Gene Therapy for Cancer Treatment - Biotechnology and Your Health: Pharmaceutical Applications - page 102

Cancer: Done in by Genes
Cancer cells of all kinds share the capacity to increase in number, free of the normal
controls on cell division. They also have the ability to survive for very long periods of
time. Normal cells generally divide and increase in number only when the body tells
them to do so through chemical signals. Cancer cells have acquired the ability to divide
without outside signals, as long as they have proper nutrition. The cancer cells get this
capacity for growth from genetic changes. Two different types of genes are changed in
cancer: oncogenes and tumor suppressor genes.
Oncogenes are mutated forms of protooncogenes—normal genes that stimulate cell
division. Studies of how certain animal RNA viruses caused cancers in animals led to
the discovery of oncogenes and protooncogenes. Scientists suspect that the viruses
picked up the oncogene sequences during their evolution. There are many different
protooncogenes. They either code for proteins that are part of the cell's internal machinery
for cell division (Figure 7.3), code for proteins that are part of the machinery that a cell
uses to respond to an outside growth signal, or code for proteins that normally prevent
the cell from dying. The mutated forms may allow the cell to survive and divide repeat-
edly, even in the absence of the growth protein. A single copy of a mutated oncogene is
enough to give rise to cancer.
Tumor suppressor genes normally function as gatekeepers to prevent cell division
when the cell's DNA is damaged or when conditions are not right—for example, when
there is a shortage of nutrients or when a protein signal required for cell division is
missing. Mutated tumor suppressor genes allow cells with damaged DNA to survive
and go through many cycles of cell division, thus increasing the chances that a mutated
cell that cannot properly control cell division will survive and increase in number. The
changes found in the genetic material of cancer cells may be very extensive. Both copies
of a tumor suppressor gene must be mutated in order to allow cells with such changes
to survive.
Because they are mutations that add properties to a cell, oncogenes may be seen
as more difficult to correct, or turn off, through gene therapy approaches. Because they
represent a loss of function, mutations in tumor suppressor genes would appear to be
easier to correct through gene therapy techniques that put the normal gene back where
it belongs.