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
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TL;DR: The present review highlights the central role of epigenetic regulations in acquiring neoplastic phenotype, metastasis, aggressiveness, resistance to chemotherapy, and immunotherapeutic approaches of SCLC, and the utility of epigenetics targets/epidrugs in combination with first-line chemotherapy and immunotherapy that are currently under investigation in preclinical and clinical studies.
31 citations
TL;DR: Naphthalene undergoes metabolic activation to the electrophilic ortho-quinone, 1,2-NQ, which reacts with DNA to form depurinating adducts, the same mechanism as other weak carcinogens, such as the natural and synthetic estrogens, and benzene.
31 citations
TL;DR: The effects of the antiestrogen tamoxifen (TAM) and the estrogen 17 beta-estradiol (E2) on several estrogen-regulated responses in GH4C1 pituitary tumor cells are examined, finding that this estrogen may stimulate cell proliferation over the course of treatment.
Abstract: We have examined the effects of the antiestrogen tamoxifen (TAM) and the estrogen 17 beta-estradiol (E2) on several estrogen-regulated responses in GH4C1 pituitary tumor cells. After 5 days of treatment with either TAM (1.0 microM) or E2 (1.0 nM), the level of PRL mRNA was markedly increased when measured by the cytosolic dot blot procedure. In contrast, only E2 was able to increase the levels of beta-actin mRNA and cytosolic protein, suggesting that this estrogen may stimulate cell proliferation over the course of treatment. This apparent difference in the abilities of TAM and E2 to stimulate GH4C1 cell proliferation was examined directly. TAM had no effect on cell proliferation as evidenced by its inability to increase cellular DNA or deoxythymidine triphosphate incorporation by nuclei isolated from treated cells. In contrast, E2 stimulated cell proliferation as evidenced by increases in cellular DNA and deoxythymidine triphosphate incorporation by isolated nuclei. The abilities of TAM and E2 to induce ...
31 citations
TL;DR: The efficacy of a panel of HA-derived NPs in identifying prostate tumors in vivo is demonstrated, and it is suggested that by tuning the structural properties of these NPs, optimized delivery can be achieved to poorly vascularized tumors.
31 citations
TL;DR: The study reveals that the CUL3‐KLHL18 ligase is required for timely entry into mitosis, as well as for the activation of Aurora‐A at centrosomes, and proposes that the PNF ligase regulates mitotic entry through an Aurora-A‐dependent pathway.
Abstract: The cullin-RING family of ubiquitin ligases regulates diverse cellular functions, such as cell cycle control, via ubiquitylation of specific substrates. CUL3 targets its substrates through BTB proteins. Here we show that depletion of CUL3 and the BTB protein KLHL18 causes a delay in mitotic entry. Centrosomal activation of Aurora-A, a kinase whose activity is required for entry into mitosis, is also delayed in depleted cells. Moreover, we identify Aurora-A as a KLHL18-interacting partner. Overexpression of KLHL18 and CUL3 promotes Aurora-A ubiquitylation in vivo, and the CUL3-KLHL18-ROC1 ligase ubiquitylates Aurora-A in vitro. Our study reveals that the CUL3-KLHL18 ligase is required for timely entry into mitosis, as well as for the activation of Aurora-A at centrosomes. We propose that the CUL3-KLHL18 ligase regulates mitotic entry through an Aurora-A-dependent pathway.
31 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 |