Institution
Eppley Institute for Research in Cancer and Allied Diseases
About: Eppley Institute for Research in Cancer and Allied Diseases is a based out in . It is known for research contribution in the topics: Pancreatic cancer & Cancer. The organization has 965 authors who have published 1396 publications receiving 58994 citations.
Topics: Pancreatic cancer, Cancer, DNA, Gene, Cancer cell
Papers published on a yearly basis
Papers
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TL;DR: Results suggest that reaction of ortho-quinones with DNA by 1,4-Michael addition is a general mechanism of weak carcinogenesis that occurs with naphthalene and a number of other aromatic compounds.
48 citations
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TL;DR: Analysis of epigenetic changes in mucin genes may be of diagnostic utility and one of the prognostic predictors for patients with pancreatic ductal adenocarcinoma.
Abstract: Purpose: Pancreatic cancer remains a disease of high mortality despite advanced diagnostic techniques. Mucins (MUC) play crucial roles in carcinogenesis and tumor invasion in pancreatic cancers. MUC1 and MUC4 expression are related to the aggressive behavior of human neoplasms and a poor patient outcome. In contrast, MUC2 is a tumor suppressor, and we have previously reported that MUC2 is a favorable prognostic factor in pancreatic neoplasia. This study investigates whether the methylation status of three mucin genes from postoperative tissue specimens from patients with pancreatic neoplasms could serve as a predictive biomarker for outcome after surgery. Experimental Design: We evaluated the methylation status of MUC1, MUC2, and MUC4 promoter regions in pancreatic tissue samples from 191 patients with various pancreatic lesions using methylation-specific electrophoresis. Then, integrating these results and clinicopathologic features, we used support vector machine-, neural network-, and multinomial-based methods to develop a prognostic classifier. Results: Significant differences were identified between the positive- and negative-prediction classifiers of patients in 5-year overall survival (OS) in the cross-validation test. Multivariate analysis revealed that these prognostic classifiers were independent prognostic factors analyzed by not only neoplastic tissues but also nonneoplastic tissues. These classifiers had higher predictive accuracy for OS than tumor size, lymph node metastasis, distant metastasis, and age and can complement the prognostic value of the TNM staging system. Conclusions: Analysis of epigenetic changes in mucin genes may be of diagnostic utility and one of the prognostic predictors for patients with pancreatic ductal adenocarcinoma.
48 citations
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TL;DR: Initial information is provided suggesting that one-electron oxidation may be a mechanism of activation for PAH in the mammary gland.
Abstract: To obtain some initial evidence on the mechanism(s) of activation of PAH in rat mammary gland, we studied the carcinogenicity of a series of PAH directly applied to this tissue. A series of PAH which are or are not expected to be activated by one-electron oxidation because of their low or high ionization potential (IP), respectively, were tested. The compounds were dispersed as fine powders on an exposed mammary gland of female Sprague-Dawley rats. 5-Methylchrysene, dibenz[a,h]anthracene and benz[a]anthracene, which have relatively high IP, were inactive. In contrast, three PAH with relatively low IP, 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene (BP), and 3-methylcholanthrene (MC), were potent carcinogens, 6-MethylBP, with low IP, and 7-methyl-benz[a]anthracene, with borderline IP, elicited only mesenchymal tumors, whereas BP 7,8-dihydrodiol and cyclopenta[cd]pyrene were inactive. A series of MC derivatives substituted at C-1 or C-2 was tested. Substituents at C-1, the position of activation in the one-electron oxidation pathway, generally suppressed carcinogenic activity. Substitution at C-2 did not eliminate carcinogenic activity, with the exception of MC2-one. These results provide initial information suggesting that one-electron oxidation may be a mechanism of activation for PAH in the mammary gland.
48 citations
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TL;DR: Results indicate that at least two Mrc1-dependent mechanisms function to reduce CAG, and suggest that the DNA damage checkpoint inhibits expansions after formation of repeat-dependent structures.
48 citations
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TL;DR: By analyzing profiles of estrogen metabolites, conjugates, and depurinating DNA adducts in urine from men with and without prostate cancer, potential biomarkers of Pca can be detected.
Abstract: BACKGROUND
Although the estrogens estrone and estradiol are recognized to play very important roles in the risk of developing prostate cancer (Pca), the molecular mechanism by which estrogens initiate and/or promote Pca is still unknown. Substantial evidence supports that specific metabolites of estrogens, catechol estrogen quinones, can react with DNA to form depurinating estrogen-DNA adducts. Apurinic sites derived from depurination of these adducts can induce mutations leading to cancer. Once released from DNA, depurinating estrogen-DNA adducts are shed from cells into the bloodstream and excreted in urine. By analyzing profiles of estrogen metabolites, conjugates, and depurinating DNA adducts in urine from men with and without prostate cancer, potential biomarkers of Pca can be detected. The goal of this case–control study was to detect and identify potential biomarkers of Pca.
METHODS
Urine samples from fourteen cases, men diagnosed with Pca, and 125 controls, men who had not been diagnosed with Pca, were partially purified by solid phase extraction and analyzed by ultraperformance liquid chromatography/tandem mass spectrometry. The urinary levels of androgens, estrogens, estrogen metabolites, conjugates and depurinating DNA adducts were measured.
RESULTS
The ratio of depurinating estrogen-DNA adducts to the sum of the corresponding estrogen metabolites and conjugates was significantly higher in cases (median: 57.34) compared to controls (median: 23.39) (P < 0.001).
CONCLUSIONS
This study suggests that depurinating estrogen-DNA adducts could serve as potential biomarkers to predict risk of Pca. They also could be useful tools for early clinical diagnosis and development of suitable strategies to prevent Pca. Prostate 69: 41–48, 2009. © 2008 Wiley–Liss, Inc.
48 citations
Authors
Showing all 965 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael R. Green | 126 | 537 | 57447 |
Henrik Clausen | 109 | 520 | 49820 |
Howard E. Gendelman | 101 | 567 | 39460 |
James O. Armitage | 97 | 558 | 59171 |
Surinder K. Batra | 87 | 564 | 30653 |
Michael L. Gross | 82 | 701 | 27140 |
Michael A. Hollingsworth | 76 | 249 | 24460 |
Peter M. J. Burgers | 73 | 167 | 16123 |
Patrick L. Iversen | 68 | 319 | 13707 |
J. Alan Diehl | 67 | 168 | 19966 |
Samuel M. Cohen | 65 | 421 | 15940 |
Kenneth H. Cowan | 64 | 178 | 14094 |
Gangning Liang | 60 | 150 | 18081 |
Michael G. Brattain | 59 | 199 | 13199 |
Thomas E. Smithgall | 57 | 184 | 8904 |