Cancer seems to be a programmed sequence. It is currently widely believed to be started by multiple DNA mutations, either from toxic triggers or natural random errors, that subvert the normal program. And once started, some aspects of the normal cell growth programs come into play and help support the growing tumor.
Cancer Cell Differences
Cancers are different to normal human cells in many ways. These differences help them to grow fast and can also help them spread.
- Rapid growth: tumor cells grow rapidly, whereas normal cells retain a steady population
- Immortality and telomeres: Normal cells have only a finite number of divisions before they die, perhaps around 50. The reason is that cells have telomeres that shrink with each cell division, and kill the cell when they run out. Some cancer cells live forever, do not have shortening telomeres, and synthesize their own enzyme telomerase that extends the telomeres. Not all cancer cells have this property.
- No contact inhibition: normal cells will stop growing when they start to touch other cells and have filled up an area. Cancer cells do not stop growing when they reach other cells, but will either push these cells, or penetrate into the cell area. Hence, lack of contact inhibition causes tumors to continue growing even when they press on other organs (causing damage or other problems), and also promotes metastasis of the cancer cells.
- No stickiness: Normal human cells stick together or stick to the site where they should stay. The most dangerous of cancer cells lose this adhesive property. The cells can then drop off easily and spread throughout the body.
- Simpler nutrients: Normal human cells are hard to grow in the laboratory and require a complex nutrient base. Cancer cells have much simpler needs for nutrition.
- No growth factors needed: Normal human cells require growth factors to grow in a lab. Cancer cells can grow without them. Cancers do not need to be stimulated to grow.
- No death (all cases?) - Loss of apoptosis (?).
- No DNA repair: Normal cells have many DNA repair mechanisms. Many types of cancer cells have damaged chromosomes.
- Abnormal chromosome structure: Normal cells have pairs of each chromosome. Many cancer cells have bizarre chromosome patterns rather than the normal disomy, having sometimes 0 or sometimes many chromosomes per cell. Major errors such as chromosome translocations are common.
How Do Cancers Grow?
Over-growth or under-death?: All cancers grow too fast, but it needs to be clarified whether this is due to a failure of the growth program or of the death program. Normal cells grow and divide, but their rate equals the rate of death of cells (except during growth spurts or healing). So do cancers increase the rate of cell growth or decrease the rate of cell death? Or possibly both? Either way will yield a net over-growth.
Cancers can grow fast, but not super-fast. They do not grow as fast as the body does during growth (e.g. fetal development and childhood) nor as fast as the healing process. Cancers are also slower than the most rapidly dividing of adult cells such as in the bone marrow or intestinal epithelium. The fact that cancers do not grow faster than all human cells indicates that the cause can be over-growth (but only partial) or under-death. It does not rule out either case, but it does mean that cancers do not get some kind of new super-growth or hyper-growth; they are just using ordinary cell growth methods.
Another interesting fact is found by S-phase testing of cancer cells. This measures the percent of cells that are in the S-phase of cell division. Rapid growing tumors are over 8%, slower growing less than 7%. The difference in percentages seems to indicate that the rate of growth, rather than a death rate, is what decides the overall rate of tumor growth. However, this does not totally rule out differing death rates.
Immaturity of cancer cells also seems to indicate that a growth rate rather than a death rate is relevant. Most cancers are of immature forms of the normal cells (e.g. blast forms), and have varying levels of maturity and differentiation. This would seem to indicate that the growth program of the cell is interrupted, causing either premature cell division, or alternatively not ever getting mature enough to get to the start of the cell death program. So immaturity could actually mean both rates are affected: cell division too early rates the growth rate, and immaturity avoids cell death.
Organ-like growth: Large tumors are somewhat like body organs. They have a blood supply via a created network of blood vessels. How does this occur? Does the growth program somehow know that whenever a large clump of cells grow, that there should also grow blood vessels there? Or does the cancer somehow also contain these as a separate aspect? The former seems more likely, that the normal growth sequence, when subverted by the tumor, still knows to build an adequate structure of blood vessels for nutrients.
Natural Cancer Causes
When you analyze the human body, it is not so surprising that people get cancer. Rather, it is surprising that we don't all get it, and that we don't get it quickly and early in life. There are so many things attacking the body that could cause cancer early and in everyone.
DNA error rates are actually very high. Simple base-pair mutations occur between 1-in-million to 1-in-10-billion for each cell division. With 6 billion base pairs in human DNA, this translates to between 1 and 6,000 errors per cellular division, and these must be repaired. Cytosine (C) is frequently converted to Uracil (U) at a high rate of about 10% per day and this must be repaired.
Repair and Anti-Cancer Body Mechanisms
The body maintains numerous defensive lines against both the innate DNA mutations and the attacks from environmental toxins and other external agents. The anti-cancer methods that occur within the body include:
- DNA repair methods: there are various methods and enzymes used to test and repair DNA sequences. A great deal of Uracil is re-converted back to Cytosine, identified by the mismatch in base pair (?? or is it that Uracil should not appear in DNA??). Other mismatched base pairs are also continually repaired. Other more general DNA repair mechanisms also exist.
- Cell shedding: the body simply sheds some types of cells that are particularly exposed to environmental carcinogens. For example, intestional epithelial cells are shed frequently, so any mutations do not get a chance to reproduce, and this process also takes place very quickly, with these cells amongst the fastest growing in the body. Cell shedding occurs in the stomach, colon, skin, and other epithelial cells.
- Cell life-span: many different types of cells only live a short time, and thus any mutation does not get a chance to replicate. For example, red blood cells are replaced at a rate of about 100 billion a day, out of a total of about a trillion.
- Cell division limits: the use of telomeres to limit the number of cell divisions that a single cell can make also helps to inhibit cancer. Even if a cell becomes cancerous, its generations of children will often die out from this limit, before the over-growth becomes a significant tumor.
- Carcinogen neutralization: many of the substances to which the body is exposed would be carcinogenic, but are quickly metabolized into harmless substances by the gut and the liver.
- Immune system: the immune system is also believed to identify any significantly altered cancerous cells, and it kills these cells, just as it kills virus-infected cells.
- Glutathione transferases defend against mutagens
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