Having a BRCA1 or BRCA2 mutation makes no difference to your survival odds

Having a BRCA1 or BRCA2 mutation makes no difference to your survival odds

After a diagnosis of breast cancer, there is no significant difference in overall survival times between patients carrying a BRCA1 or BRCA2 gene and patients without.

 


 

 

 


A study(1) published in top cancer medical journal, the Lancet Oncology, dispelled a few myths. First, the researchers studied 2733 younger women aged between 18 and 40. They did this because this is the group in which breast cancer risk is seeing the fastest growth. This is contrary to the Cancer Research UK view that cancer is a disease of older people. 40 per cent of breast cancer is now found in women under 60. 

 

 


 

 

 


In particular, there was a ‘belief’ that the growth in breast cancers such as Triple Negative Breast cancer (TNBC) was linked to these gene mutations. Cancer Research have talked in the past about women with BRCA1 or BRCA 2 accounting for 25 per cent of breast cancers, even though just 7 per cent of the population has the mutations.

 

 


 

 

 


In the study the women with breast cancer came from 127 hospitals across the UK and data from 2000-2008 was used. Only 12 per cent had either mutation, not 25 per cent.

 

 


 

 

 


The women’s records were followed for 10 years. At the 2, 5 and 10 year stage there was absolutely no difference in survival whether a woman had the gene mutations or not.

 

 


 

 

 


About a third of the women with a mutation had a double mastectomy to improve survival. However, the surgery did not appear to make any difference to the 10-year survival rate. 

 

 


 

 

 


Chris Woollams, former Oxford University Biochemist and Founder of CANCERactive said, “And another Medical Myth or two bites the dust. How many women have I helped over the years, who were scared stiff because they had breast cancer and been told by their oncologist that they had the BRCA1 or BRCA2 gene mutation? And if the Oncologist talks ‘Doom and Gloom’ to the patient, it becomes a sad and self-fulfilling prophecy. If you are told your odds of survival are poor, it prays on the mind. And the mind is a crucial factor in beating cancer. 

 

 


 

 

 


Mutations like this occur in just 7% of the population, yet we were told authoritatively by charities who should know, that they accounted for 25% of breast cancers! It turns out that figure is not true.



Go toBreast cancer overview - symptoms, causes and treatment alternatives

 

 


 

 

 


The definition of the word ‘mutation’ is a sequence change in your DNA.  And be clear. At worst, the mutation is only in one strand of your DNA; you have two. The other is perfectly healthy and works. The same process that affects the single strand will affect both strands. Genes work in pairs, and cancer is caused by lost messages. Lost messages are caused by blockages – the results of histone build up caused, in turn, by environmental toxins, stress, poor diet and hormones like oestrogen. This is the proven theory of cancer – the Science of Epigenetics – that cancer is caused by metabolic changes, not by mutation i.e. DNA sequence changes (which rarely occur – except by specific damage, for example by radiation or EMFs).   

 

 


 

 

 


If you have the genes and breast cancer, some UK oncologists put patients under real stress to have their breasts removed because they argued it lessened the risk of death. It may well still be true that there is a case for preventative surgery to remove susceptible parts of the body, as with Angelina Jolie, if you don’t yet have the disease (Go to: the research that led Angelina Jolie to have a Preventative Double Mastectomy, or PDM).  But you also could be ultra, ultra, careful and try to restrict environmental damage. But that, in itself, might be a huge stress and result in cancer.”  

 

 


 

 

 


The research showed that in the early stages of breast cancer, those with the either gene actually showed a greater survival.

 

 


 

 

 


The Research was conducted by a team from the Cancer Sciences Academic Unit at the University of Southampton and University Hospital Southampton NHS Foundation Trust in the UK, with senior author Professor Diana M Eccles.

 

2012 Research
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