Spring Break
Tennessee professor delivers lecture on discoveries about damaged DNA
Betsy Cohen
Issue date: 12/5/08 Section: News
12/05/08 - Damaged human Deoxyribonucleic acid, (DNA), is responsible for cancers and other diseases, according to professor Yue Zou of East Tennessee State University.
Zou, a professor who works in the Department of Biochemistry and Molecular Biology, spoke yesterday evening in Fogarty Hall.
The presentation, titled "DNA Damage, Repair and Checkpoints in Human Cells," discussed human nucleotide excision repair (NER) on a molecular level and the interactions of damaged checkpoints of DNA in conjunction with NER.
The fully attended lecture was part of the 2008-2009 Rhode Island Idea Network of Biomedical Research Excellence Seminar Series.
Zou, in collaboration with professor Mamuka Kvaratskhelia of Ohio State University and professor John J. Turchi of Indiana University's Medical School and 10 other researchers, obtained results that have significantly contributed to the research of nucleotide repair. Zou and his team determined that RPA hyperphosphorylation and Xeroderma pigmentosum (XPA) are two health issues directly linked to various consequences of DNA damage.
"Fortunately, all of our bodies have DNA repair mechanisms," Zou said. "DNA damage is ultimately responsible for most of human cancers."
Replication errors lead to an accumulation of DNA mutations, instability in an organism's genome and cancers and other diseases, Zou said.
DNA repair recognizes the damage and "controls the cell cycle in response to DNA damage," he said.
The four classifications of DNA damage and repair pathways are Base Excision Repair of base damage, Mismatch Repairs of mismatched bases, DNA double-strand Break Repair and Nucleotide Excision Repair of large DNA lacerations.
The NER pathway is composed of two sub pathways, the Global Genome Repair (GGR) and Transcription-coupled Repair (TCR). These two repair types are important when studying the repair of DNA and how it affects patients with DNA damage.
Xeroderma pigmentosum is an example of an illness related to DNA damage. Patients exhibiting the XPA disease are extremely sensitive to sunlight, have an elevated susceptibility to skin cancer and may have other mutations associated with the site of DNA damage.
Another disease associated with DNA damage is Hutchinson-Gilford progeria Syndrome (HOPS).
"This is a devastating disease," Zou said. "Kids with this disease have a [lifespan] average of 30 years."
The lecture was "very interesting, it relates to my research and he made a lot of interesting points about XPA," Michelle Cavanna, a graduate student working in the Cellular Molecular Biology Department at URI, said.
Cavanna, who studies Fanconi Anemia, a DNA damage disorder syndrome also known for increasing cancer susceptibleness, thought this lecture was beneficial to the URI community.
"There are many laboratories on campus that study these DNA damage pathways," she said.
Zou and his team of researchers are still in the midst of discovering new potential methods to treat illnesses caused by DNA damage.
Zou, a professor who works in the Department of Biochemistry and Molecular Biology, spoke yesterday evening in Fogarty Hall.
The presentation, titled "DNA Damage, Repair and Checkpoints in Human Cells," discussed human nucleotide excision repair (NER) on a molecular level and the interactions of damaged checkpoints of DNA in conjunction with NER.
The fully attended lecture was part of the 2008-2009 Rhode Island Idea Network of Biomedical Research Excellence Seminar Series.
Zou, in collaboration with professor Mamuka Kvaratskhelia of Ohio State University and professor John J. Turchi of Indiana University's Medical School and 10 other researchers, obtained results that have significantly contributed to the research of nucleotide repair. Zou and his team determined that RPA hyperphosphorylation and Xeroderma pigmentosum (XPA) are two health issues directly linked to various consequences of DNA damage.
"Fortunately, all of our bodies have DNA repair mechanisms," Zou said. "DNA damage is ultimately responsible for most of human cancers."
Replication errors lead to an accumulation of DNA mutations, instability in an organism's genome and cancers and other diseases, Zou said.
DNA repair recognizes the damage and "controls the cell cycle in response to DNA damage," he said.
The four classifications of DNA damage and repair pathways are Base Excision Repair of base damage, Mismatch Repairs of mismatched bases, DNA double-strand Break Repair and Nucleotide Excision Repair of large DNA lacerations.
The NER pathway is composed of two sub pathways, the Global Genome Repair (GGR) and Transcription-coupled Repair (TCR). These two repair types are important when studying the repair of DNA and how it affects patients with DNA damage.
Xeroderma pigmentosum is an example of an illness related to DNA damage. Patients exhibiting the XPA disease are extremely sensitive to sunlight, have an elevated susceptibility to skin cancer and may have other mutations associated with the site of DNA damage.
Another disease associated with DNA damage is Hutchinson-Gilford progeria Syndrome (HOPS).
"This is a devastating disease," Zou said. "Kids with this disease have a [lifespan] average of 30 years."
The lecture was "very interesting, it relates to my research and he made a lot of interesting points about XPA," Michelle Cavanna, a graduate student working in the Cellular Molecular Biology Department at URI, said.
Cavanna, who studies Fanconi Anemia, a DNA damage disorder syndrome also known for increasing cancer susceptibleness, thought this lecture was beneficial to the URI community.
"There are many laboratories on campus that study these DNA damage pathways," she said.
Zou and his team of researchers are still in the midst of discovering new potential methods to treat illnesses caused by DNA damage.
