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
More filters
••
TL;DR: Overall, it is identified that metabolic alterations in precancerous lesions are maintained during cancer development and are largely mirrored by cancer cells in culture conditions.
Abstract: Pancreatic cancer is the third leading cause of cancer-related deaths in the USA. Pancreatic tumors are characterized by enhanced glycolytic metabolism promoted by a hypoxic tumor microenvironment and a resultant acidic milieu. The metabolic reprogramming allows cancer cells to survive hostile microenvironments. Through the analysis of the principal metabolic pathways, we identified the specific metabolites that are altered during pancreatic cancer progression in the spontaneous progression (KPC) mouse model. Genetically engineered mice exhibited metabolic alterations during PanINs formation, even before the tumor development. To account for other cells in the tumor microenvironment and to focus on metabolic adaptations concerning tumorigenic cells only, we compared the metabolic profile of KPC and orthotopic tumors with those obtained from KPC-tumor derived cell lines. We observed significant upregulation of glycolysis and the pentose phosphate pathway metabolites even at the early stages of pathogenesis. Other biosynthetic pathways also demonstrated a few common perturbations. While some of the metabolic changes in tumor cells are not detectable in orthotopic and spontaneous tumors, a significant number of tumor cell-intrinsic metabolic alterations are readily detectable in the animal models. Overall, we identified that metabolic alterations in precancerous lesions are maintained during cancer development and are largely mirrored by cancer cells in culture conditions.
41 citations
••
TL;DR: Tumor suppressor functions of DnMT3a and Dnmt3b in the prevention of malignant mouse lymphopoiesis are inhibited and cell death is prevented in mice treated with F508(B) deletion.
Abstract: Tumor suppressor functions of Dnmt3a and Dnmt3b in the prevention of malignant mouse lymphopoiesis
41 citations
••
TL;DR: More than 60% of the patients in the cohort were considered unsuitable for radical cystectomy and their survival was poor, whether treated with full dose radiotherapy or transurethral resection of the bladder alone.
41 citations
••
TL;DR: Research at the laboratory, translational and clinical levels that supports the use of curcumin for various musculoskeletal disorders, such as osteoarthritis, osteoporosis, musculocartilaginous disorders, and sarcoma is comprehensively summarized.
Abstract: The Indian spice turmeric, in which the active and dominant biomolecule is curcumin, has been demonstrated to have significant medicinal properties, including anti-inflammatory and anti-neoplastic effects. This promise is potentially very applicable to musculoskeletal disorders, which are common causes of physician visits worldwide. Research at the laboratory, translational and clinical levels that supports the use of curcumin for various musculoskeletal disorders, such as osteoarthritis, osteoporosis, musculocartilaginous disorders, and sarcoma is here in comprehensively summarized. Though more phase I-III trials are clearly needed, thus far the existing data show that curcumin can indeed potentially be useful in treatment of the hundreds of millions worldwide who are afflicted by these musculoskeletal disorders.
41 citations
••
TL;DR: In vivo and in vitro studies show that ERβ-mediated upregulation of QR are involved in the protection against estrogen-induced mammary tumorigenesis, representing a possible novel mechanism of tamoxifen prevention against breast cancer.
Abstract: We previously reported that antiestrogen-liganded estrogen receptor β (ERβ) transcriptionally activates the major detoxifying enzyme quinone reductase (QR) (NAD(P)H:quinone oxidoreductase). Further studies on the functional role of ERβ-mediated upregulation of antioxidative enzymes indicated protective effects against estrogen-induced oxidative DNA damage (ODD). We now report on in vivo and in vitro studies that show that ERβ-mediated upregulation of QR are involved in the protection against estrogen-induced mammary tumorigenesis. Using the August Copenhagen Irish (ACI) model of estrogen-induced carcinogenesis, we observed that increased ODD and decreased QR expression occur early in the process of estrogen-induced mammary tumorigenesis. Prevention of ACI mammary gland tumorigenesis by tamoxifen was accompanied by decreased ODD and increased QR levels. These correlative findings were supported by our findings that downregulation of QR levels led to increased levels of estrogen quinone metabolites and enhanced transformation potential of 17β-estradiol treated MCF10A non-tumorigenic breast epithelial cells. Concurrent expression of ERβ and treatment with 4-hydroxytamoxifen decreased tumorigenic potential of these MCF10A cells. We conclude that upregulation of QR, through induction by tamoxifen, can inhibit estrogen-induced ODD and mammary cell tumorigenesis, representing a possible novel mechanism of tamoxifen prevention against breast cancer.
41 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 |