Wednesday, November 15, 2017

CANCER: A PROBLEM OF CELL REGULATION

a problem of cell regulation
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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