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Stress Hormones Hastens Blood Cancer Progression

by Medindia Content Team on November 21, 2007 at 7:34 PM
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Stress Hormones Hastens Blood Cancer Progression

A new in-vitro study using cell culture has shown that norepinephrine, the stress hormone, may cause growth and spread of certain tumour cells by hastening the biochemical signals that stimulate them. This may consequently quicken the progression of certain blood cancers.

The finding, if verified, may suggest a way of slowing the progression and spread of some cancers enough so that conventional chemotherapeutic treatments would have a better chance to work.

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The study also showed that stress hormones may play a totally different role in cancer development than researchers had once thought.

"We would not be surprised if we see similar effects of norepinephrine on tumor progression in several different forms of cancer," explained Eric Yang, first author of the paper and a research scientist with the Institute for Behavioral Medicine Research (IBMR) at Ohio State University.
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The researchers looked at a different type of blood cancer - multiple myeloma, focussing on three multiple myeloma tumor cell lines, each representing a different stage in the life of the disease, for their experiments. While all three-tumour cell lines reacted to the presence of norepinephrine, only one, a cell line known as FLAM-76, responded strongly to the hormone.

"The fact that this one cell line, of the three multiple myeloma cell lines studied, closely represents the early stages of the tumour, and that this is where we see the biggest effect, is what makes this work more clinically relevant," Yang said.

The norepinephrine binds to receptors on the surface of the cells, sending a signal to the nucleus to produce a compound known as VEGF --vascular endothelial growth factor - that is key to the formation of new blood vessels, which the tumour must have to grow.

The FLAM-76 cell line was prepared from multiple myeloma tumour cells taken from a patient whose disease had not yet progressed too far from its original site in the bone marrow where blood cells are formed.

"It turns out that FLAM-76 tumour cells more closely represent the earlier stages of the disease when blood vessel formation, a process called angiogenesis, is needed for disease progression," Yang said.

The researchers believe that blocking these receptors would slow the process of the growth of more blood vessels to the tumour, delaying disease progression and perhaps allowing treatments to be more effective. Widely used "beta-blocker" drugs now prescribed for high blood pressure work by blocking these same particular cell surface receptors, Yang said.

"This approach wouldn't kill the tumour cells but it would diminish the blood supply to the tumour cells and slow them down, and that could translate into a longer and better quality of life for the patient," said Ron Glaser, a professor of molecular virology, immunology and medical genetics, and an author of the study.

The researchers and their colleagues are now working with other forms of cancer to test the effects of stress hormones like norepinephrine on their growth.

Glaser added that these kinds of results might change the way scientists are looking at a link between stress and the development and spread of cancer. In the past, he said, the focus was on how stress hormones weakened the immune system, allowing certain tumours to evade the body's defenses.

"Now we have these stress hormones, not only affecting the immune response, but also acting directly on the tumour cells and inducing changes in the molecules made by those same tumour cells," Glaser said.

The results appear in the current issue of the journal Brain, Behavior and Immunity.

Source: ANI
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