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: The hydrazine class, unlike the polycyclic aromatic hydrocarbons, N-nitroso compounds, and aromatic amines, poses a greater environmental risk to the human population and appears reasonable to proceed with additional experimentation in this field of interest.
Abstract: This writing details the natural occurrence, synthetic production and use of the carcinogenic hydrazines and related chemicals. Twenty-three such chemicals were found in nature in mushrooms, tobacco, bay leaves, antibiotics, soil and other sources. The synthetically-produced hydrazines and related chemicals include 61 compounds which were or are in use as pharmaceutical drugs, agricultural substances, industrial chemicals and fuels for military and space vehicles and rockets. Because there is an overlap between the naturally-occurring and synthetically-produced compounds, their total number is 76. Altogether, 98 hydrazines and related chemicals were studied for carcinogenic action thus far, of which 84 were found to be carcinogenic and the remaining 14 were inactive. This means that the human population is exposed in various degrees to a substantial number of these agents. Therefore, the hydrazine class, unlike the polycyclic aromatic hydrocarbons, N-nitroso compounds, and aromatic amines, poses a greater environmental risk to the human population. In view of these considerations, it appears reasonable to proceed with additional experimentation in this field of interest.
48 citations
••
TL;DR: It is demonstrated that Ets2, which is expressed in F9-differentiated cells along with Elf3, does not stimulate or bind to the TβR-II promoter in these cells, and it is shown that PU.1 exerts little or no effect on the activity of the T βR- II promoter.
48 citations
••
TL;DR: In vivo NIR imaging demonstrated that ICG conjugated micelles prolonged its circulation and increased tumor accumulation through enhanced permeability and retention (EPR) effect and suggested that ICg conjugation micells can be potentially utilized for PT and imaging of melanoma.
48 citations
••
TL;DR: It is found that use of canertinib or afatinib resulted in reduction of MUC4 and abrogation of in vitro and in vivo oncogenic functions of M UC4 in pancreatic cancer cells.
Abstract: // Parthasarathy Seshacharyulu 1 , Moorthy P. Ponnusamy 1 , Satyanarayana Rachagani 1 , Imayavaramban Lakshmanan 1 , Dhanya Haridas 1 , Ying Yan 2,3 , Apar K. Ganti 4 and Surinder K. Batra 1,2 1 Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA 2 Fred and Pamela Buffett Cancer Center, Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA 3 Department of Radiation Oncology, University of Nebraska Medical Center, Omaha, NE, USA 4 Department of Internal Medicine, VA Nebraska-Western Iowa Health Care System and University of Nebraska Medical Center, Omaha, NE, USA Correspondence: Surinder K. Batra, email: // Keywords : Afatinib, Canertinib, Pancreatic cancer, MUC4, EGFR Received : November 28, 2014 Accepted : December 30, 2014 Published : December 31, 2014 Abstract Transmembrane proteins MUC4, EGFR and HER2 are shown to be critical in invasion and metastasis of pancreatic cancer. Besides, we and others have demonstrated de novo expression of MUC4 in ~70-90% of pancreatic cancer patients and its stabilizing effects on HER2 downstream signaling in pancreatic cancer. Here, we found that use of canertinib or afatinib resulted in reduction of MUC4 and abrogation of in vitro and in vivo oncogenic functions of MUC4 in pancreatic cancer cells. Notably, silencing of EGFR family member in pancreatic cancer cells decreased MUC4 expression through reduced phospho-STAT1. Furthermore, canertinib and afatinib treatment also inhibited proliferation, migration and survival of pancreatic cancer cells by attenuation of signaling events including pERK1/2 (T202/Y204), cyclin D1, cyclin A, pFAK (Y925) and pAKT (Ser473). Using in vivo bioluminescent imaging, we demonstrated that canertinib treatment significantly reduced tumor burden ( P =0.0164) and metastasis to various organs. Further, reduced expression of MUC4 and EGFR family members were confirmed in xenografts. Our results for the first time demonstrated the targeting of EGFR family members along with MUC4 by using pan-EGFR inhibitors. In conclusion, our studies will enhance the translational acquaintance of pan-EGFR inhibitors for combinational therapies to combat against lethal pancreatic cancer.
47 citations
••
TL;DR: The findings suggest that the assembly of Cx43 and Cx32 into GJs is differentially modulated by E-cadherin-mediated cell-cell adhesion and that direct or indirect cross-talk between carboxyl tails of Cxs and actin cytoskeleton via ZO-1 may regulate GJ assembly and growth.
47 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 |