The Cell/Tissue Morphology Core (Core B) is strategically established to address the shared needs of morphological characterization of tumor samples atthe histological, cellular, and organelle levels. Based on the specific aims proposed by the 3 Project Leaders, this Core will have 2 essential components: (1) Histopathology to perform histological analysis of tumors, quantitative and qualitative assessment of cell death/survival pathways, and interactions between tumor cells and microenvironment from animal and cell culture models. The core will also perform quantitative immunohistochemistry (IHC) analysis of hypoxia and key UPR antigens identified by this programmatic group to assess the expression of critical molecules. (2) Electron Microscopy (EM) analysis of ultrastructural changes to cell organelles, particularly the changes of ER compartment and other secretory organelles, subcellular evidence of cell injury and cell death, and the dynamic changes of organelles involved in autophagic pathway. It is oiir strong believe that the Core B will be able to provide project-oriented technological support with consistence, high quality, and scientific interaction in a much more efficient and economic fasliion than that performed and maintained by each individual group.

Public Health Relevance

CORE B is not a General Core. All of its expertise, technology, and services are specifically dedicated to addressing the scientific needs shared by most, if not all, members of this program. Every core protocol and techniques listed is tested and optimized to carry-out projects from 2 or 3 of the proposed study projects. It is therefore completely relevant to the successful execution of all Specific Aims of this application.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA165997-02
Application #
8754469
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2014-09-01
Budget End
2015-08-31
Support Year
2
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Pennsylvania
Department
Type
DUNS #
City
Philadelphia
State
PA
Country
United States
Zip Code
19104
Bu, Yiwen; Diehl, J Alan (2016) PERK Integrates Oncogenic Signaling and Cell Survival During Cancer Development. J Cell Physiol 231:2088-96
Xia, Chuan; Vijayan, Madhuvanthi; Pritzl, Curtis J et al. (2016) Hemagglutinin of Influenza A Virus Antagonizes Type I Interferon (IFN) Responses by Inducing Degradation of Type I IFN Receptor 1. J Virol 90:2403-17
Gui, Jun; Gober, Michael; Yang, Xiaoping et al. (2016) Therapeutic Elimination of the Type 1 Interferon Receptor for Treating Psoriatic Skin Inflammation. J Invest Dermatol 136:1990-2002
Zhang, Kangjian; Yin, Xiao-Fei; Yang, Yuan-Qin et al. (2016) A potent in vivo anti-tumor efficacy of novel recombinant type I interferon. Clin Cancer Res :
Xu, Zhenhua; Bu, Yiwen; Chitnis, Nilesh et al. (2016) miR-216b regulation of c-Jun mediates GADD153/CHOP-dependent apoptosis. Nat Commun 7:11422
Katlinskaya, Yuliya V; Katlinski, Kanstantsin V; Yu, Qiujing et al. (2016) Suppression of Type I Interferon Signaling Overcomes Oncogene-Induced Senescence and Mediates Melanoma Development and Progression. Cell Rep 15:171-80
Bu, Yiwen; Diehl, J Alan (2016) Stressing out melanoma with an anti-GRP78 compound. Pigment Cell Melanoma Res 29:490-1
Katlinskaya, Yuliya V; Katlinski, Kanstantsin V; Lasri, Audrey et al. (2016) Type I Interferons Control Proliferation and Function of the Intestinal Epithelium. Mol Cell Biol 36:1124-35
Davar, Diwakar; Fuchs, Serge Y; Kirkwood, John M (2016) BRAF Inhibitors and IFNα: Plus, Minus, or Indeterminate? J Natl Cancer Inst 108:
Yu, Qiujing; Zhao, Bin; Gui, Jun et al. (2015) Type I interferons mediate pancreatic toxicities of PERK inhibition. Proc Natl Acad Sci U S A 112:15420-5

Showing the most recent 10 out of 19 publications