Dr. Andrej Podlutsky of LECOM Erie


Dr. Andrej Podlutsky is an Associate Professor of Biochemistry and Medical Genetics at LECOM-Erie.  He received an MSc degree from the Kharkiv State University, Ukraine, with a specialization in Cytology and Genetics.  He earned his Ph.D. degree from the Institute of Theoretical and Experimental Biophysics, Puschino, Moscow Region, Russia, with a specialization in Biophysics and Molecular Biology.  He completed postdoctoral training in the laboratory of Prof. Bo Lambert, Stockholm, Sweden, where he studied the mutagenesis of the HPRT gene in lung cancer patients, comparing the spectrum of mutations between smokers and nonsmokers.

After moving to the United States, he worked in the laboratory of Dr. Wilhelm Bohr at the National Aging Institute in Baltimore, and with Dr. Nikki Holbrook at Yale Medical School, where he focused on the biochemistry of the DNA repair process and oxidative stress in mammalian cells.  Before joining the University of Alaska Fairbanks (UAF), he studied the DNA repair efficiency of blood cells isolated from children diagnosed with cancer in a study conducted at the Children Cancer Research Institute in San Antonio.  As a faculty member at UAF, he focused chiefly on the DNA repair efficiency in cancerous cell lines and chronic inflammatory response concerning dietary habits, metabolism, and obesity among Alaska Native people.  Since joining LECOM in January 2022, he continues to study DNA repair in virally infected cells and in cancerous cell lines.

Research Interests

The biology of cancer, the biology of aging, DNA damage and repair

Project-1: Viral infection and DNA repair

Background: The stability of DNA in host cells is constantly challenged by a variety of errors in replication or by the action of reactive oxidative species. A combination of any of these challenges is linked to a plethora of diseases, including cancer. Some viruses might contribute to genetic instability by inserting viral DNA into the host cell’s DNA. For example, individuals infected with HIV show a significant increase in certain types of cancer. Cancer is currently one of the leading causes of death in patients with HIV. By understanding the mechanisms linking viral infection and the efficiency of DNA repair, a new treatment strategy might be developed, leading to decreased cancer occurrences in HIV patients.

Hypothesis: We hypothesize that the virus-infected cells could not repair their damaged DNA properly; and as a result, the damage is passed on to subsequent generations in the form of mutations.


Project-2: DNA repair efficiency in cancerous cell lines

Background: It is well known that DNA repair plays a vital role in cancer initiation and progression, also in a patient’s response to radiation- and chemotherapy. Such knowledge would be precious for any research aimed at developing a new drug or treatment strategy. The National Cancer Institute, NIH lists approximately one hundred cell lines commonly used in cancer research. The catalog contains cell lines corresponding to common types of cancer. Because most of them are used for drug discovery and testing, studying DNA repair capacity and dynamics in one laboratory would be essential. Our project is the first attempt to compare the DNA repair between various cell lines for different cancers.

Hypothesis: Using the X-ray radiation and UV-C light exposures, we monitor the repair dynamics of two pathways: the base excision repair and the nucleotide excision repair.


Project-3: Genome stability in breast cancer survivors

Background: The long-term survival following breast cancer treatment continues to improve. However, the molecular and cellular mechanisms involved in the disease-free life of former breast cancer patients are poorly understood. Approximately 30% of women treated for breast cancer would develop secondary tumors ten years following the initial recovery period. Such secondary tumors might result from delayed malignant growth of the original tumor or the cancerous transformation caused by chemo- or radiation therapy of the primary tumor. Genome stability plays an essential role in overall cancer risk development. Comparing DNA repair capacity in cancer patients before the beginning of the treatment and following 5-8 years of the conclusion of the treatment might lead to the understanding of cellular mechanisms behind the risk of secondary cancer occurrence. In collaboration with the local oncology doctors, we would analyze repair dynamics in the lymphocytes of current and survivors of breast cancer patients.

Hypothesis: The treatment protocol for breast cancer patients might be adjusted based on the overall DNA repair capacity of the patient’s cells, which would lower the risk of secondary tumors.


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