In the past, I have posted my theory of cancer, at this newsgroup, and
applied it to cancer of the breast. I will give a short abstract at this
time. Basically, my principle hypothesis is that DHEA is necessary for
transcription and replication of DNA, in all tissues. I suggest that
oncogenes may be triggered by reductions in the hormone,
dehydroepiandrosterone (DHEA). (See my earlier posts for explanation.)
DHEA naturally starts to decline sometime after age 20, to reach very low
levels in the aged. It is the low levels of DHEA, I suggest, that trigger
oncogene function in the elderly. Another part of my explanation of cancer
suggests that, once cancers are initiated, cancer depend on DHEA for
growth. (I suggest all tissues must have DHEA for DNA function, so must
cancer.) If you put these two phenomena together, you have an explanation
for why cancers appear more in the elderly, but grow much less rapidly.
In my earlier posts, I cited reports that demonstrated that breast tumor
tissues concentrate DHEA more than non-tumor tissues. This means that the
cancer is absorbing DHEA more rapidly than noncancerous tissue. DNA of
cancers is more "juvenile-like," so its DNA is rapidly dividing. DNA that
is rapidly dividing, according to my theory, must have more DHEA than
differentiated tissues. Now carefully follow the following to avoid some
confusion. I have suggested (explained in my earlier posts) that reduced
DHEA triggers oncogenes. When these genes are triggered, they must have
more DHEA to survive. I suggest they must stimulate an increase in DHEA in
order to continue. In the following quotation, note that in postmenopausal
women, DHEA, and its primary blood source, DHEAS, are increased.
"Relationship of serum dehydroepiandrosterone (DHEA), DHEA sulfate, and
5-androstene-3 beta, 17 beta-diol to risk of breast cancer in
postmenopausal women," Cancer Epidemiol Biomarkers Prev 6 (3): 177-181 (Mar
1997)
Dorgan JF, Stanczyk FZ, Longcope C, Stephenson HE Jr, Chang L, Miller R,
Franz C, Falk RT, Kahle L, Division of Cancer Prevention and Control,
National Cancer Institute, NIH, Bethesda, Maryland 20892-7326, USA.
"Laboratory evidence suggests a role for dehydroepiandrosterone (DHEA) and
its metabolite 5-androstene-3 beta, 17 beta-diol (ADIOL) in mammary tumor
growth. Serum DHEA also has been related to breast cancer in postmenopausal
women, but the relationship of ADIOL to risk has not been evaluated
previously. To assess the relationship of serum DHEA, its sulfate (DHEAS),
and ADIOL with breast cancer risk in postmenopausal women, we conducted a
prospective nested case-control study using serum from the Columbia, MO
Breast Cancer Serum Bank. Cases included 71 healthy postmenopausal
volunteers not taking replacement estrogens when they donated blood and who
were diagnosed with breast cancer up to 10 years later (median, 2.9 years).
Two randomly selected controls, who also were postmenopausal and not taking
estrogens, were matched to each case on exact age, date (+/-1 year), and
time (+/-2 h) of blood collection. Significant (trend P = 0.02) gradients
of increasing risk of breast cancer were observed for increasing
concentrations of DHEA and ADIOL, and women whose serum levels of these
hormones were in the highest quartiles were at a significantly elevated
risk compared to those in the lowest; their risk ratios were 4.0 [95%
confidence interval (CI), 1.3-11.8) and 3.0 (95% CI, 1.0-8.6),
respectively. The relationship of DHEAS to breast cancer was less
consistent, but women whose serum DHEAS concentration was in the highest
quartile also exhibited a significantly elevated risk ratio of 2.8 (95% CI,
1.1-7.4). Results of this prospective study support a role for the adrenal
androgens, DHEA, DHEAS, and ADIOL, in the etiology of breast cancer."
