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We began analyzing https://link.springer.com/article/10.1007/s00534-005-1056-2, but it redirected us to https://link.springer.com/article/10.1007/s00534-005-1056-2. The analysis below is for the second page.

Title[redir]:
Epigenetic alterations in intraductal papillary mucinous neoplasms of the pancreas | Journal of Hepato-Biliary-Pancreatic Sciences
Description:
Intraductal papillary mucinous neoplasm (IPMN), an increasingly recognized cystic neoplasm of the pancreas with a broad spectrum of malignant potential, has been considered a precursor to infiltrating ductal adenocarcinoma. Because of its unique clinical, radiological, pathological, and molecular features, IPMN has attracted considerable interest among clinicians and researchers. Although some genetic alterations have been described in IPMNs, the molecular features that characterize the evolution and progression of these neoplasms are largely unknown. Recent studies have shown that aberrant methylation of the promoter cytosine-phospho-guanine (CpG) island is a common mechanism associated with the silencing of tumor-suppressor and cancer-related genes in IPMNs. Importantly, the prevalence of such methylation increases along with the grade of neoplasia, suggesting that these epigenetic events may contribute to the progression of IPMNs. Further studies of epigenetic alterations in IPMN will shed light on the molecular pathogenesis of this unique neoplasm and lead to the identification of epigenetic markers that can be applied in the clinical setting.

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Keywords {πŸ”}

google, scholar, pubmed, article, cas, pancreas, intraductal, pancreatic, cancer, mucinous, papillary, neoplasms, sato, fukushima, methylation, tumors, goggins, surg, yeo, ductal, res, pathol, papillarymucinous, hruban, tumor, matsubayashi, epigenetic, adenocarcinoma, clin, gene, iacobuziodonahue, analysis, ipmn, clinical, progression, aberrant, genes, clinicopathologic, ann, expression, molecular, neoplasia, access, patients, cameron, privacy, cookies, content, journal, research,

Topics {βœ’οΈ}

iacobuzio-donahue jg herman albores-saavedra av biankin wilentz ca iacobuzio-donahue matsubayashi ca iacobuzio-donahue dc%2bd38%2fgs1slta%3d%3d 10 klimstra kc conlon fernandez-del-castillo rh hawes rb/p16 tumor-suppressive pathway argani ta sohn matsubayashi jl cameron dc%2bd38vhvvsktq%3d%3d 10 dc%2bd3c7kvvwrsq%3d%3d 10 dc%2bd2mxnt1wlsa%3d%3d 10 dc%2bd3mvotvymug%3d%3d 10 dc%2bd3sxht1yltw%3d%3d 10 dc%2bd28xlsfonuw%3d%3d 10 month download article/chapter takaori rh hruban goggins cj yeo schutte rh hruban intraductal papillary-mucinous neoplasms intraductal papillary-mucinous carcinoma intraductal papillary-mucinous tumor intraductal papillary-mucinous tumors kitagawa ta unger ueki cj yeo mucus-secreting pancreatic cancer k-ras gene mutations parsons se kern activating k-ras mutations promoter cytosine-phospho-guanine dc%2bd3mxks1oru78%3d 10 dc%2bd38xptfcjtl4%3d 10 dc%2bd3sxmtvemsly%3d 10 dc%2bd2cxhsfohtro%3d 10 dc%2bd28xhvfomsr0%3d 10 dc%2bd38xmt1ahs7c%3d 10 dc%2bd3sxit1yms7c%3d 10 dc%2bd38xkvvgktlw%3d 10 dc%2bd3mxkslclsbs%3d 10 dc%2bd3sxlsvaktro%3d 10 dc%2bd38xktvkgtrg%3d 10 dc%2bd2mxlvvght7y%3d 10 dc%2bd3sxisfajtl4%3d 10 dc%2bd2mxnsl2ksl4%3d 10 dyak2m3ktlcnsg%3d%3d 10 dyak2svlt1eisg%3d%3d 10 dyak1czjvvemsg%3d%3d 10 yeo cj dyak2m7itvwrtq%3d%3d 10

Questions {❓}

  • (2005) Multicenter analysis of clinicopathologic features of intraductal papillary mucinous tumor of the pancreas: is it possible to predict the malignancy before surgery?

Schema {πŸ—ΊοΈ}

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         headline:Epigenetic alterations in intraductal papillary mucinous neoplasms of the pancreas
         description:Intraductal papillary mucinous neoplasm (IPMN), an increasingly recognized cystic neoplasm of the pancreas with a broad spectrum of malignant potential, has been considered a precursor to infiltrating ductal adenocarcinoma. Because of its unique clinical, radiological, pathological, and molecular features, IPMN has attracted considerable interest among clinicians and researchers. Although some genetic alterations have been described in IPMNs, the molecular features that characterize the evolution and progression of these neoplasms are largely unknown. Recent studies have shown that aberrant methylation of the promoter cytosine-phospho-guanine (CpG) island is a common mechanism associated with the silencing of tumor-suppressor and cancer-related genes in IPMNs. Importantly, the prevalence of such methylation increases along with the grade of neoplasia, suggesting that these epigenetic events may contribute to the progression of IPMNs. Further studies of epigenetic alterations in IPMN will shed light on the molecular pathogenesis of this unique neoplasm and lead to the identification of epigenetic markers that can be applied in the clinical setting.
         datePublished:
         dateModified:
         pageStart:280
         pageEnd:285
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         keywords:
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            Hypermethylation
            IPMN
            Precursor
            Pancreatic cancer
            Abdominal Surgery
            Hepatology
            Gastroenterology
            Surgical Oncology
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      headline:Epigenetic alterations in intraductal papillary mucinous neoplasms of the pancreas
      description:Intraductal papillary mucinous neoplasm (IPMN), an increasingly recognized cystic neoplasm of the pancreas with a broad spectrum of malignant potential, has been considered a precursor to infiltrating ductal adenocarcinoma. Because of its unique clinical, radiological, pathological, and molecular features, IPMN has attracted considerable interest among clinicians and researchers. Although some genetic alterations have been described in IPMNs, the molecular features that characterize the evolution and progression of these neoplasms are largely unknown. Recent studies have shown that aberrant methylation of the promoter cytosine-phospho-guanine (CpG) island is a common mechanism associated with the silencing of tumor-suppressor and cancer-related genes in IPMNs. Importantly, the prevalence of such methylation increases along with the grade of neoplasia, suggesting that these epigenetic events may contribute to the progression of IPMNs. Further studies of epigenetic alterations in IPMN will shed light on the molecular pathogenesis of this unique neoplasm and lead to the identification of epigenetic markers that can be applied in the clinical setting.
      datePublished:
      dateModified:
      pageStart:280
      pageEnd:285
      sameAs:https://doi.org/10.1007/s00534-005-1056-2
      keywords:
         Epigenetics
         Hypermethylation
         IPMN
         Precursor
         Pancreatic cancer
         Abdominal Surgery
         Hepatology
         Gastroenterology
         Surgical Oncology
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