According to [Friedman2013, pg 86], there are three steps that lead to the initiation of most cancers:
- Cell division rate in excess of cell apoptosis rate,
- Defective tumor-suppressor genes (e.g. TP53),
- The lengthening of telomeres that allows cancer cells to become immortal and replicate indefinitely.
These steps may result from hormone imbalances, immune system failures, genetic mutations, metagenetic changes in gene expression, etc.
In a healthy individual, cells are constantly being "born" (by cell division or from adult stem cells), and "dying"
(via a process called apoptosis), and after adolescence the rates of birth and death should be balanced.
Cells become cancerous (immortal) when they mutate
[Dr. Weyrich: or undergo metagenetic changes ]
that prevent normal cellular apoptosis.
Apoptosis (also known as "programmed cell death") is a process that protects the body from defective or old cells, and is triggered
by the immune system when a cell appears to be problematic.
Some authors contend that the body is constantly forming cancerous cells, but the vast
majority of the cancer cells are detected by the immune system and destroyed before they
can multiply to the point of becoming a problem.
Some practitioners have noted an association with
inflammatory process mediated by homocysteine [Rogers2008, pg 9]. Note that the common
diuretic hydrochlorothiazide (HCTZ) increases homocysteine levels [Westphal2003 🕮 ].
Hypothyroid
conditions may be associated with low immune system activity,
which compromises the body's defense against all forms of cancer.
[ONeill2008] has discussed the role of Toll-Like receptors in cancer.
- Low-dose naltrexone targets the opioid growth factor - opioid growth factor receptor pathway to
inhibit cell proliferation: mechanistic evidence from a tissue culture model [Donahue2011b 🕮 ]
- Interaction of opioid growth factor (OGF) and opioid antagonist and their significance in cancer therapy [Wang2019 🕮 ]
- Naltrexone at low doses upregulates a unique gene expression not seen with normal doses:
Implications for its use in cancer therapy [Liu2016 🕮 ]