Relevant bibliographies by topics / INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM, PANCREAS, INDOLENT PRECURSOR, PANCREATIC CANCER

Academic literature on the topic 'INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM, PANCREAS, INDOLENT PRECURSOR, PANCREATIC CANCER'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM, PANCREAS, INDOLENT PRECURSOR, PANCREATIC CANCER"

1

Marchegiani, Giovanni, Stefano Andrianello, Tommaso Pollini, Andrea Caravati, Giuseppe Malleo, Marco Biancotto, Claudio Bassi, and Roberto Salvia. "Natural History of Intraductal Papillary Mucinous Neoplasm of the Pancreas Reappraisal of the Indolent Precursor of Pancreatic Cancer." Journal of the American College of Surgeons 227, no. 4 (October 2018): e37-e38. http://dx.doi.org/10.1016/j.jamcollsurg.2018.08.099.

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Marchegiani, G., S. Andrianello, T. Pollini, A. Caravati, M. Biancotto, G. Malleo, C. Bassi, and R. Salvia. "The natural history of intraductal papillary mucinous neoplasm of the pancreas: Reappraisal of the indolent precursor of pancreatic cancer." HPB 20 (September 2018): S195. http://dx.doi.org/10.1016/j.hpb.2018.06.051.

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3

Marchegiani, Giovanni, Stefano Andrianello, Tommaso Pollini, Andrea Caravati, Marco Biancotto, Giuseppe Malleo, Claudio Bassi, and Roberto Salvia. "The natural history of intraductal papillary mucinous neoplasms of the pancreas: Reappraisal of the indolent precursor of pancreatic cancer." Pancreatology 18, no. 4 (June 2018): S2—S3. http://dx.doi.org/10.1016/j.pan.2018.05.011.

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4

Ferri-Borgogno, Sammy, Sugata Barui, Amberly M. McGee, Tamara Griffiths, Pankaj K. Singh, Cortt G. Piett, Bidyut Ghosh, et al. "Paradoxical Role of AT-rich Interactive Domain 1A in Restraining Pancreatic Carcinogenesis." Cancers 12, no. 9 (September 21, 2020): 2695. http://dx.doi.org/10.3390/cancers12092695.

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Background & Aims: ARID1A is postulated to be a tumor suppressor gene owing to loss-of-function mutations in human pancreatic ductal adenocarcinomas (PDAC). However, its role in pancreatic pathogenesis is not clear despite recent studies using genetically engineered mouse (GEM) models. We aimed at further understanding of its direct functional role in PDAC, using a combination of GEM model and PDAC cell lines. Methods: Pancreas-specific mutant Arid1a-driven GEM model (Ptf1a-Cre; KrasG12D; Arid1af/f or “KAC”) was generated by crossing Ptf1a-Cre; KrasG12D (“KC”) mice with Arid1af/f mice and characterized histologically with timed necropsies. Arid1a was also deleted using CRISPR-Cas9 system in established human and murine PDAC cell lines to study the immediate effects of Arid1a loss in isogenic models. Cell lines with or without Arid1a expression were developed from respective autochthonous PDAC GEM models, compared functionally using various culture assays, and subjected to RNA-sequencing for comparative gene expression analysis. DNA damage repair was analyzed in cultured cells using immunofluorescence and COMET assay. Results: Retention of Arid1a is critical for early progression of mutant Kras-driven pre-malignant lesions into PDAC, as evident by lower Ki-67 and higher apoptosis staining in “KAC” as compared to “KC” mice. Enforced deletion of Arid1a in established PDAC cell lines caused suppression of cellular growth and migration, accompanied by compromised DNA damage repair. Despite early development of relatively indolent cystic precursor lesions called intraductal papillary mucinous neoplasms (IPMNs), a subset of “KAC” mice developed aggressive PDAC in later ages. PDAC cells obtained from older autochthonous “KAC” mice revealed various compensatory (“escaper”) mechanisms to overcome the growth suppressive effects of Arid1a loss. Conclusions: Arid1a is an essential survival gene whose loss impairs cellular growth, and thus, its expression is critical during early stages of pancreatic tumorigenesis in mouse models. In tumors that arise in the setting of ARID1A loss, a multitude of “escaper” mechanisms drive progression.
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Panic, Nikola, Gabriele Capurso, Fabia Attili, Giovanna Vitale, Serena Stigliano, Gianfranco Delle Fave, Emanuele Leoncini, et al. "Risk for Colorectal Adenomas Among Patients with Pancreatic Intraductal Papillary Mucinous Neoplasms: a Prospective Case- Control Study." Journal of Gastrointestinal and Liver Diseases 24, no. 4 (December 1, 2015): 445–50. http://dx.doi.org/10.15403/jgld.2014.1121.244.rsk.

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Background & Aims: It has been reported that patients with intraductal papillary mucinous neoplasms of the pancreas are at an increased risk of colorectal cancer. The aim of our study was to investigate whether patients with intraductal papillary mucinous neoplasms are at a higher risk of colorectal adenomas with respect to the general population, as this condition represents the precursor of sporadic colorectal cancer. Methods: A case–control study was conducted at the Catholic University and University Sapienza, Rome, Italy. The cases were patients with intraductal papillary mucinous neoplasms without history of colorectal cancer, who had underwent screening colonoscopy for the first time. The controls were individuals who had underwent first time colonoscopy for screening or evaluation of non-specific abdominal symptoms. Chi-square and Fisher tests were used to compare the distributions of categorical variables. Results: We enrolled 122 cases and 246 controls. Colorectal polyps were found in 52 cases (42.6%) and 79 controls (32.1%) (p<0.05). In 29 cases (23.8%) and 57 controls (23.2%) histological examination disclosed adenomatous polyps (p=0.90). There was no difference between the groups in relation to the presence of polyps with low-grade (19.7% vs. 19.8%, p=0.98) and high-grade dysplasia (4.9% vs. 4.5%, p=0.85). Conclusion: Patients with intraductal papillary mucinous neoplasms of the pancreas are not at an increased risk for the development of adenomatous colorectal polyps. Abbreviations: BD-IPMN: branch duct intraductal papillary mucinous neoplasm; CRC: colorectal cancer; FAP: familiar adenomatous polyposis; FNA: fine needle aspiration; FOBT: fecal occult blood test; HNPCC: hereditary non-polyposis colorectal cancer; IPMN: intraductal papillary mucinous neoplasm; M-IPMN: mixed intraductal papillary mucinous neoplasm; MD-IPMNs: main duct intraductal papillary mucinous neoplasm; PDAC: pancreatic ductal adenocarcinoma; S-MRCP: magnetic resonance cholangiopancreatography with secretin stimulation.
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6

Wei, Tao, Qi Chen, Tingbo Liang, and Xueli Bai. "Clinical-relevant model of intraductal papillary mucinous neoplasm induced by ARID1A loss." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14696-e14696. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14696.

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e14696 Background: Intraductal papillary mucinous neoplasm (IPMN) constitutes a precursor lesion for malignancy of pancreas. Genes encoding subunits of SWI/SNF chromatin-remodeling complexes like ARID1A are collectively mutated in a significant proportion of patients with pancreatic neoplasm. In the present study, we characterize the role of ARID1A in pancreatic tumorigenesis using genetic engineering mouse models. Methods: Various mouse strains were interbred to obtain pancreas-specific Arid1aflox, KrasLSL-G12D/+; Arid1aflox, KrasLSL-G12D/+; Tgfbr2flox; Arid1aflox, and various littermate control animals. Tissue microarrays were used to determine the expression of ARID1A in human pancreatic ductal adenocarcinoma and IPMN. Results: Arid1a loss in pancreas of mice incurred pancreatic duct dilation and development of cystic lesions. Concomitant Kras mutation and Arid1a inactivation accelerated formation of cystic neoplasm resembling human IPMN. These lesions were reminiscent of specific subtype of IPMN given their morphology and expression pattern of mucin proteins. Histological examination further revealed the step-wise progression of these neoplasm from low-grade to high-grade dysplasia and even invasive carcinoma. TGFBR2 deletion promoted the malignant transformation of IPMN to invasive carcinoma in the background of Kras and Arid1a alterations. Analysis of human tissues consistently showed negative or low expression of ARID1A in over half of IPMN patients. Moreover, patients with pancreatic adenocarcinoma also exhibited downregulated ARID1A expression, and reduced expression correlated with worse prognosis. Conclusions: We have established a preclinical mouse model of pancreatic cystic tumor closely resembling human IPMN. This is helpful for the further understanding of biology of IPMN and highlight therapeutic niches for patient tailored treatment in those with altered SWI/SNF function.
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7

Chung, Wen-Cheng, Lavanya Challagundla, Yunyun Zhou, Min Li, Azeddine Atfi, and Keli Xu. "Loss of Jag1 cooperates with oncogenic Kras to induce pancreatic cystic neoplasms." Life Science Alliance 4, no. 2 (December 2, 2020): e201900503. http://dx.doi.org/10.26508/lsa.201900503.

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Notch signaling exerts both oncogenic and tumor-suppressive functions in the pancreas. In this study, deletion of Jag1 in conjunction with oncogenic KrasG12D expression in the mouse pancreas induced rapid development of acinar-to-ductal metaplasia and early stage pancreatic intraepithelial neoplasm; however, culminating in cystic neoplasms rather than ductal adenocarcinoma. Most cystic lesions in these mice were reminiscent of serous cystic neoplasm, and the rest resembled intraductal papillary mucinous neoplasm. Jag1 expression was lost or decreased in cystic lesions but retained in adenocarcinoma in these mice, so was the expression of Sox9. In pancreatic cancer patients, JAG1 expression is higher in cancerous tissue, and high JAG1 is associated with poor overall survival. Expression of SOX9 is correlated with JAG1, and high SOX9 is also associated with poor survival. Mechanistically, Jag1 regulates expression of Lkb1, a tumor suppressor involved in the development of pancreatic cystic neoplasm. Collectively, Jag1 can act as a tumor suppressor in the pancreas by delaying precursor lesions, whereas loss of Jag1 promoted a phenotypic switch from malignant carcinoma to benign cystic lesions.
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8

Ilies, Maria, Praveen Kumar Sappa, Cristina Adela Iuga, Felicia Loghin, Manuela Gesell Salazar, Frank Ulrich Weiss, Georg Beyer, et al. "Plasma protein profiling of patients with intraductal papillary mucinous neoplasm of the pancreas as potential precursor lesions of pancreatic cancer." Clinica Chimica Acta 477 (February 2018): 127–34. http://dx.doi.org/10.1016/j.cca.2017.12.008.

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