Geneticists identify four new breast-cancer genes
Discovery adds to understanding of individuals' susceptibility.
A large-scale genetic study has identified four new genes that significantly affect a woman's risk of developing breast cancer.
Read more here.
Comments
I am wondering if the newly found mutations in sporadic breast cancer are also in either or both parents of the affected woman or maybe man. Are these inherited mutations or are they sporadic germ line mutations?
Posted by: Leslie Feldman | May 29, 2007 07:34 PM
The identification of FGFR2 gene will provied a new paradigm for the diagnosis of early stage breast tumor in women and could be use as early stage biomarker.
Posted by: Subhash Chandra Gupta | May 30, 2007 12:58 PM
The disease is Interstitial Cystitis (I.C.) of the bladder. The bladder is inflamed and pain worsens when urine fills it. Women are disproportionately afflicted with I.C. Conventional therapy is palliative treatment for an unknown etiology without a cure.
My wife had I.C. Her doctor allowed me to offer a therapy that promotes the production of mucin, a protective glycoprotein on the bladder membrane. Most over the counter products for menstrual discomfort can inhibit mucin production. The trade name drug Cytotec, prostaglandin agonist for gastric ulcer, was chosen because it can increase mucin production. I designed the drug protocol for my wife. After nine months of treatment, she has remained asymptomatic for five years.
It is possible for a drug or drugs to interfere with mucin secretion. An interruption of glycoprotein secretion may expose the lipid bilayer to strong hydrophilic forces. An occurrence of a breach will trigger VEGF and inflammatory mediators’ response or an inflammatory lining disease. One of the downstream signals of VEGF is PI (3) K. Using a prostaglandin agonist to stimulate glycophorin A dimmer will increase mucin secretion. An over expression of g-protein couple receptors will send deactivation signals to VEGF and over expressing PPAR, using nicotinic acid to utilize PLC-γ to increase endothelial nitric oxide synthesis, will downgrade transport for inflammatory mediators. The affected cells will return to normal cell noise, both extrinsic and intrinsic cell noise. Where the actin cytoskeleton is not re-arranged then normal transduction and cargo transport will resume.
The control over VEGF and inflammatory mediators in inflammatory lining disease has potential for other metabolic disorders including cancer. In the situation of cancer, the cells have abandon social-cooperation for self-survival. Cancer cells, probably coerce, have activated a conserved evolutionary gene(s) that allowed the cells to survive when environmental conditions are harsh and toxic. Although independent, the cancer cell still possesses the ability to respond to signals from the community. Therefore, a high frequency signaling induction will arrest VEGF and cytokines, and reestablish normal modulation of extrinsic and intrinsic cell noise, an eventual return to the community.
Drug regiment that I developed for treating I.C. is available upon request.
Sincerely,
Norman A. Smith
normanasmith@cox.net
Posted by: norman a smith | June 6, 2007 06:23 AM
I cant help but wonder how reliable this testing is, (http://www.thenewsroom.com/details/543066/Health?c_id=wom=kg-jlt
)people have that DNA was going to be the holy grail for a long time now, and so far, not a lot has changed. Kate from the womens health desk at thenewsroom.com
Posted by: Kate | July 29, 2007 03:42 PM