Section: Research

Zdenka Matijasevic, Ph.D.

Academic Role: Assistant Professor

Faculty Appointment(s) In:
   Cell Biology

Joint Faculty In:
   Biochemistry and Molecular Pharmacology

Cellular responses to hypothermia

Hypothermia increases the levels of tumor suppressor p53 protein in human fibroblasts and causes a p53-dependent cell cycle arrest in mouse fibroblasts; (Matijasevic et al., 1998). These findings suggest that hypothermia has applications in two areas, cancer treatment and protection from environmental carcinogens.

Hypothermia and cancer treatment

Since many human tumors lack wild type p53 function, hypothermia may provide conditions for selective targeting of tumor cells; cell cycle arrest of normal cells at low temperature may protect them from cytotoxicity of drugs that target proliferating cells. Therefore, we are studying the effects of hypothermia on cell cycle progression in p53-deficient human tumor cells and ask whether or not it decreases the sensitivity of normal cells to drugs such as 5-fluorouracil (Matijasevic, 2002).

Hypothermia and DNA damage/repair

Acute and delayed toxicities from exposure to DNA-damaging agents such as sulfur mustard (SM) can be prevented or diminished by the activities of cellular DNA repair processes. At least two DNA repair mechanisms act upon SM-damaged DNA: base excision repair (BER) (Matijasevic et al., 1996) and nucleotide excision repair (NER) (Matijasevic et al., 2001). Our finding that hypothermia improves recovery of human fibroblasts after exposure to SM suggests that the reversible cell cycle arrest at low temperature provides more time for the DNA repair to take place. We are now investigating the effects of hypothermia on DNA repair activities in vivo and in vitro.

Office: S7-318
Phone: 508-856-2459
E-mail: Zdenka.Matijasevic@umassmed.edu
Keywords: Centrosome, Cancer, DNA Repair, Cell Cycle, Mitosis

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