A New Hypothesis of Cancer

By Xiaolong Meng, M.D.

Current theories hold that cancers are abnormal tissues triggered by gene mutations. Standard cancer treatments are primary removal via surgery and/or attempts to destroy tumor tissue using radiation and/or chemotherapy. In spite of huge improvements in earlier detection and diagnosis, current treatments have not radically improved survival.  From 1950 to 2001, five-year survival rates for 50% malignant tumor types (such as pancreas, liver stomach, lung, brain, larynx, uterus, cervix, oral cavity and esophagus) have increased less than 15%.

From 1950 to 2001, five year survival rates for 50% malignant tumor types have increased less than 15%.

Why is this happening? Is the diagnosis still not early enough? Is the treatment not precise enough? Or are we going in the wrong direction? Let’s look at some facts first.

Fact A: Wounds are involved in pre-cancer diseases:
• Smoking causes chronic inflammation of the lungs and is a risk factor for lung cancer.
• Inflammation of the liver, colon, and prostate increases the risk of cancer developing in those tissues.
• Cervical erosion is a risk factor for cervical cancer.
• Ulcers are risk factors for gastric cancer.

Fact B: Oncogenes are involved in growth and wound healing:
An oncogene is originally defined as a gene that contributes to the production of a cancer. However, oncogenes are expressed not only in cancer, but also in pregnancy, embryonic development, wound healing, and growth factor synthesis. Oncogenes also have broad anti-apoptotic functions.

How can the commonalities of wound healing and cancer be explained? How can the relationships among oncogene, anti-apoptosis, and wound healing be interpreted? If gene mutations cause a cancer, why do they never cause a new organ formation?

Here we generate a new hypothesis tying those phenomena together. During growth or reproduction phases, growth and repair genes (GR genes, all tissue growth and repair genes, such as oncogenes, proto-oncogenes, etc.) are activated to reproduce cells so tissues can develop. When a wound occurs, the healing process begins. Platelets seal broken capillaries. T cells, macrophages, and NK cells migrate into the tissue to remove debris and dead cells. Leaked platelets, T cells, monocytes, and macrophages secrete growth and repair factors (GR factors, all tissue growth and repair promoting substances, such as cytokines, growth factors, growth and repair related hormones, etc). GR genes in surrounding cells are activated and secrete more GR factors. GR factors can recruit stem cells from neighboring tissues and the bone marrow to the wound site. Stem cells differentiate into various tissues under GR factor influence and finally repair the wound in concert with other cells. When repair is complete, the GR genes are turned off (or tumor suppressor genes are turned on) and homeostasis is restored.

However, if the wound is persistent due to chronic physical damage (radiation, electromagnetic field, trauma, particles, etc.), chemical damage (carcinogens, toxic chemicals, heavy metals, etc.) or biological damage (aging, free radicals, inflammation, nutrient deficiency, bacteria and virus infections, stress, etc.), local and neighboring stem cells may become exhausted. As the wound persists, more and more GR genes activated in surrounding cells induce malignant transformation that can lead to a small clinical cancer. After the wound is healed, the cancer cells can be re-differenciated or apoptotic. Then the tumor mass will be gone. If a small cancer cannot heal the wound, the tumor mass will continue to grow until the wound is healed or the whole system is exhausted.

Therefore, a cancer may not be a passive mutated mass. Rather, they are functional tissues produced by GR gene activation to secrete GR factors in an effort to heal persistent wounds. Cancerization is a programmed event of a cell. This program, like the other programs from the fertilized egg to a mature body, is necessary to our human life.

Evidence to support the hypothesis:
• Tumor cells secrete functional repair molecules, many of which are produced during wound healing, indicating tumor cells may help wound healing.
• The expansion potential of stem cells is lower in cancer patients than in controls, indicating stem cells are consumed in cancer.
• The fact that pathological cancers are found during autopsy at a higher incidence than clinical cancer suggests that the sub clinical cancer may be working on the underlying wounds.
• If the tumor suppressor gene, p53, is activated all the time, mice do not get cancer. However, they display an early onset of aging in their lives, including reduced longevity, osteoporosis, generalized organ atrophy, and less stress tolerance. This phenomenon indicates that cancerization is a necessary mechanism in the mammal lifespan.

Potential therapies based on hypothesis:

Traditional cancer treatments, including surgery, radiation, and chemotherapy aim to eliminate cancer masses. However, cancer tissue produces vital factors for repair of non-healing wounds. Therefore, traditional cancer treatments may actually be working against an organism’s attempts to heal.

Based on this new hypothesis, cancer treatment strategies should be comprised of three facets: (1) removal of known physical, chemical, or biological causes of persistent wounds; (2) provision of repair cells to the site of malignancy, such as stem cells; (3) delivery of growth and repair factors and substrates required for wound healing to the site of malignancy.

Too many factors around our living environment are harmful to our body, leading to wounds, wound healing, and cancerization. Some foods and food additives might induce cell death directly (such as heterocyclic amines from deep fried foods, BHA/BHT, and alcohol). Pollution and smoking can cause free radical formation, leading to cell damage. Electromagnetic field exposure and sunburn have been shown to cause apoptosis (programmed cell death). Mental depression, psychological tension, and physical stress were shown to cause apoptosis inside the body.

All those harmful factors present in daily life contribute to tissue damage. Persistent wounds will lead to continuous activation of GR genes and eventually to clinical cancer. Therefore, to treat cancer, it is very important to limit those harmful factors in daily life to avoid new cancerization. Detoxification therapies (such as chelation and enema) can remove the accumulated toxins inside the body and are reported to be of benefit. If risk factors cannot be found for an existing cancer, changes in living environment and lifestyle may be good solutions to avoid the harmful factors.

Supplying enough repair cells to wound sites for a sufficient amount of time to elicit termination of wound healing is one of three cornerstones of successful cancer therapy based on the hypothesis. Stem cells are the most likely candidates for repair cells. Stem cells are known to home in on, and repair, damaged tissue. Some immune stimulants that show an anticancer effect are found to be stem cell stimulants also, such as glucans. Stem cell stimulators alone have demonstrated benefit to cancer patients, i.e. granulocyte-macrophage
colony stimulating factor.

Wound healing is a series of complex physicochemical interactions that require various micronutrients at every step. Multiple nutrients are necessary for optimal wound healing. They are also being added to conventional cancer therapies (chemo-, surgical, and radiation therapy) and recently became the “fourth arm” of cancer treatment. Clinical cancer often accompanies substrate deficiencies. These substrate deficiencies affect cell replication and stem cell activities (proliferation, differentiation, responses to growth hormone and growth factors, etc.). If supplemented
substrates are not adequate to overcome localized deficiencies at the wound site, completion of wound healing is unlikely and cancerization will never end. One study found that vitamin C treatment of patients with a variety of cancer resulted in 10% excellent responders versus 40% in patients treated with vitamin C plus other nutrients. Because deficiencies of individual nutrients at the wound site are not generally measurable, provision of whole cellular nutrients (WCN) to cover any potential deficiency is desirable. The WCN include GR factors, vitamins, minerals, nucleic acids, amino acids, fatty acids, glycosaminoglycans, carbohydrates, antioxidants, oxygen, etc. The risk, if WCN are supplied in known non-toxic concentrations, is minimal to none.

Spontaneous regressions of cancer, although rare, may be successful examples of wound healing treatments in cancer. Standard therapies aimed at killing cancer cells, such as surgery, should be limited to adjuvant status for limiting symptoms or buying time for completion of the wound healing process. Attempts to destroy cancer cells without healing underlying wounds will allow for eventual cancer recurrence. Since chemo- and radiation therapies kill both normal and cancer cells and cause new underlying wounds, they should be limited in cancer treatments.