a Cell goes Bad - How Cancer Starts
Weinberg’s book “One Renegade Cell” makes for fascinating reading.
Weinberg’s book emphasizes how many bizarre things must happen
for a cancer cell to be produced, implanted and eventually, silently, and
mysteriously grow to such proportions that it threatens the very existence
of its host. With this in mind, we will briefly explore the various
phases which neoplasms go through on their way to becoming a life
have I seen this summarized better than in John Boik’s remarkable book
“Natural Compounds in Cancer Therapy. (www.ompress.com)”
Within its 500 pages are thorough explanations of the molecular
biology of cancer, tumor immunology, and of course splendid research on
promising natural compounds (including their mechanisms of action).
Quoting directly from Mr. Boik’s book, we see how healthy cells
are supposed to act.
a healthy tissue containing thousands of cells.
Each cell serves the greater good, which is the continuation of a
person’s life. Each cell is
programmed so that when the cell is old or no longer needed, it dies a
peaceful and timely death. This
death is call apoptosis. All
cells are in communication, which allows for the smooth repair and
replacement of tissues and other aspects of cell behavior.
Communication takes place either indirectly, via exchange of
messenger compounds such as hormones and growth factors, or directly via
cell-to-cell contact. Contact
allows cells to respond to the “feel” of neighboring cells, via cell
adhesion molecules, and to exchange messenger molecules through
cell-to-cell portals called gap junctions.
With the help of proper communication, appropriate cells
proliferate when new cells are needed, and when enough new cells have been
produced, cell division stops.”
cells don’t act like the healthy cells described above.
Let’s discuss the pathogenesis of cancer.
The transformation of a normal cell into a neoplastic cell occurs
in response to one or more initiating factors.
The primary initiating factors appear to be chemical carcinogens,
viruses, and ionizing radiation. No
matter what the source of insult, the result is damaged DNA, leading to
mistakes when the cell divides with the eventual outcome of transformation
into a cancer cell (neoplasm). Actually
mistakes in DNA replication happen all the time and our cells are equipped
to handle this by either repairing the DNA, or by the cell committing a
programmed cell death (apoptosis). Therefore,
in order for the cell to become cancerous, it must escape these protective
In order for the individual cancer cell to propagate itself by
division, it must also overcome numerous obstacles.
Actually, cancer cells do die, and the only way for the individual
cells to become a tumor is for the rate of cell growth to overcome the
rate of cell death. It is
believed that the cancer cells achieve their growth through the initiation
of stem cells. Stem cells are
abundant in actively growing tissues, such as in tissue repair, but they
are controlled. In neoplasms,
the stem cells proliferate unchecked.
Also, in cancers, the daughter cells are not fully differentiated,
that is they do not exactly match the cell of origin.
For example a malignant liver cell is not exactly like a liver
cell; it is a mutant. Complementary
approaches to cancer treatment employ natural agents that stimulate
redifferentiation of the DNA.
Tumors could only reach a certain size before they would exhaust
themselves of nutrients if it were not for angiogenesis.
Simply put, this is the tumor’s ability to coax the body to
supply it with a vigorous blood supply.
The mechanism by which this happens is complex, and will be the
subject of an entire article in the near future.
A number of natural products interfere with angiogenesis and
prescription drugs are in development that target angiogenesis.
Invasion is one of the hallmark characteristics of a cancerous
tumor. Normally different types of tissues have very well defined borders
which is why you won’t normally find skin cells growing in deep muscle,
or liver cells growing in the stomach.
The amazing human body uses a myriad of mechanisms to maintain
order and boundaries, yet somehow cancerous tumors have the ability to
invade and pierce these protective barriers.
The biochemistry by which this happens is complex and in many
respects not well understood.
Metastases is another “hallmark” of cancerous tumors, and
involves the ability of the primary tumor to “seed” via the blood
stream or lymph system to distant sites where new colonies are
established. Metastasis is
actually not very efficient. In
fact in a study of patients with renal cell carcinoma, it was found that
their tumors released from ten million to one billion cancer cells into
the bloodstream every day, but only 20% developed distant tumors.
(Boik, “Cancer and Natural Medicine, 1996) .
of the mechanisms via which cancer cells grow and metastasize is leading
towards promising complementary approaches.
Every stage of development mentioned in this article can be
addressed via natural products and many by prescription drugs.
Genetics of Cancer
Cancer is fundamentally
genetic, in that it arises from mutations distorting the information
contained in genes. For the
most part, the genetic dysfunction is not inherited, but acquired during
life. In fact, probably less
than 10% of cancer patients have a strongly predisposing inheritance and
another 20 to 30% have a moderately predisposing inheritance (Ross,
“Introduction to Oncogenes and Molecular Cancer
All of this genetics
talk can become quite confusing, so we’ll try to keep it as simple as
possible. There is no doubt
that some cancers are strongly associated with a genetic
predisposition…and let’s reemphasize the word predisposition.
Along with the predisposition, there almost always has to be
subsequent events that damage the DNA of a cell for that cell to begin its
course towards malignancy. In fact the damage occurs with specific genes
that you will be hearing much more about: proto-oncogenes, and tumor
Perhaps the most
notorious inherited mutations are those of the genes BRCA1 and BRCA2.
Mutation at either site carries a 70% probability of breast or
ovarian cancer BUT, 95% of the time, breast cancer occurs without this
The press has recently
been buzzing with news of the human genome project.
Basically, scientists are mapping the approximately 50,000 genes
that are present in human DNA. About
100 of these genes are now known to be proto-oncogenes (Ross, 1998).
These genes are very important in the process of producing growth
factors that assure that cells grow and multiply especially during fetal
growth. Many of these
proto-oncogenes are normally “turned off” like a switch.
The turning on of genetic switches is referred to by scientists as
the “expression” or “over-expression” of the gene.
When proto-oncogenes are mutated they become oncogenes, and the
switch changes to the on position. Often
a whole series of these genes become activated into oncogenes (Dollinger,
“Everyone’s Guide to Cancer Therapy,” 1997).
If and when proto-oncogenes
misbehave, the damage is normally arrested by another type of gene, called
a tumor suppressor gene. Many have heard of the P53 gene.
This is a tumor suppressor gene.
So far about 20 tumor suppressor genes have been identified.
In the case of p53, we have a remarkable smart gene.
Somehow this gene detects when DNA has been damaged.
In this case, p53 slows down the cell cycle and allows the DNA to
repair itself. If that
doesn’t happen, the p53 gene instructs the cell to commit suicide
The dynamics of proto-oncogenes
and tumor suppressor genes usually create a regulated and controlled
environment of cell growth. In
the case of cancer, something, in fact many things have gone terribly
On a final note, it is
interesting to note that it appears that proto-oncogene defects are not
inherited. Damage to the
proto-oncogene occurs after birth. Conversely,
there is a genetic link to many tumor suppressor genes, such as p53.
Still, this defect alone does not cause cancer.
Further DNA “hits,” occurring throughout one’s lifetime are
required to permanently shut down the p53 gene.
Unraveling of the
genetics of cancer is paving the way for novel treatments such as gene
therapy. Even now, scientists
are finding that certain natural products such as the herb andrographis
paniculata may re-express the p53 gene when it is damaged.
IP-6 appears to have similar “reparative” effects.