p53 gene

http://apbrwww5.apsu.edu/thompsonj/Anatomy%20&%20Physiology/2010/2010%20Exam%20Reviews/Exam%201%20Review/03-30_CellCycle.JPG

My company reassures me that the continuing education credits I complete with them is sufficient for the continuing ed requirements to renew my license.  For reasons that would just stress me out to rehash online I don't believe them, not for a slight second.  So I'm pursuing continuing ed credits through some Illinois Edition Elite Continuing Education magazine that came to my house, presumably via the ANA, and it is, by far, the most annoying magazine in the world.  It has typos. Actually, that's being generous.  It has entire sentences that are illogically constructed, however, if one can set aside those few annoyances, it actually has some interesting information.

The first section of study was about cancer, and in it, it talks about the p53 gene.

To understand why the p53 gene is important, you have to understand that each somatic cell in the human body is designed to grow when exposed to certain commands.  Inversely, the cell is commanded not to grow under certain commands.  These commands come in the form of stimuli: proper amounts of nutrients and energy to grow more cell membrane, to increase cytoplasm, etc.

Another important signal is the proximity of one cell to another.  In other words, if a cell has the proper amount of nutrients and energy, it will want to grow, but if the edges of one cell are being touched by other cells, the cell will be prohibited from duplicating.  But, if there aren't other cells touching that one cell, like in the case of a cut, the cells that aren't touching each other (like the cells on the edges of the cut) will be compelled to grow.

The gene that maintains the integrity of those checks is p53, and these checks by p53 occur in the G1 phase (the beginning of cell replication).

This means:

• if p53 is correctly functioning, potentially abnormal cells will be appropriately suppressed.
• if p53 is not correctly functioning, injured, or damaged, potentially abnormal cells will not be appropriately suppressed.
• if p53 is mutated, the cell carrying the mutation will copy itself regardless of the presence of growth promoting stimuli.
• if p53 is damaged, it causes that cell carrying the damaged gene to proliferate ineffective, deformed, mutated daughter cells that divide rapidly and without control, resulting in an irreversible growth--a tumor.

And here's the real kicker: Scientists have discovered that cigarette smoke is the most contributing factor inducing mutation of the p53 gene.  This is why it is never too late to quit smoking.  Even if the patient already has cancer, quitting smoking will prevent the formation of additional mutated cells, which will, in turn, prevent additional tumors.


References:

• CDC: Smoking and tobacco use (2004). Retrieved online February 22, 2008 at http://www.cancerhelp.org.uk/help/default.asp?page=119 
• Ko, A., Dollinger, M., & Rosenbaum, E. (2002). Everyone's guid to cancer therapy. (5th ed) Andrews McMeel: Kansas City.
• National Cancer Institute.  Screening Mammogram: Questions and Answers.  Retrieved online March 15, 2008 at http://www.nci.nih.go/cancertopics/factsheet/Detection/screening-mammograms.
• Sacher, R. & McPherson, R. (2000).  Widwams clinical interpretation of laboratory tests.  F.A. Davis: Philadelphia.