Diane L. Carlisle, PhDAssistant Professor of Neurological Surgery
Diane Carlisle, PhD, joined the Department of Neurological Surgery in October 2010. She received her undergraduate degree in molecular biology from Washington and Jefferson College and her graduate degree in molecular and cellular oncology from George Washington University where she identified new signaling pathways involved in occupational causes of lung cancer. Dr. Carlisle came to the University of Pittsburgh after a postdoctoral fellowship at Johns Hopkins University under the mentorship of Robert Casero Jr., PhD, in drug development for lung cancer. She then developed her independent research program investigating the fetal basis for adult disease, including the effects of prenatal exposures on development. In addition, she serves as the course coordinator of the NIH-funded stem cell course Frontiers in Stem Cells and Regeneration, which is held annually at the Marine Biological Laboratories in Woods Hole Massachusetts.
Dr. Carlisle's publications can be reviewed through the National Library of Medicine's publication database.
Professional Organization Membership
American Society for Cell Biology
American Association for Cancer Research
International Society for Stem Cell Research
Women in Cancer Research
In the United States, each year approximately 1 in 10 newborns is exposed to cigarette smoke during gestation. Cigarette smoke exposure during this critical time of organogenesis and subsequent organ growth and maturation causes morbidity and mortality after birth. In the lung, prenatal cigarette smoke exposure causes decreased lung function at birth and into childhood as well as increased incidence of asthma and allergies. The mechanisms by which cigarette smoke has these effects is not known; however, it is modeled in non-human primates exposed during pregnancy to nicotine, a major component of cigarette smoke. These studies find that although there are thousands of chemicals in cigarette smoke, NHP infants subjected to nicotine alone via a maternal exposure during development have increased thickness of the inner airway wall and altered complexity of branching, decreased respiratory volumes, and altered response to airway challenges. This is possible because nicotine easily crosses the placenta and accumulates in amniotic fluid with average concentrations of 150 nM. The physiological alterations described above that are caused by nicotine exposure may be linked to altered regulation of proliferation and apoptosis during organogenesis and organ growth. Our preliminary data demonstrate that nicotine may affect differentiation by altering the expression of a key regulators of proliferation and apoptosis during development.