It’s something of a puzzle. Scientists know that ethyl alcohol (the drinking kind) tends to suppress the spread of cancer yet worsen the patient’s overall condition.
And Washington State University researchers have learned that alcohol administered to cancerous lab mice causes loss of body fat but not protein. Loss of both is a common experience of advanced cancer patients.
Finding the “why” of these two phenomena is the current pursuit of Gary Meadows and former graduate student Nomelí Núñez and collaborator Patrick Carter, a WSU associate professor. They are getting help in funding from the NIAAA branch of the National Institute of Health.
25 years of study
Meadows, the current Dorothy O. Kennedy Distinguished Professor, has been at WSU since 1976.
“It was the only university in the country offering a position in my field,” he said. That field was pharmacognosy, which is “knowing all about” drugs and natural products having therapeutic benefits.
He earned his bachelor’s and master’s from Idaho State, and the University of Washington presented him with a Ph.D. in pharmacy sciences. He accepted the position at WSU as an assistant professor. The university promoted him to full professor in 1989.
Meadows developed a pharmacy course, dealing with immunology and vaccines, in his early years at WSU, then with the help of the College of Pharmacy, led an effort to make this a required course in the professional pharmacy curriculum. He directed the pharmaceutical sciences unit from 1987 – 1990, and when the unit expanded to a department within the college, he accepted the position of chair until 1996.
Last year, he became executive director of the Inland Northwest Cancer Research Consortium in Spokane, which is an alliance of two major health provider corporations in the region — Empire Health Services and Providence Services of Eastern Washington — and WSU.
“The consortium facilitates clinical cancer research,” he said. “My role is to promote professional cooperation among colleagues.”
Meadows has also directed WSU’s Cancer Prevention & Research Center since 1998.
Personal motivation
Ask him why the particular interest in cancer research and he’ll tell you the disease got to be personal.
“I grew up on an Idaho farm,” he explains, “and I saw family deaths from cancer, possibly as a result from pollution and agricultural chemicals. And my mother is a breast cancer survivor.”
So Meadows takes on the challenge of finding blocking mechanisms to limit or prevent metastasis, the spreading of cancer through the body from the point of origin. He works on melanoma, which he says has the highest rate of increase in the United States, and on prostate and breast cancer.
And the challenge is real, even after years of intensive cancer research in this country. Meadows explains cancer as uncontrolled growth of any cell due to an accumulation of genetic defects or mutations. Cells have built-in replication control mechanisms and an ability to repair low incidences of genetic damage. But four or five mutations break down the controls and cancer begins.
When metastasis happens, cancer becomes difficult to treat. The immune system gets overwhelmed, other bodily systems and functions get choked out, the body deteriorates and the person dies. Restoring genetic control functions would be a major breakthrough, and genetic therapy research is being conducted across the country. Meadows and his team are also looking at “signaling proteins.”
Cells communicate death
“Cells communicate through surface and secreted molecules,” he said. “Normal cells in physical contact relay a message to not divide. This is the control mechanism that damaged (cancerous) cells lack. And cells also have a ‘death pathway’ for life termination that is also signaled. This message pathway is ‘off’ in cancerous cells. We’re looking for a way to selectively switch on the death pathway for the cancerous cells but not the healthy cells.”
Alcohol, killer cells, obesity
And then there is the investigation into the alcohol-cancer link.
“Cancer researchers have known for awhile that heavy consumers of alcohol have a greater tendency toward cancer,” said Meadows. “We just don’t know why.” He says the speculation is that heavy alcohol use suppresses the immune system and destroys “killer cells” that are toxic to tumors and may contribute to the genetic mutation that gets cancer started.
But it is the loss of body fat in cancerous laboratory mice that is the intriguing research topic of the day.
“There are interesting human implications,” said Meadows. “When we eventually learn how alcohol consumption by cancerous mice selectively induces the metabolism of fat, but not protein, it may one day be possible to design a safer and more effective way to treat obesity.”
