(note: there is an essential video that accompanies this post at the bottom of the page.)
Cancer is hard to define. Would-be cancer cells are routinely destroyed by your immune system prior to becoming clinically apparent. That may have happened billions of times already but “if a tree falls in the woods, and no one hears it…”
Cancers can also fail to travel or invade very well, leading to cancers of “low malignant potential” that you can live with indefinitely, like Steve Jobs’ Neuroendocrine pancreatic cancer.
And if cancer-like behavior, such as loss of contact inhibition or uncontrolled replication, occurs in a telomerase-inactive cell, then its lineage is dead within 50 divisions due to the Hayflick limit, so who cares?
What we can say without hesitation about both Cancer (and Aging) is that they may not be diseases like Scurvy (Vitamin C deficiency) or a Heart Attack (coronary artery blockage) but they are both the result of DNA damage which can be caused by radiation, oxidation, but most of all, telomere shortening and dysfunction.
Since it is Breast Cancer Awareness month, let’s look at the infamous “breast cancer gene,” or BRCA1. A BRCA1 mutation is associated with a 60% chance of breast and ovarian cancer by age 90. But did you know that “BRCA,” although it sounds like “breast cancer,” is really named after Berkeley, California?
Even more surprising, BRCA1 is no more a “cancer gene” than policemen are crime-inducers. They don’t cause cancer but if they aren’t policing the DNA, cancers will develop.
This policeman’s role of BRCA1 is to keep the telomeres healthy and repair DNA breaks. That is what they do 99.99% of the time. When a breast ‘stem cell,’ which is already immortal by virtue of telomerase activation, loses its heterozygosity (LOH), it loses its only good copy of the BRCA1 gene and then the “bad” copy (or no copy) is all that is left. As a result, the cell can no longer protect the telomeres and bad things happen.
LOH occurs with high frequency in BRCA1 patients who get cancer because chromosomes are not evenly segregated between a cells two daughters, a process described in the video about chromosome damage at the end of this posting.
In your car, friction causes your pistons to wear out, the brakes to fail, and the tires to go bald.
Just as motion creates friction in your car, so replicative senescence grinds down the cells in your body. Cells are constantly “in motion” because they must copy their 46 chromosomes 50 billion times a day. With each division, telomeres shorten and that’s why cells age.
Analogies are not even needed when it comes to radiation and oxidative stress. Radiation can cause DNA breaks just as radiation causes paint to crack and upholstery to fade. And oxidation causes DNA damage in cells just as it causes rust to your undercarriage.
————Other cancer syndromes
When I say there is only one cause of breast cancer, I mean that DNA damage is the sina qua non of all cancers. And when I say there are many cures, just look at this chart because all of these pathways are constantly at work to repair DNA or cause cell apoptosis (forced death) in order to prevent cancer. When any of them are disabled, as in the case of BRCA1 gene mutation, your DNA surveillance is compromised and like a city without cops, crime ensues.
Interestingly, 10 of 11 premature aging syndromes (aka Progerias) are related to DNA repair problems as I describe in this video, so the premature aging and the premature cancer syndromes are cut from the same cloth: failure of DNA repair and/or cell apoptosis.
Now that we have a telomerase activator in TA-65, we can assist DNA repair by preventing the telomere decay that causes breaks and incorrect chromosome separation at cell division. Don’t let another day pass without naturally recharging your stem cells by safely activating your telomerase.
To really increase your breast cancer awareness, you must watch this video which explains how DNA damage occurs and explains why cancer-prevention genes like BRCA1 are so essential.