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
Zhao, Bin; Bhattacharya, Sabyasachi; Yu, Qiujing et al. (2018) Expression of the IFNAR1 chain of type 1 interferon receptor in benign cells protects against progression of acute leukemia. Leuk Lymphoma 59:171-177
Bu, Yiwen; Yoshida, Akihiro; Chitnis, Nilesh et al. (2018) A PERK-miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival. Nat Cell Biol 20:104-115
Nguyen, Hao G; Conn, Crystal S; Kye, Yae et al. (2018) Development of a stress response therapy targeting aggressive prostate cancer. Sci Transl Med 10:
Hong, Feng; Liu, Bei; Wu, Bill X et al. (2017) CNPY2 is a key initiator of the PERK-CHOP pathway of the unfolded protein response. Nat Struct Mol Biol 24:834-839
Rozpedek, W; Nowak, A; Pytel, D et al. (2017) Molecular Basis of Human Diseases and Targeted Therapy Based on Small-Molecule Inhibitors of ER Stress-Induced Signaling Pathways. Curr Mol Med 17:118-132
Ortiz, Angélica; Fuchs, Serge Y (2017) Anti-metastatic functions of type 1 interferons: Foundation for the adjuvant therapy of cancer. Cytokine 89:4-11
Katlinski, Kanstantsin V; Gui, Jun; Katlinskaya, Yuliya V et al. (2017) Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment. Cancer Cell 31:194-207
Davar, Diwakar; Fuchs, Serge Y; Kirkwood, John M (2016) BRAF Inhibitors and IFN?: Plus, Minus, or Indeterminate? J Natl Cancer Inst 108:
Bu, Yiwen; Diehl, J Alan (2016) PERK Integrates Oncogenic Signaling and Cell Survival During Cancer Development. J Cell Physiol 231:2088-96
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

Showing the most recent 10 out of 28 publications