scispace - formally typeset
Search or ask a question
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
More filters
Journal ArticleDOI
TL;DR: It is demonstrated that JNK signaling contributes to muscle wasting in cancer cachexia and its inhibition has the potential to be utilized as an anti-cachectic therapy.

21 citations

Journal ArticleDOI
14 Feb 2020-Cancers
TL;DR: This review provides a succinct overview of the main structural features of the TSG101 protein and their suggested roles in molecular and cellular functions, and summarizes critical issues that need to be addressed to gain a better understanding of biologically significant roles of TSG 101 in cancer.
Abstract: The multidomain protein encoded by the Tumor Susceptibility Gene 101 (TSG101) is ubiquitously expressed and is suggested to function in diverse intracellular processes. In this review, we provide a succinct overview of the main structural features of the protein and their suggested roles in molecular and cellular functions. We then summarize, in more detail, key findings from studies using genetically engineered animal models that demonstrate essential functions of TSG101 in cell proliferation and survival, normal tissue homeostasis, and tumorigenesis. Despite studies on cell lines that provide insight into the molecular underpinnings by which TSG101 might function as a negative growth regulator, a biologically significant role of TSG101 as a tumor suppressor has yet to be confirmed using genuine in vivo cancer models. More recent observations from several cancer research teams suggest that TSG101 might function as an oncoprotein. A potential role of post-translational mechanisms that control the expression of the TSG101 protein in cancer is being discussed. In the final section of the review, we summarize critical issues that need to be addressed to gain a better understanding of biologically significant roles of TSG101 in cancer.

21 citations

Journal ArticleDOI
TL;DR: Mutation of the native M-PMR3 element to create perfect homopurine/homopyrimidine mirror symmetry alters the preferred folding to the more common H-y3 triplex DNA isomer, demonstrating that imperfections in mirror symmetry can alter the relative stabilities of different H-DNA isomers.

21 citations

Book ChapterDOI
TL;DR: This chapter describes the establishment and characterization of telomerase-immortalized human pancreatic duct-derived cells to study mechanisms of Ras growth transformation and utilizes this cell system to evaluate the antitumor activity of small molecule inhibitors of the Raf-MEK-ERK mitogen-activated protein kinase cascade.
Abstract: Mutational activation of the K-Ras oncogene is well established as a key genetic step in the development and growth of pancreatic adenocarcinomas. However, the means by which aberrant Ras signaling promotes uncontrolled pancreatic tumor cell growth remains to be fully elucidated. The recent use of primary human cells to study Ras-mediated oncogenesis provides important model cell systems to dissect this signaling biology. This chapter describes the establishment and characterization of telomerase-immortalized human pancreatic duct-derived cells to study mechanisms of Ras growth transformation. An important strength of this model system is the ability of mutationally activated K-Ras to cause potent growth transformation in vitro and in vivo. We have utilized this cell system to evaluate the antitumor activity of small molecule inhibitors of the Raf-MEK-ERK mitogen-activated protein kinase cascade. This model will be useful for genetic and pharmacologic dissection of the contribution of downstream effector signaling in Ras-dependent growth transformation.

21 citations

Journal ArticleDOI
02 Nov 2011-PLOS ONE
TL;DR: Results indicate that MUC1 downregulation alters the phenotype and tumorigenicity of MKN45 gastric carcinoma cells and also the expression of several molecules that can be involved in tumorigenic events.
Abstract: Background Gastric carcinoma is the second leading cause of cancer-associated death worldwide. The high mortality associated with this disease is in part due to limited knowledge about gastric carcinogenesis and a lack of available therapeutic and prevention strategies. MUC1 is a high molecular weight transmembrane mucin protein expressed at the apical surface of most glandular epithelial cells and a major component of the mucus layer above gastric mucosa. Overexpression of MUC1 is found in approximately 95% of human adenocarcinomas, where it is associated with oncogenic activity. The role of MUC1 in gastric cancer progression remains to be clarified.

20 citations


Authors

Showing all 965 results

NameH-indexPapersCitations
Michael R. Green12653757447
Henrik Clausen10952049820
Howard E. Gendelman10156739460
James O. Armitage9755859171
Surinder K. Batra8756430653
Michael L. Gross8270127140
Michael A. Hollingsworth7624924460
Peter M. J. Burgers7316716123
Patrick L. Iversen6831913707
J. Alan Diehl6716819966
Samuel M. Cohen6542115940
Kenneth H. Cowan6417814094
Gangning Liang6015018081
Michael G. Brattain5919913199
Thomas E. Smithgall571848904
Network Information
Related Institutions (5)
National Institutes of Health
297.8K papers, 21.3M citations

94% related

Laboratory of Molecular Biology
24.2K papers, 2.1M citations

91% related

Scripps Research Institute
32.8K papers, 2.9M citations

91% related

Albert Einstein College of Medicine
56.4K papers, 2.7M citations

90% related

University of Texas Southwestern Medical Center
75.2K papers, 4.4M citations

90% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20223
202188
202069
201964
201842
201757