The research of the Fels Research Institute at Temple University School of Medicine in Philadelphia is divided into three broad areas, the Chemical Carcinogenesis Program, the Cell Biology Program and the Biochemistry Program. The main aim of the Program on Chemical Carcinogenesis is the better understanding, at the molecular and cellular levels, of how certain chemicals cause cancer in animals in vivo and induce malignant transformation of cells in vitro. Investigation is on a broad front using carcinogenic nitrosamines and other N-nitroso compounds, as well as other chemical carcinogens in the study of their distribution in the body, metabolic activation and deactivation, interaction with nucleic acids and proteins, DNA repair mechanisms and morphological studies of tumor development and tumor modification in vivo and in vitro. Members of the Cell Biology Program study, at the molecular and cellular level, the genes and gene products that control cell growth and cell death in neoplastic and normal cells. Areas of study include regulation of the cell cycle by oncoviral antigens, growth factors, genes involved in hybrid cells, effects of chemical and viral carcinogens on human lymphoblastoid cell lines and biochemical mechanisms of cell death. The Biochemistry Program is concerned mainly with biologically active proteins. Areas under investigation include metabolite and steroid binding proteins including ligandin, modification of proteins by protein methylases, including membrane proteins and specific catalytic sites of proteins and relationships between isoenzymes in adult, fetal and tumor tissues.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
Project #
Application #
Study Section
Cancer Center Support Review Committee (CCS)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Temple University
Schools of Medicine
United States
Zip Code
Sjin, Robert M Tjin Tham; Krishnaraju, Kandasamy; Hoffman, Barbara et al. (2002) Transcriptional regulation of myeloid differentiation primary response (MyD) genes during myeloid differentiation is mediated by nuclear factor Y. Blood 100:80-8
Adelson, M E; Martinand-Mari, C; Iacono, K T et al. (1999) Inhibition of human immunodeficiency virus (HIV-1) replication in SupT1 cells transduced with an HIV-1 LTR-driven PKR cDNA construct. Eur J Biochem 264:806-15
Murali, R; Helmer-Citterich, M; Sharkey, D J et al. (1998) Structural studies on an inhibitory antibody against Thermus aquaticus DNA polymerase suggest mode of inhibition. Protein Eng 11:79-86
Domashenko, A D; Latham, K E; Hatton, K S (1997) Expression of myc-family, myc-interacting, and myc-target genes during preimplantation mouse development. Mol Reprod Dev 47:57-65
Krishnaraju, K; Hoffman, B; Liebermann, D A (1997) Lineage-specific regulation of hematopoiesis by HOX-B8 (HOX-2.4): inhibition of granulocytic differentiation and potentiation of monocytic differentiation. Blood 90:1840-9
Latham, K E; Cosenza, S; Reichenbach, N L et al. (1996) Inhibition of growth of estrogen receptor positive and estrogen receptor negative breast cancer cells in culture by AA-etherA, a stable 2-5A derivative. Oncogene 12:827-37
Zhu, J; Nabissa, P M; Hoffman, B et al. (1996) Activated abl oncogenes and apoptosis: differing responses of transformed myeloid progenitor cell lines. Blood 87:4368-75
Latham, K E; Litvin, J; Orth, J M et al. (1996) Temporal patterns of A-myb and B-myb gene expression during testis development. Oncogene 13:1161-8
Zhu, J; Shore, S K (1996) c-ABL tyrosine kinase activity is regulated by association with a novel SH3-domain-binding protein. Mol Cell Biol 16:7054-62
Gross, J; Rajavel, M; Segura, E et al. (1996) Energy coupling in Salmonella typhimurium nicotinic acid phosphoribosyltransferase: identification of His-219 as site of phosphorylation. Biochemistry 35:3917-24

Showing the most recent 10 out of 44 publications