How Cancer Buffaloes its Host
Growing a cancer is a multi-step process. For a cancerous growth to occur, a previously
normal, healthy gene is transformed into something that no longer recognizes normal growth
constraints. At the point that unbridled growth occurs, whether in flesh, bone, or blood, it is called a tumor.
Once growth eludes constraint, there yet
remains the question of whether, and to what extent, a tumor
will spread. Metastasis is far from uniform.
When a tumor is content to proliferate in one place, without spreading, it is known as benign. Those that metastasize are of course malignant.
But for metastasis to occur, the tumor does not act alone. It requires cooperation
from its host, the cancer-bearer. Although this seems unnatural—why in nature would a body help a cancer to spread?, and all living creatures contain internal defenses against such aberrations as cancer or the species would not have survived— sometimes the requested cooperation is achieved, and the tumor, well-fed by the host's own nutrients and provided by host with a highway, commences exploration.
If you are wondering why certain creatures are betrayed by their own body's collusion with a tumor, read on. I will explain this process as best I can.
While it is true that some external event—chemical, physical, or viral—can instigate from without carcinogenic growth, still the growth occurs initially in one cell within the host, and sometimes occurs in the absence of tangible external persuasion. One cell, previously operating in effect by the rules, suddenly ignores restraint. It proliferates. As it grows, it may influence surrounding cells likewise to abandon their restraints.
Although people speak of getting cancer, as though it is visited upon them, actually cancer is a part of its own host gone awry.
Tumor growth is distinct from tumor spread. Unchecked physical growth is the primary difference between normal cells and malignant cancer cells. A benign tumor, however, can still be life-threatening or even fatal, if it happens to grow in a place, such as areas in the brain, from which it interferes and is difficult or impossible to remove. Physical spread, however, distinguishes malignant from benign.
As the cancer grows and if it is to spread, it must not only resist the defenses of its host but also, at certain points, enlist the aid of its host. This assistance is both passive and active.
Passively, the host provides transport systems—the blood and lymph vessels—for transport of metastatic cancer cells. Before transport, these cells must escape the confines of the tumor. Once free, tumor cells work their way to nearby vessels for transport.
But it is in its recruitment of active host assistance that the process of cancer appears almost malevolently ordained.
For growth to continue, the cancer must be fed. The host complies. The tumor, like newly laid fat cells, is vascularized— supplied with nutrient-providing blood vessels—by the body. Without nutrients supplied by its host a fledgling tumor colony would languish.
Both plant and animal cells contain genes that influence development in themselves, as well as in their neighbors. The genes provide structural and chemical cues for cell growth and differentiation.
Cues can take the form of hormones, growth factorsA naturally occurring protein or chemical that stimulates cells to grow and differentiate. , and structures that influence growth of neighboring as well as distant cells. These cues provide the architecture, for example, for embryonic neuronal development in the central nervous system. The process is not random. Certain cells contain genes that seem to have greater influence. This influence can be normal or abnormal.
One gene considered a potent influencer of abnormal development is the oncogeneA gene that causes a previously normal cell to become cancerous. ; as genes govern normal development, oncogenes instruct aberration.
Oncogenes can be native to the host or introduced by viruses in viral genomesThe entire DNA sequence of any organism. Recall the human-genome project. . One such gene functions as a growth factor in normal healing after abrasion.
Growth and division in normal cells is limited by control mechanisms, one of which is contact inhibition.When cells of a developing tissue fill their space and their surfaces touch, reproduction decreases and genes that induce cell division stop doing so.
In cancer cells, contact inhibition is broken. Unchecked cell reproduction forms a mass of tumor within normal tissue, a zone where growth continues unabated. Tumor cells may divide indefinitely and will do so in culture dishes, subject only to nutritional requirements. Cancer cells may even evade the dictates of normal aging.
As of the end of the 20th century, cancer metastasis was thought to be a two-part process commencing within the genes of a single cell. The stage is set when genes with essential roles in control of cell growth and development become oncogenes. When they contain such abnormalities as these, they have developed into oncogenes:
Chromosome translocation—When chromosomes are broken and rejoined erratically, oncogenes may occur in the new joint region, separated from their normal control regions.
Gene amplification—Multiple copies of a normally single gene may occur within a cell.
Gene transposition—An oncogene or a regulatory gene may be located eccentrically.
Mutation—Oncogenes may contain altered nucleotide sequences and thus produce proteins more active or less resistant to degradation than normal.
Oncogenes with such abnormalities are no longer subject to customary controls; they are sensitized, ready to be triggered. Triggering occurs when the DNA within them is mutated. DNA mutation may be caused by physical agents such as x-rays, chemical factors such as carcinogens, transcription by virus, or something as yet unnamed within the gene itself.
Of course, all mutations do not cause cancer. Current belief holds that cancer begins when something activates the primed oncogene.
Cells that multiply excessively but do not spread to other locations are considered benign tumors. Malignant tumors, however, contain differences other than simply the yen to move. They may have abnormal numbers of chromosomes, deranged metabolic processes, or unusual cell surfaces, some of which may have preceded their induction into malignancy.
For while normal cell surfaces facilitate cohesion with like cells, which orchestrates containment, the cell surfaces of cancerous cells encourage their spread in the body. Their migration occurs in blood and lymph vessels and in organ parenchyma. Surfaces of cancer cells may also differ from normal cell surfaces by receptor type.
Another apparently invariable difference between benign and malignant tumors lies in the capsule that contains them. Benign tumors lie in unbroken basement membrane while malignant tumors inhabit capsules containing sieve-like defective zones. Substantial loss of basement membrane around a tumor correlates significantly with increased metastasis, or spread, and poor ultimate survival rates in certain forms of cancer.
How does the cancer spread?
