Isle doc helps find gene that hunts cancer
A gene called ASPP2 triggers a mechanism that kills mutant cells
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A breakthrough in understanding how the body fights the formation of cancerous tumors was announced this week by an Oregon research team that included a Hawaii doctor.
Working with lab mice, the researchers found that a gene known as ASPP2 triggers biological pathways that tell cancer cells to die.
"By identifying the steps that a cell takes to change from a normal cell to a cancer cell, we can identify what risk factors for cancer might be and also what potential treatments might be available," said Dr. Jared Acoba, of Honolulu, who took part in the study.
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An Oregon research team that included a Honolulu doctor announced this week a breakthrough that identifies a genetic mechanism for eliminating cancer cells.
The gene, known as ASPP2, triggers a key protein by the same name, activating biological pathways that tell cancer cells to die.
The research was presented Wednesday at the annual meeting of the American Association of Cancer Research in San Diego.
"What we've shown is that ASPP2 is important for cancer formation, and by identifying the steps that a cell takes to change from a normal cell to a cancer cell, we can identify what risk factors for cancer might be and also what potential treatments might be available," said Dr. Jared Acoba, who participated in the research during the last two years of his three-year fellowship at Oregon Health and Science University Cancer Institute.
Acoba has returned home to Hawaii and now serves as assistant clinical professor at the John A. Burns School of Medicine at the University of Hawaii, running the resident oncology clinic.
"This finding was important because expression of this gene is frequently suppressed in many cancers, such as lymphoma and breast cancers," Dr. Charles Lopez of the OHSU Cancer Institute and School of Medicine said in a news release. "This research helps us understand the basics of why cancer cells grow and what kills them so that one day we can develop better therapies and better cancer care for patients."
The research team set out to prove the hypothesis Lopez had developed while at Stanford University that ASPP2 was a tumor suppresser by genetically engineering mice predisposed to cancer because they lacked one of the genes encoding ASPP2.
"Basically what we did was created a mouse, called a 'knockout mouse,' which was missing a copy of ASPP2 ... which made it more susceptible to forming cancer -- at least that was our hypothesis," said Acoba, who cared for the mouse colony and performed necropsies to identify the tumors. He also ran the statistics and the survival curves to show the statistically significant difference between the two colonies in the rate of tumor formation.
The researchers compared normal mice, which have two copies of ASPP2, with the knockout mice with only one copy, and discovered the latter formed tumors faster, Acoba said.
Acoba said they manipulated the mouse embryo at an early stage, and identified the mice that had the gene knocked out.
"The more we're able to identify the protein and the genes involved in the onset of cancer, the better understanding we have, the better we can treat people. Then we can target patients we need to basically cure cancer.
"If we can find a genetic change that makes a cell more susceptible to becoming cancerous, we can design drugs to target that gene or that protein, or we can look for things in the environment to cause that genetic mutation to come about more easily," Acoba said.