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: The results indicate that optimum dietary selenium provides partial protection from the toxic effects of TCDD, and aryl hydrocarbon hydroxylase, glutathione S-transferase, and glutathion reductase activities were induced by T CDD.
Abstract: TCDD has been shown to inhibit selenium-dependent glutathione peroxidase activity. The role of selenium in TCDD toxicity is not known. We have therefore examined the effect of TCDD administration on hepatic glutathione peroxidase, aryl hydrocarbon hydroxylase, glutathione reductase, and glutathione S-transferase activities, glutathione content, and lipid peroxidation in rats fed 0, 0.10, and 2.0 ppm dietary selenium. TCDD treatment significantly inhibited selenium-dependent glutathione peroxidase in animals on diets containing 0.10 and 2.0 ppm selenium. The selenium-dependent glutathione peroxidase activities in rats on 0.10 and 2.0 ppm dietary selenium were 8.3-and 4.7-fold greater than in animals fed a diet containing 0 ppm selenium. TCDD administration enhanced hepatic microsomal lipid peroxidation by factors of 4.0, 4.9, and 9.8 in animals fed diets containing 0, 0.10, and 2.0 ppm selenium, respectively. The administration of a lethal dose of TCDD to rats fed diets containing 0, 0.10, and 2.0 ppm selenium resulted in 0, 46, and 7% survival, respectively, after 66 d. Aryl hydrocarbon hydroxylase, glutathione S-transferase, and glutathione reductase activities were induced by TCDD. The results indicate that optimum dietary selenium provides partial protection from the toxic effects of TCDD.
26 citations
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TL;DR: A major focus of the review is the use of p160 Rho-associated coiled-coil kinase inhibitors for improving both the cloning efficiency and the recovery of cryopreserved human embryonic stem cells and human induced pluripotent stem cells.
Abstract: Until recently, culturing human pluripotent stem cells was hampered by three prominent technical problems: a high degree of unwanted cellular stress when the cells are passaged, unacceptably low cloning efficiency and poor recovery of cryopreserved stocks. This review discusses recent developments that address these problems. A major focus of the review is the use of p160 Rho-associated coiled-coil kinase inhibitors for improving both the cloning efficiency and the recovery of cryopreserved human embryonic stem cells and human induced pluripotent stem cells. An underlying theme of this review is that the three problems have a common cause: separation of human pluripotent stem cells from one another increases cellular stress, which greatly decreases their viability unless special steps are taken.
26 citations
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TL;DR: It is shown for the first time that β‐catenin directly governs MUC4 in PC, and factors deregulated in early PC progression, such as Wnt/β‐ catenin signaling are examined.
26 citations
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TL;DR: The results suggest that aberrant expression of truncated O‐glycans in PDAC cells enhances the tumour aggressiveness through the induction of EMT and stemness properties.
Abstract: Aberrant expression of Sialyl-Tn (STn) antigen correlates with poor prognosis and reduced patient survival. We demonstrated that expression of Tn and STn in pancreatic ductal adenocarcinoma (PDAC) is due to hypermethylation of Core 1 synthase specific molecular chaperone (COSMC) and enhanced the malignant properties of PDAC cells with an unknown mechanism. To explore the mechanism, we have genetically deleted COSMC in PDAC cells to express truncated O-glycans (SimpleCells, SC) which enhanced cell migration and invasion. Since epithelial-to-mesenchymal transition (EMT) play a vital role in metastasis, we have analysed the induction of EMT in SC cells. Expressions of the mesenchymal markers were significantly high in SC cells as compared to WT cells. Equally, we found reduced expressions of the epithelial markers in SC cells. Re-expression of COSMC in SC cells reversed the induction of EMT. In addition to this, we also observed an increased cancer stem cell population in SC cells. Furthermore, orthotopic implantation of T3M4 SC cells into athymic nude mice resulted in significantly larger tumours and reduced animal survival. Altogether, these results suggest that aberrant expression of truncated O-glycans in PDAC cells enhances the tumour aggressiveness through the induction of EMT and stemness properties.
26 citations
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TL;DR: This finding suggests that NAcCys, a common dietary supplement, could be used as a potential chemopreventive agent to block the initial step in the genotoxicity caused by catechol estrogen quinones.
26 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 |