Abnormalities of tumor suppressor gene p16 in pancreatic carcinoma: immunohistochemical and genetic findings compared with clinicopathological parameters

Ohtsubo, Koushiro; Watanabe, Hiroyuki; Yamaguchi, Yasushi; Hu, Yuxin; Motoo, Yoshiharu; Okai, Takashi; Sawabu, Norio

doi:10.1007/s00535-003-1119-6

Cited by 46 publications

(40 citation statements)

References 42 publications

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“…A study evaluating the prognostic value of p16 mutation in patients with PC found that the tumour was significantly larger and the survival period significantly shorter for patients with PC with p16 mutation or hypermethylation than for those with pancreatic carcinoma with an intact p16 gene, suggesting that p16 alterations may participate in the aggressiveness of pancreatic carcinoma [48].…”

Section: K-rasmentioning

confidence: 99%

Molecular markers of pancreatic cancer: development and clinical relevance

Fry

Mönkemüller

Malfertheiner

2008

Langenbecks Arch Surg

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Section: K-rasmentioning

confidence: 99%

Molecular markers of pancreatic cancer: development and clinical relevance

Fry

Mönkemüller

Malfertheiner

2008

Langenbecks Arch Surg

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“…It is difficult to predict which patient is at risk of early relapse following surgery, or which patient with advanced stage disease will show good long-term survival. K-ras point mutations and inactivation of p53, p16, and SMAD4 are often associated with malignant characteristics in pancreatic cancers, but mutations of K-ras and p53 are not significantly associated with the prognosis of patients with pancreatic cancer (21,23,24). In the prognosis of patients with pancreatic cancer, there seems to be a significant correlation between microvessel density and the expression of vascular endothelial growth factor (VEGF) and PD-ECGF in the tumor, as well as with E-cadherin, p27, PEDF, and SMAD4 expression (24)(25)(26)(27).…”

Section: Introductionmentioning

confidence: 99%

Tumor Growth Suppression in Pancreatic Cancer by a Putative Metastasis Suppressor Gene Cap43/NDRG1/Drg-1 through Modulation of Angiogenesis

Maruyama

Ono

Kawahara³

et al. 2006

Cancer Research

152

146

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Cap43 has been identified as a nickel-and calcium-induced gene, and is also known as N-myc downstream-regulated gene 1 (NDRG1), Drg-1 and rit42. It is also reported that overexpression of Cap43 suppresses metastasis of some malignancies, but its precise role remains unclear. In this study, we asked how Cap43 could modulate the tumor growth of pancreatic cancer. Stable Cap43 cDNA transfectants of pancreatic cancer cells with Cap43 overexpression showed similar growth rates in culture as their control counterparts with low Cap43 protein level. By contrast, Cap43 overexpression showed a marked decrease in tumor growth rates in vivo. Moreover, a marked reduction in tumor-induced angiogenesis was observed. Gelatinolytic activity by matrix metalloproteinase-9 and invasive ability in Matrigel invasion activity were markedly decreased in pancreatic cancer cell lines with high Cap43 expression. Cellular expression of matrix metalloproteinase-9 and two major angiogenic factors, vascular endothelial growth factor and interleukin-8, were also significantly decreased in cell lines with Cap43 overexpression as compared with their parental counterparts. Immunohistochemical analysis of specimens from 65 patients with pancreatic ductal adenocarcinoma showed a significant association between Cap43 expression and tumor microvascular density (P = 0.0001) as well as depth of invasion (P = 0.0003), histopathologic grading (P = 0.0244), and overall survival rates for patients with pancreatic cancer (P = 0.0062). Thus, Cap43 could play a key role in the angiogenic on-or offswitch of tumor stroma in pancreatic ductal adenocarcinoma.

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“…This abstract has only four non-standard references to mutation: "CDKN2A alterations" (one instance) and "(epi)genetic modifications" (three instances). Similarly, articles PMID: 12898359 (Ohtsubo, et al, 2003) and PMID: 12721243 (Schneider-Stock, et al, 2003) both mention "mutation(s)" and either "homozygous deletion" or "loss of heterozygosity" sporadically, but each usually instead refers to "abnormalities", and the focus of the articles are on methylation status and immunohistochemical analysis of tumors. PMID:11159196 (Schraml, et al, 2001), specifically mentions "mutation analysis" and "24-bp deletion" as the only two direct instances of mutation mentions, while most of the abstract describes results of a chromosomal deletion analysis.…”

Section: Resultsmentioning

confidence: 99%

An automated procedure to identify biomedical articles that contain cancer-associated gene variants

et al. 2006

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The proliferation of biomedical literature makes it increasingly difficult for researchers to find and manage relevant information. However, identifying research articles containing mutation data, a requisite first step in integrating large and complex mutation data sets, is currently tedious, time-consuming and imprecise. More effective mechanisms for identifying articles containing mutation information would be beneficial both for the curation of mutation databases and for individual researchers. We developed an automated method that uses information extraction, classifier, and relevance ranking techniques to determine the likelihood of MEDLINE abstracts containing information regarding genomic variation data suitable for inclusion in mutation databases. We targeted the CDKN2A (p16) gene and the procedure for document identification currently used by CDKN2A Database curators as a measure of feasibility. A set of abstracts was manually identified from a MEDLINE search as potentially containing specific CDKN2A mutation events. A subset of these abstracts was used as a training set for a maximum entropy classifier to identify text features distinguishing "relevant" from "not relevant" abstracts. Each document was represented as a set of indicative word, word pair, and entity tagger-derived genomic variation features. When applied to a test set of 200 candidate abstracts, the classifier predicted 88 articles as being relevant; of these, 29 of 32 manuscripts in which manual curation found CDKN2A sequence variants were positively predicted. Thus, the set of potentially useful articles that a manual curator would have to review was reduced by 56%, maintaining 91% recall (sensitivity) and more than doubling precision (positive predictive value). Subsequent expansion of the training set to 494 articles yielded similar precision and recall rates, and comparison of the original and expanded trials demonstrated that the average precision improved with the larger data set. Our results show that automated systems can effectively identify article subsets relevant to a given task and may prove to be powerful tools for the broader research community. This procedure can be readily adapted to any or all genes, organisms, or sets of documents. Classifying text for cancer mutations AbstractThe proliferation of biomedical literature makes it increasingly difficult for researchers to find and manage relevant information. However, identifying research articles containing mutation data, a requisite first step in integrating large and complex mutation data sets, is currently tedious, time-consuming and imprecise. More effective mechanisms for identifying articles containing mutation information would be beneficial both for the curation of mutation databases and for individual researchers. We developed an automated method that uses information extraction, classifier, and relevance ranking techniques to determine the likelihood of MEDLINE abstracts containing mentions of genomic variation data suitable for inclusion in mutation d...

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Abnormalities of tumor suppressor gene p16 in pancreatic carcinoma: immunohistochemical and genetic findings compared with clinicopathological parameters

Abstract: These findings suggest that p16 alterations may participate in the aggressiveness of pancreatic carcinoma.

Cited by 46 publications

References 42 publications

Molecular markers of pancreatic cancer: development and clinical relevance

Molecular markers of pancreatic cancer: development and clinical relevance

Tumor Growth Suppression in Pancreatic Cancer by a Putative Metastasis Suppressor Gene Cap43/NDRG1/Drg-1 through Modulation of Angiogenesis

An automated procedure to identify biomedical articles that contain cancer-associated gene variants

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