Possible, New Support of my Explanation of Breast Cancer… including Arch Intern Med. 2006;166:1483-1489
These represent possible, new support of my explanation of breast cancer. These are articles to which I have responded. If you are reading these, you may already know my hypotheses, however, since these are responses to investigators who may not know my hypotheses, I have included my basic hypotheses.
Medicinski arhiv (Med Arh) 2005;59(1):33-5.
Circulating levels of
prolactin in breast cancer patients.
Mujagic Z, Mujagic H, Prnjavorac B.
Department of Biochemistry, University of Tuzla, Bosnia and Herzegovina.
OBJECTIVES: In order to assess diagnostic value of prolactin (PRL) in breast cancer (BC), we examined its serum levels and frequencies of its increase in breast cancer patients (BCP), and compared them to those in two controls. We also determined circulating levels of PRL in localised and advanced BC and calculated sensitivity and specificity of PRL in BC. Patients and METHODS: The main experimental group consisted of 47 female patients with histologically confirmed diagnosis of BC. The obtained results were compared to those in two control groups: clinically healthy women, and female patients with other types and locations of cancer. Serum levels of PRL were measured by means of radioimmunoassay. Results were processed by means of t-test and two way analysis of variance. RESULTS: The serum levels of PRL before treatment, as well as the frequencies of its increase, were significantly higher in BCP in comparison to controls (p<0.01, 0.02). The average circulating levels of PRL in patients with advanced BC were significantly higher (p<0.0001) in comparison to patients with localised disease. Sensitivity for PRL in BC was 50%, and specificity was 100%. CONCLUSIONS: Increased levels of PRL can be detected in the majority of patients with advanced BC. PRL has high specificity for BC, especially for metastatic BC, which leads to its diagnostic and prognostic importance in this disease.
It is my hypothesis that low dehydroepiandrosterone (DHEA) may trigger breast cancer (Annals of Internal Medicine 2005; 142: 471-472). Your findings in Med Arh 2005; 59: 33-5 may support my explanation of cancer.
It is known that prolactin stimulates DHEA production. I suggest that when sufficient DHEA is stimulated, prolactin production is reduced. That is, DHEA inhibits prolactin production when DHEA reaches a proper level. This is a “feed back” mechanism. I intend to suggest that high prolactin indicates that DHEA is not available to reduce prolactin production. This could be why prolactin is high in breast cancer.
Therefore, according to my explanation of breast cancer, prolactin levels should be high. Prolactin levels should be higher in women of low DHEA, therefore, prolactin levels should be high in breast cancer compared to controls. It is also part of my work that all tissues use DHEA for growth. Therefore, cancer will also depend upon DHEA for growth and, I suggest, will use DHEA at the expense of normal tissues. I think cancer will cause DHEA levels to be reduced even lower. This reduction in DHEA should increase prolactin levels. I suggest this is why you found that prolactin increases with increased intensity of breast cancer and metastasis. That is, as cancer increases, it uses more DHEA which increases prolactin because of the lack of DHEA feedback on prolactin levels.
Again, I suggest your findings directly support my explanation of DHEA and breast cancer. DHEA naturally declines in old age. Therefore, my explanation of low DHEA and cancer explains why cancer incidence increases during old age. This is also supported by the increase of prolactin in old age. Since DHEA declines in old age, the DHEA feedback mechanism does not decrease prolactin. Also, since DHEA is decreased in old age, cancer grows less rapidly in old age. The use of DHEA by cancer in elderly people may explain “cachexia” of caner. Cachexia results from loss of DHEA for all tissues because of use of DHEA by cancer. This could also explain mental illness which often occurs with cancer in the elderly as the brain also uses DHEA.
International Journal of Cancer (Int J Cancer) 2006 Jan 31; [Epub ahead of print]
Metabolic syndrome as a
prognostic factor for breast cancer recurrences.
Pasanisi P, Berrino F, De Petris M, Venturelli E, Mastroianni A, Panico S.
Department of Preventive and Predictive Medicine, Istituto Nazionale Tumori,
Several studies have shown that hormonal, metabolic and inflammatory mechanisms may affect breast cancer progression. We tested the prognostic value of metabolic syndrome in 110 postmenopausal breast cancer patients, who participated in a 1-year dietary intervention study. The risk of adverse events after 5.5 years of follow-up was examined by Cox' proportional hazard modelling, adjusting for hormone receptor status, stage at diagnosis and serum testosterone level, which were shown to significantly affect prognosis. The adjusted hazard ratio of recurrence for the presence of metabolic syndrome at baseline was 3.0 (95% CI 1.2-7.1). Combining metabolic syndrome and serum testosterone, the adjusted hazard ratio of recurrence among women with metabolic syndrome and testosterone levels higher than 0.40 ng/ml (median value) was 6.7 (95% CI 2.3-19.8) compared with that among women without metabolic syndrome and testosterone levels </=0.40 ng/ml. The results suggest that metabolic syndrome may be an important prognostic factor for breast cancer. (c) 2006 Wiley-Liss, Inc.
It is my hypothesis that breast cancer, and other cancers, may be initiated by increased testosterone (International Journal of Cancer 2005; 115: 497) and low dehydroepiandrosterone (DHEA) (Annals of Internal Medicine 2005; 142: 471-472).
Rasanisi, et al., report that women with increased testosterone and “with metabolic syndrome” are at increased risk of breast cancer (International Journal of Cancer 2006. It has been reported that “DHEA replacement could play a role in prevention and treatment of the metabolic syndrome” (Journal of the American Medical Association 2004; 292: 2243-8).
I suggest the findings of Rasanisi, et al., may support my explanation of the combined connections of increased testosterone and low DHEA with breast cancer.
Annals of Oncology (Ann Oncol) 2006 Feb;17(2):341-345. Epub 2005 Oct 25.
Consumption of sweet foods and breast cancer
risk in Italy.
Tavani A, Giordano L, Gallus S, Talamini R, Franceschi S, Giacosa A, Montella M, La Vecchia C.
Istituto di Ricerche Farmacologiche 'Mario Negri',
BACKGROUND: The relation between the intake of sugar and sweets and the risk of breast cancer has been considered in ecological, prospective and case-control studies, but the results are unclear. We analyzed such a relation in a case-control study conducted between 1991 and 1994 in
It is my hypothesis that increased testosterone may trigger breast cancer (International Journal of Cancer 2005; 115: 497). It is known that "increased glucose and insulin concentrations are associated with increased free testosterone and decreased sex hormone binding globulin" (Am J Med 1995; 98: 40S-47S).
I suggest the findings of Tavani, et al., may be explained by increased testosterone in the subjects and that increased testosterone may trigger breast cancer
Combined Estrogen and Testosterone Use and Risk of Breast Cancer in Postmenopausal Women
Rulla M. Tamimi, ScD; Susan E. Hankinson, ScD; Wendy Y. Chen, MD; Bernard Rosner, PhD; Graham A. Colditz, MD, DrPH
Arch Intern Med. 2006;166:1483-1489.
Background The role of androgens in breast cancer etiology has been unclear. Epidemiologic studies suggest that endogenous testosterone levels are positively associated with breast cancer risk in postmenopausal women. Given the increasing trend in the use of hormone therapies containing androgens, we evaluated the relation between the use of estrogen and testosterone therapies and breast cancer.
Methods We conducted a prospective cohort study in the Nurses' Health Study from 1978 to 2002 to assess the risk of breast cancer associated with different types of postmenopausal hormone (PMH) formulations containing testosterone. During 24 years of follow-up (1 359 323 person-years), 4610 incident cases of invasive breast cancer were identified among postmenopausal women. Information on menopausal status, PMH use, and breast cancer diagnosis was updated every 2 years through questionnaires.
Results Among women with a natural menopause, the risk of breast cancer was nearly 2.5-fold greater among current users of estrogen plus testosterone therapies (multivariate relative risk, 2.48; 95% confidence interval, 1.53-4.04) than among never users of PMHs. This analysis showed that risk of breast cancer associated with current use of estrogen and testosterone therapy was significantly greater compared with estrogen-only therapy (P for heterogeneity, .007) and marginally greater than estrogen and progesterone therapy (P for heterogeneity, .11). Women receiving PMHs with testosterone had a 17.2% (95% confidence interval, 6.7%-28.7%) increased risk of breast cancer per year of use.
Conclusion Consistent with the elevation in risk for endogenous testosterone levels, women using estrogen and testosterone therapies have a significantly increased risk of invasive breast cancer.