Just as a corporation depends on individuals to staff
its various departments, the body depends on its basic units of function, the
cells. Cells band together as tissues,
such as muscle tissue, to perform a prescribed function. Tissues in turn joint to form organs, such as
the heart, and organs are assembled into the body’s several organ system, such
as the cardiovascular system. Such is
the “corporate structure” of the body.
If individual and cells are the basic units of
function for their respective organizations, the failure of either to perform
in a prescribed, dependable manner can erode the overall organization to the
extent that it might not be able to continue.
Cancer, the second leading cause of death among adults, is a condition
reflecting cell dysfunction in its most extreme form. In cancer, the normal behavior of cells
ceases.
Cell
Regulation
Most of the body’s tissue lose cells over time. This continual loss requires that replacement
cells come from areas of young and less specialized cells. The process of specialization required to
turn the less specialized cells into mature cells is controlled by genes within
the cells. On becoming specialized,
these newest cells copy, or replicate, themselves. These two processes are carefully monitored
by the cells’ regulatory genes. Failure
to regulate specialization and replication results in abnormal, or potentially
cancerous, cells.
In addition to genes that regulate specialization and
replication, cells also have genes designed to repair mistakes in the copying
of genetic material (the basis of replication) and genes to suppress the growth
of abnormal cells should it occur. Thus,
repair genes and tumor suppressor genes, such as the p53 gene (altered or
missing in half of all cancers), can be also be considered regulatory genes in
place to prevent the development of abnormal cells. Should these genes fail to function properly,
resulting in the development of malignant (cancerous) cells, the immune system
will ideally recognize their presence and remove them before a clinical case of
cancer can develop.
Because specialization, replication, repair, and
suppressor genes can become cancer-causing genes, or oncogenes, when not
working properly, these four types of genes could also be referred to as
proto-oncogenes, or potential oncogenes.
How proto-oncogenes become oncogenes is a question that cannot be
completely answered at this time.
Regardless, abnormal cells produce abnormal proteins, and the absence of
normal proteins alters the body’s ability to function approximately, from the molecular
to the organ system level.
Oncogene
Formation
Recognizing that all cell have proto-oncogenes, what
events alter otherwise normal regulatory genes so that they become
cancer-causing genes? Three mechanisms,
genetic mutations, viral infections, and carcinogens, have received much
attention.
Genetic mutations develop when dividing cells miscopy
genetic information. If the gene that is
miscopied is a gene that controls specializations, replication, repair, or
tumor suppression (a proto-oncogene), the oncogene that results will allow the
formation of cancerous cells. A variety
of factors, and radiation, are associated with the miscopying of the complex
genetic information that comprises the genes found within the cells, including
those intended to prevent cancer.
In both animals and humans, cancer-producing viruses,
such as the feline leukemia virus in cats and the human immunodeficiency virus
(HIV) and multiple forms of the human papilloma virus (HPV) in humans have been
identified. These viruses seek out cells
of a particular type, such as cells of the immune system, or the lining of the
cervix, and substitute some of their genetic material for some of the cells’
thus converting them into virus-producing cells. In so doing, however, they change the makeup
of the specialization, replication, repair, or suppressors genes, converting
the proto-oncogenes into oncogenes. Once
converted into oncogenes, the altered genes are passed on through cell
division.
A third possible explanation for the conversion of
proto-oncogenes into oncogenes involves the presence of environmental agents
known as carcinogens. Over an extended period, carcinogens, such as
chemicals found in tobacco smoke, polluted air and water, toxic wastes, and
even high-fat foods, may convert proto-oncogenes into oncogenes. These carcinogens may work alone or in
combination with co-carcinogenic promoters to alter the genetic material,
including regulatory genes, within cells.
Thus people might develop lung cancer only if they are exposed to the
right combination of carcinogens over an extended period.
You may already see that some of the specific risk
factors in each area such as radiation in the development of mutations,
sexually transmitted viruses in cancers of the reproductive tract, and smoking
introduced carcinogens in the development of lung cancer – can be moderated by
adopting health-promoting behaviors.
In light of the complexity of cancer, some in the
scientific community believe that cancer never be truly prevented. Rather, they feel that the ability to stop
and then reverse cancerous changes at an early stage of their development is
more likely than prevention of this complex disease process. However, this text will address the concepts
of prevention in the belief that prevention based practices reflect our
personal contribution to the “war on cancer.”
The Cancerous
Cell
Compared with noncancerous cells, cancer cells
function in similar and dissimilar ways.
It is the dissimilar aspects that often make them unpredictable and
difficult to manage.
Perhaps the most unusual aspect of cancerous cells is
their infinite life expectancy.
Specifically, it appears that cancerous cells can produce an enzyme, telomerase, that blocks the cellular biological clock that informs normal
cells that it is time to die. In spite
of this ability to live forever, cancer cells do not necessarily divide more
quickly than normal cells. In fact, they
can divide at the same rate or even on occasion at a slower rate.
In addition, cancerous cells do not possess the contact inhibition (a mechanism that
influences the number of cells that can occupy a particular space at a
particular time) of normal cells. In the
absence of this property, cancer cells accumulate, altering the functional
capacity of the tissue or organ they occupy.
Further, the absence of cellular
cohesiveness (a property seen in
normal cells that “keeps them at home”) allows cancer cells to spread through
the circulatory or lymphatic system to distant points via metastasis. Interestingly, once migrating cancer cells
arrive at a new area of the body, the “rediscover” their cellular cohesive
capabilities. A final unique
characteristic of cancerous cells in their ability to command the circulatory
system to send them additional blood supply to meet their metabolic needs and
to provide additional routes for metastasis.
This angiogenesis capability of cancer cells makes them
extremely hardy compared with noncancerous cells.
Benign Tumors
Noncancerous,
or benign, tumors can also form in the body.
These tumors are usually enclosed by a membrane and do not spread from
their point of origin. Benign tumors can
be dangerous when they crowd out normal tissue within a confined space.
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