Fri, Apr-09-10, 09:05
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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http://www.cbc.ca/health/story/2009...er-vaccine.html
Quote:
Diabetes drug may help fight cancer, mouse study suggests
A commonly prescribed diabetes drug also has the potential to boost the immune system's response to cancer treatments, Canadian and American researchers have found.
In studies on mice published in Wednesday's issue of the journal Nature, Prof. Yongwon Choi, a professor of pathology and laboratory medicine at the University of Pennsylvania in Philadelphia, and his colleagues found the drug metformin increases the effectiveness of an experimental anti-cancer vaccine.
'I like to think of it as an immune system booster.'— Prof. Russell Jones
Cancer and diabetes may seem quite different, but researchers are uncovering common metabolic pathways in both diseases.
Cancer vaccines aim to treat the disease rather than prevent it, by priming the immune system to recognize cancerous cells as a threat before they grow out of control.
The challenge of cancer vaccines is to get the immune system to recognize the threat posed by cancer cells and mount enough of a response to eliminate the tumour, said study co-author Russell Jones, a professor at McGill University's Goodman Cancer Centre in Montreal.
The team said they serendipitously discovered that the immune system's specialized white blood cells known as CD 8 T-cells switch from burning glucose to fatty acids following infection.
"While I definitely would stop short of saying, 'Let's take it as a prophylactic therapy' [for cancer], because I think it's more complex than that, it certainly gives hope," said Jones, who also works in McGill's pathology department.
"Essentially, I like to think of it as an immune system booster."
Metformin is known to bring down blood sugar levels by mimicking starvation.
In the experiments, mice engineered to lack immunological memory were unable to switch from using glucose as a fuel source to using fatty acids.
Giving metformin "tricked" the T-cells into thinking they were starved, and restored their immunological memory, Jones explained.
The immunological memory of normal mice also improved.
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Besides the effect on T-cells, metformin could reduce glucose availability to cancer cells, reducing their ability to fight or subvert the immune process.
http://www.jimmunol.org/cgi/content/abstract/158/1/40
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Although female mice readily reject organs from allogeneic or semiallogeneic male donors, they do not reject the fetuses sired by those same donors. An explanation for this that has been made in the past is that the fetus influences its mother's immune response by sending fetal cells into the maternal circulation. To determine the frequency and magnitude of fetal to maternal cell migration, we employed a sensitive quantitative PCR technique to assess the numbers of male cells in the thymus, spleen, liver, lymph nodes, and peripheral blood of normal mice undergoing their first pregnancy. We found that fetal cell migration is not universal but occurs in only a fraction of pregnancies. Using a kinetic analysis of normal mice mated to syngeneic or allogeneic males, a comparison of normal and SCID mice, and testing of multiparous mice for CTL against fetal Ags, we found that migrating fetal cells were cleared by the maternal immune system. Thus the mother is not continuously exposed to circulating fetal cells and, in fact, has the capacity to eliminate them without eliminating the fetus.
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Maybe the fetus has the ability to "subvert" the immune response, but individual fetal cells do not? Sort of like with cancer? (What does this say about drinking Neu5Gc isolated from red meat, and the immune response to that? No guarantees that those immune cells will go off and attack tissue that contains Neu5Gc, is there?)
This next is from the article posted by Valtor;
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In other words, normal mitochondrial function would facilitate expression of the differentiated state thereby suppressing the tumorigenic or undifferentiated state. This concept can link mitochondrial function to the long-standing controversy on cellular differentiation and tumorigenicity [5,163]. Respiration is required for the emergence and maintenance of differentiation, while loss of respiration leads to glycolysis, dedifferentiation, and unbridled proliferation [8,25]. These observations are consistent with the general hypothesis presented here, that prolonged impairment of mitochondrial energy metabolism underlies carcinogenesis. New studies are necessary to assess the degree to which cellular energy balance is restored in cybrids and in reprogrammed tumor cells.
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