, no. 1 (June 23, 2016): 54–61. http://dx.doi.org/10.1177/1457496916645963.

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Objectives: Since the early 1990s, low long-term survival rates following pancreatic surgery for pancreatic ductal adenocarcinoma have challenged us to improve treatment. In this series, we aim to show improved survival from pancreatic ductal adenocarcinoma during the era of centralized pancreatic surgery. Methods: Analysis of all pancreatic resections performed at Helsinki University Hospital and survival of pancreatic ductal adenocarcinoma patients during 2000–2013 were included. Post-operative complications such as fistulas, reoperations, and mortality rates were recorded. Patient and tumor characteristics were compared with survival data. Results: Of the 853 patients undergoing pancreatic surgery, 581 (68%) were pancreaticoduodenectomies, 195 (21%) distal resections, 28 (3%) total pancreatectomies, and 49 (6%) other procedures. Mortality after pancreaticoduodenectomy was 2.1%. The clinically relevant B/C fistula rate was 7% after pancreaticoduodenectomy and 13% after distal resection, and the re-operation rate was 5%. The 5- and 10-year survival rates for pancreatic ductal adenocarcinoma were 22% and 14%; for T1-2, N0 and R0 tumors, the corresponding survival rates were 49% and 31%. Carbohydrate antigen 19-9 >75 kU/L, carcinoembryonic antigen >5 µg/L, N1, lymph-node ratio >20%, R1, and lack of adjuvant therapy were independent risk factors for decreased survival. Conclusion: After centralization of pancreatic surgery in southern Finland, we have managed to enable pancreatic ductal adenocarcinoma patients to survive markedly longer than in the early 1990s. Based on a 1.7-million population in our clinic, mortality rates are equal to those of other high-volume centers and long-term survival rates for pancreatic ductal adenocarcinoma have now risen to some of the highest reported.

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Kim, Hyo-Sup, Seung-Hyun Hong, Seung-Hoon Oh, Jae-Hyeon Kim, Myung-Shik Lee, and Moon-Kyu Lee. "Activin A, exendin-4, and glucose stimulate differentiation of human pancreatic ductal cells." Journal of Endocrinology 217, no. 3 (March 15, 2013): 241–52. http://dx.doi.org/10.1530/joe-12-0474.

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Islet transplantation is one treatment option for diabetes mellitus. However, novel sources of pancreatic islets or insulin-producing cells are required because the amount of donor tissue available is severely limited. Pancreatic ductal cells are an alternative source of β-cells because they have the potential to differentiate into insulin-producing cells. We investigated whether treatment of human pancreatic ductal cells with activin A (ActA) and exendin-4 (EX-4) stimulated transdifferentiation of the cells, bothin vitroandin vivo. We treated human pancreatic ductal cells with ActA and EX-4 in high-glucose media to induce differentiation into insulin-producing cells and transplanted the cells into streptozotocin-induced diabetic nude mice. Co-treatment of mice with ActA and EX-4 promoted cell proliferation, induced expression of pancreatic β-cell-specific markers, and caused glucose-induced insulin secretion compared with the ActA or EX-4 mono-treatment groups respectively. When pancreatic ductal cells treated with ActA and EX-4 in high-glucose media were transplanted into diabetic nude mice, their blood glucose levels normalized and insulin was detected in the graft. These findings suggest that pancreatic ductal cells have a potential to replace pancreatic islets for the treatment of diabetes mellitus when the ductal cells are co-treated with ActA, EX-4, and glucose to promote their differentiation into functional insulin-producing cells.

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Ushio, Jun, Atsushi Kanno, Eriko Ikeda, Kozue Ando, Hiroki Nagai, Tetsurou Miwata, Yuki Kawasaki, et al. "Pancreatic Ductal Adenocarcinoma: Epidemiology and Risk Factors." Diagnostics 11, no. 3 (March 20, 2021): 562. http://dx.doi.org/10.3390/diagnostics11030562.

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The number of new cases of pancreatic ductal adenocarcinoma is increasing with a cumulative total of 495,773 cases worldwide, making it the fourteenth most common malignancy. However, it accounts for 466,003 deaths per year and is the seventh leading cause of cancer deaths. Regional differences in the number of patients with pancreatic ductal adenocarcinoma appear to reflect differences in medical care, as well as racial differences. Compared to the prevalence of other organ cancers in Japan, pancreatic ductal adenocarcinoma ranks seventh based on the number of patients, eighth based on morbidity, and fourth based on the number of deaths, with a continuing increase in the mortality rate. Risk factors for developing pancreatic ductal adenocarcinoma include family history, genetic disorders, diabetes, chronic pancreatitis, and intraductal papillary mucinous neoplasms. An issue that hinders improvement in the prognosis of patients with pancreatic ductal adenocarcinoma is the development of a strategy to identify patients with these risk factors to facilitate detection of the disease at a stage when intervention will improve survival.

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Park, Jong Y. "MicroRNAs in pancreatic ductal adenocarcinoma." World Journal of Gastroenterology 17, no. 7 (2011): 817. http://dx.doi.org/10.3748/wjg.v17.i7.817.

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Pilarsky, Christian, and Robert Grützmann. "Genomics of pancreatic ductal adenocarcinoma." Hepatobiliary & Pancreatic Diseases International 13, no. 4 (August 2014): 381–85. http://dx.doi.org/10.1016/s1499-3872(14)60281-2.

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Horvat, Natally, Davinia E. Ryan, Maria D. LaGratta, Pari M. Shah, and Richard Kinh Do. "Imaging for pancreatic ductal adenocarcinoma." Chinese Clinical Oncology 6, no. 6 (December 2017): 62. http://dx.doi.org/10.21037/cco.2017.11.03.

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Mozheiko, L. A. "HISTOPHYSIOLOGY OF DUCTAL PANCREATIC SECRETION." Hepatology and Gastroenterology 3, no. 1 (2019): 22–27. http://dx.doi.org/10.25298/2616-5546-2019-3-1-22-27.

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31

Tracy, Thomas F. "Pancreatic ductal abnormalities in children." Journal of Pediatric Surgery 27, no. 6 (June 1992): 788. http://dx.doi.org/10.1016/s0022-3468(05)80136-8.

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Bakman, Y. G., K. Safdar, and M. L. Freeman. "PANCREATIC STENT-INDUCED DUCTAL INJURY." Pancreas 37, no. 4 (November 2008): 461. http://dx.doi.org/10.1097/01.mpa.0000335330.72933.0f.

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Al-Hawary, Mahmoud M., Ravi K. Kaza, Shadi F. Azar, Julie A. Ruma, and Isaac R. Francis. "Mimics of pancreatic ductal adenocarcinoma." Cancer Imaging 13, no. 3 (2013): 342–49. http://dx.doi.org/10.1102/1470-7330.2013.9012.

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Kawai, Hiromi, Mizuho Kojima, Masaki Yokota, Haruo Iguchi, Hideyuki Wakasugi, Atsuo Jimi, and Akihiro Funakoshi. "Erythropoietin-Producing Pancreatic Ductal Adenocarcinoma." Pancreas 21, no. 4 (November 2000): 427–29. http://dx.doi.org/10.1097/00006676-200011000-00015.

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Bakman, Yan, and Martin Freeman. "Pancreatic Stent-Induced Ductal Injury." American Journal of Gastroenterology 103 (September 2008): S62. http://dx.doi.org/10.14309/00000434-200809001-00157.

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Pandol, Stephen, Mouad Edderkaoui, Ilya Gukovsky, Aurelia Lugea, and Anna Gukovskaya. "Desmoplasia of Pancreatic Ductal Adenocarcinoma." Clinical Gastroenterology and Hepatology 7, no. 11 (November 2009): S44—S47. http://dx.doi.org/10.1016/j.cgh.2009.07.039.

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37

Yamasaki, Akio, Kosuke Yanai, and Hideya Onishi. "Hypoxia and pancreatic ductal adenocarcinoma." Cancer Letters 484 (August 2020): 9–15. http://dx.doi.org/10.1016/j.canlet.2020.04.018.

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38

Gallego, J., C. López, R. Pazo-Cid, F. López-Ríos, and A. Carrato. "Biomarkers in pancreatic ductal adenocarcinoma." Clinical and Translational Oncology 19, no. 12 (June 14, 2017): 1430–37. http://dx.doi.org/10.1007/s12094-017-1691-5.

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Vera, R., L. Díez, E. Martín Pérez, J. C. Plaza, A. Sanjuanbenito, and A. Carrato. "Surgery for pancreatic ductal adenocarcinoma." Clinical and Translational Oncology 19, no. 11 (June 23, 2017): 1303–11. http://dx.doi.org/10.1007/s12094-017-1688-0.

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Muñoz Martín, A. J., J. Adeva, J. Martínez-Galán, J. J. Reina, and M. Hidalgo. "Pancreatic ductal adenocarcinoma: metastatic disease." Clinical and Translational Oncology 19, no. 12 (June 16, 2017): 1423–29. http://dx.doi.org/10.1007/s12094-017-1690-6.

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Djanani, Angela, Andreas Schmiderer, Lukas Niederreiter, Markus Niederreiter, and Herbert Tilg. "Management of ductal pancreatic cancer." European Surgery 51, no. 3 (May 15, 2019): 135–38. http://dx.doi.org/10.1007/s10353-019-0583-z.

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Habtezion, Aida, Mouad Edderkaoui, and Stephen J. Pandol. "Macrophages and pancreatic ductal adenocarcinoma." Cancer Letters 381, no. 1 (October 2016): 211–16. http://dx.doi.org/10.1016/j.canlet.2015.11.049.

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43

Storz, Peter, and Howard C. Crawford. "Carcinogenesis of Pancreatic Ductal Adenocarcinoma." Gastroenterology 158, no. 8 (June 2020): 2072–81. http://dx.doi.org/10.1053/j.gastro.2020.02.059.

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Tijeras-Raballand, Annemilaï, Marc Hilmi, Lucile Astorgues-Xerri, Rémy Nicolle, Ivan Bièche, and Cindy Neuzillet. "Microbiome and pancreatic ductal adenocarcinoma." Clinics and Research in Hepatology and Gastroenterology 45, no. 2 (March 2021): 101589. http://dx.doi.org/10.1016/j.clinre.2020.101589.

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Carpenter, Eileen, Sarah Nelson, Filip Bednar, Clifford Cho, Hari Nathan, Vaibhav Sahai, Marina Pasca Magliano, and Timothy L. Frankel. "Immunotherapy for pancreatic ductal adenocarcinoma." Journal of Surgical Oncology 123, no. 3 (February 17, 2021): 751–59. http://dx.doi.org/10.1002/jso.26312.

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Betriu, Nausika, Juan Bertran-Mas, Anna Andreeva, and Carlos E. Semino. "Syndecans and Pancreatic Ductal Adenocarcinoma." Biomolecules 11, no. 3 (February 25, 2021): 349. http://dx.doi.org/10.3390/biom11030349.

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Abstract:

Pancreatic Ductal Adenocarcinoma (PDAC) is a fatal disease with poor prognosis because patients rarely express symptoms in initial stages, which prevents early detection and diagnosis. Syndecans, a subfamily of proteoglycans, are involved in many physiological processes including cell proliferation, adhesion, and migration. Syndecans are physiologically found in many cell types and their interactions with other macromolecules enhance many pathways. In particular, extracellular matrix components, growth factors, and integrins collect the majority of syndecans associations acting as biochemical, physical, and mechanical transducers. Syndecans are transmembrane glycoproteins, but occasionally their extracellular domain can be released from the cell surface by the action of matrix metalloproteinases, converting them into soluble molecules that are capable of binding distant molecules such as extracellular matrix (ECM) components, growth factor receptors, and integrins from other cells. In this review, we explore the role of syndecans in tumorigenesis as well as their potential as therapeutic targets. Finally, this work reviews the contribution of syndecan-1 and syndecan-2 in PDAC progression and illustrates its potential to be targeted in future treatments for this devastating disease.

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Permert, Johan, Masatoshi Mogaki, Åke Andrén-Sandberg, Katherine Kazokoff, and Parviz M. Pouf. "Pancreatic mixed Ductal-Islet tumors." International Journal of Pancreatology 11, no. 1 (February 1992): 23–29. http://dx.doi.org/10.1007/bf02925989.

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Montag, A. G., N. Fossati, and F. Michelassi. "Pancreatic Microcystic Adenoma Coexistent with Pancreatic Ductal Carcinoma." American Journal of Surgical Pathology 14, no. 4 (April 1990): 352–55. http://dx.doi.org/10.1097/00000478-199004000-00006.

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Iwase, Kazuhiro, Masahiko Miyata, Tokio Yamaguchi, Takanobu Kawaguchi, Yasuhiro Tanaka, and Hikaru Matsuda. "Pancreatic ductal cell carcinoma producing pancreatic elastase 1." Journal of Surgical Oncology 54, no. 3 (November 1993): 199–202. http://dx.doi.org/10.1002/jso.2930540316.

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Sharaiha, Reem Z., Jessica Widmer, and Michel Kahaleh. "Palliation of Pancreatic Ductal Obstruction in Pancreatic Cancer." Gastrointestinal Endoscopy Clinics of North America 23, no. 4 (October 2013): 917–23. http://dx.doi.org/10.1016/j.giec.2013.06.010.

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