A source on BRCA1 Selenium and DCA

Evaluation of the effect of obesity on selected haemostatic and fibrinolytic parameters in peri- and postmenopausal women

Polac I, Stetkiewicz T, Stachowiak G, Jedrzejczyk S, Pertynski T, Pakalski A, Kowalska E.
Klinika Ginekologii i Chorob Menopauzy Instytutu Centrum Zdrowia Matki Polki w Lodzi.

Localization of adipose tissue influence on obesity-dependent diseases. In obese people many abnormalities are observed connected with coagulation factors and fibrinolysis. We studied 47 peri- and postmenopausal female patients, who were operated on for benign changes within the pelvis minor. The patients were divided according to BMI (group I--BMI <25 kg/m2, group II--BMI > 29 kg/m2). In obese women lower SHBG concentration, higher insulin and glucose fasting blood levels, higher LDL, higher total fatty tissue content, higher fibrinogen level and elevated PAI-1 activity were found. A positive correlation between area under insulin curve and PAI-1 activity and a negative correlation between fasting insulin levels and tPA were also observed.

Based on the studies performed it can be said that:

1. Fatty tissue content in postmenopausal women exerts an influence on PAI-1 activity.
2. Obesity influences coagulation and fibrinolysis system in peri- and postmenopausal women.
3. Carbohydrate metabolism disturbances have influence on PAI-1 activity in peri- and postmenopausal women.

PMID: 12474565 [PubMed - indexed for MEDLINE]

Pol Merkur Lekarski. 2002 Sep;13(75):182-4

[I edited the date of first posting to bring this one to the top of the blog ~ originally 2nd January 2006]
can be edited under 'advanced properties' time stamp

Metabolic Targeting as an Anticancer Strategy: Dawn of a New Era?

James G. Pan1* and Tak W. Mak2*

1Campbell Family Institute for Breast Cancer Research, University Health Network TMDT East Tower, MaRs Centre, 101 College Street, 5-705, Toronto, ON M5G 1L7, Canada.
2Campbell Family Institute for Breast Cancer Research, University Health Network and Departments of Medical Biophysics and Immunology, University of Toronto, 620 University Avenue, Suite 706, Toronto, ON, M5G 2C1, Canada.

http://dx.doi.org/10.1126/stke.3812007pe14

http://www.signaling-gateway.org/update/updates/200705/nrm2168.html

Gain-of-function mutations in the tumor suppressor p53 promote oncogenesis by interfering with DNA repair.

[[...The authors argue that "a novel gain-of-function of common p53 cancer mutants in disrupting critical DNA DSB damage responses will have significant implications on the therapeutic interventions for human cancers that express p53 cancer mutants."...]]