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BRCA1 and BRCA2 are the well known genes associated with the development of breast cancer. They are tumor-suppressor genes that produce proteins to help repair damaged DNA.

If these genes get mutated or damaged, they fail to produce the right proteins, and the DNA may not be repaired. This can lead to more mutations and, eventually, the development of cancer.

What does the research say about the association of BRCA1 and BRCA2 with breast cancer? According to the Journal of Epidemiology Community Health, ‘Genetic inheritance is an infrequent but not the main cause of breast cancer.

The consensus is that breast cancer susceptibility or cancer predisposition genes are associated with only 4%–8% of breast cancer cases. It is apparent therefore that 92%–96% of cases are sporadic. The New England Journal of Medicine states that only 7% of women from families with a history of breast cancer had BRCA1 mutations. Last, the journal Carcinogenesis states that mutations of the BRCA1 and BRCA2 genes account for 5% of breast cancer in the US annually.

Is there another genetic abnormality other than the famous and infamous BRCA genes that may spark breast cancer? Allow me to introduce P53.

The P53 gene appears to be the protector of the genome (genetic material of an organism) by using several functions. P53 can help to repair damaged DNA and also acts as a tumor suppressor. It can put the brakes on cell function long enough for the cell to repair itself; if the damage can’t be repaired, the P53 gene causes the cell to commit suicide.

As with other genes, the P53 gene can become damaged/mutated and cease to function normally.

The resulting genetic damage can lead to abnormal cell growth and proliferation, thus causing the development of cancer and tumor formation.

Somewhere along the life of a specific individual, genes can become damaged and fail to do their jobs. As a result, breast cancer can develop.

Factors that can affect the genes include body composition (percentage of body fat and lean muscle), hormone profile, nutrient intake, stressors, toxins, emotions, exposure to radiation, viral load (amount of viruses), oxidative stress (free radical damage), drugs, and alcohol.

It appears that the majority of breast cancer is due to metabolic alterations inside the body, rather than from an inherited gene.

However, when considering genetics and genes, BRCA1 and BRCA2 mutations account for only 5% of breast cancer. Yet, according to Clinical Cancer Research, mutations in the tumor-suppressor gene P53 are present in 18%–25% of primary breast carcinomas.

Research found in the journal Cancer Research showed that of 137 breast-cancer tumors examined, the P53 mutation was found in 40% of the tumors . . . 40%! It is obvious that dysfunctional P53 genes are more prevalent than the well known BRCA genes in their contribution to the development of breast cancer. The fact that P53 is not talked about or investigated makes no sense.

With breast cancer the third-most-common tumor globally, it would behoove anyone with a family history of breast cancer, or anyone who has dealt with breast cancer diagnosis and treatment, to get evaluated for mutations of the P53 gene, along with BRCA1 and BRCA2.

While genes are not your fate, having a greater understanding of your specific blueprint, as well as the environmental factors that can alter your genetic profile, can and will give you greater control, instead of waiting for a disaster to happen.


O’Donovan P, and Livingston D.  BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair. Carcinogenesis vol.31 no.6 pp.961–967, 2010

Wiseman R. Breast cancer hypothesis: a single cause for the majority of cases. Journal of Epidemiology & Community Health 2000;54:851–858

Alsner J, Yilmaz M, Guldberg P, et al., Heterogeneity in the Clinical Phenotype of TP53 Mutations in Breast Cancer Patients,  Clinical Cancer Research Vol. 6, 3923–3931, October 2000

Coles C, Condie A, Chetty U, et al.  p53 Mutations in Breast Cancer.  Cancer Research 1992;52:5291-5298.