home   genetic news   bioinformatics   biotechnology   literature   journals   ethics   positions   events   sitemap
 
  HUM-MOLGEN -> Genetic News | search  
 

Genes, Time And Breast Cancer

 
  December, 2 2000 3:47
your information resource in human molecular genetics
 
     
An established hypothesis that explains the increase in risk of cancer with advancing age is centred on cell division. The older one gets, the more times one’s cells must divide (or undergo mitosis), the greater the chance that something will ‘go wrong’, thus causing a cell to become malignant. The model must be tweaked to accommodate the risk of breast cancer in women, which rises steeply between the puberty and menopause, and levels thereafter. It is thought that this is because cells in breast epithelial tissue proliferate (and then undergo cell death) each month, in response to changes of hormone levels that are part of the menstrual cycle—which takes place between puberty and menopause. So the cyclical growth of breast epithelium superimposes an additional risk over that incurred by age.

Epidemiologists Julian Peto (Institute of Cancer Research, UK) and Thomas Mack (University of Southern California) now present data that support the need for yet another tweak to the breast-cancer model (Nature Genetics, Vol. 26, Issue 4, 01 Dec 2000). It is known that women who have had breast cancer run a relatively high, constant risk (about 0.7% per year) of developing cancer in the other breast. Peto and Mack carried out a prospective study of women with breast cancer and their immediate relatives; they purposely included women with identical twins in the study. They find that the risk of an identical twin developing breast cancer is also 0.7%, regardless of age of onset of the initial breast cancer in her sister. Of course, identical twins tend to share environments (including the that of the womb), and so there may be environmental factors that confound this interpretation. But when Peto and Mack charted the risk of breast cancer in the mothers and (non-twin) sisters of index patients, they found a similar result. These women have an elevated constant risk (0.3–0.4%/year) that does not vary with age after initial diagnosis of breast cancer in the daughter/sister. The investigators interpret this to indicate that a woman’s risk of breast cancer starts from a genetically determined age, and that a high proportion of breast cancers arise in a small, susceptible group.

As Douglas Easton (of the Cancer Research Campaign) points out in an accompanying News & Views article, this model does not account for the inflection of risk seen at menopause. He suggests that overall risk of breast cancer is akin to a multi-factorial equation and that the finding of Peto and Mack may be one such factor in the equation—although cautions that epidemiological observations alone are probably too weak to provide a clear answer regarding which type of model, or mixture of models, most accurately accounts for the pattern of risk of breast cancer.

CONTACT

(Authors)

Dr. Thomas Mack
University of Southern California
Los Angeles, California
Telephone: +1 323 865 0445
E-mail: tmack@hsc.usc.edu

Dr. Julian Peto
Institute of Cancer Research
Sutton, United Kingdom
Telephone: +44 20 8643 0424
Fax: +44 20 8770 7876
E-mail: j.peto@icr.ac.uk

(News & Views)

Dr. Doug Easton
Strangeways Research Laboratories
Cambridge, United Kingdom
Telephone: +44 1223 740 160
Fax: +44 1223 740 159
E-mail: douglas.easton@srl.cam.ac.uk

(C) Nature Genetics press release.


Message posted by: Trevor M. D'Souza

print this article mail this article
Bookmark and Share this page (what is this?)

Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.

Use the links below to share this article on the social bookmarking site of your choice.

Read more about social bookmarking at Wikipedia - Social Bookmarking

Latest News
Variants Associated with Pediatric Allergic Disorder

Mutations in PHF6 Found in T-Cell Leukemia

Genetic Risk Variant for Urinary Bladder Cancer

Antibody Has Therapeutic Effect on Mice with ALS

Regulating P53 Activity in Cancer Cells

Anti-RNA Therapy Counters Breast Cancer Spread

Mitochondrial DNA Diversity

The Power of RNA Sequencing

‘Pro-Ageing' Therapy for Cancer?

Niche Genetics Influence Leukaemia

Molecular Biology: Clinical Promise for RNA Interference

Chemoprevention Cocktail for Colon Cancer

more news ...

Generated by News Editor 2.0 by Kai Garlipp
WWW: Kai Garlipp, Frank S. Zollmann.
7.0 © 1995-2016 HUM-MOLGEN. All rights reserved. Liability, Copyright and Imprint.