Fighting Cancer at the Genetic Level
I have often written about the future of cancer research and cancer treatment increasingly being genetically-based. One of the earliest targeted therapies for cancer, and the very earliest for breast cancer, was tamoxifen, a drug that is very commonly used today. Most of the newest targeted breast cancer drugs are helpful for women who have her2 positive cancers. That over-producing her2 gene becomes a target that scientists can explore.
This is a very nice article from Cure Today about development of targeted/genetic therapies. It is quite brief and easily understandable; I know that I sometimes and enjoy and share journal articles about this topic, but they are much harder to comprehend (at least for me).
Here is the start and a link to read more:
Future Frontier: Fighting Cancer at the Genetic Level
BY LAURA BEIL
Rita Doerner was stunned earlier this year when doctors told her she had stage 2
breast cancer. The 77-year-old from St. Louis did not have any symptoms.
Although her sister died from ovarian cancer, Doerner did not think she had any
particular risk. She figured genetics were on her side. “When they told me I had
cancer, I didn’t believe it,” she says. In addition to standard hormone therapy,
Doerner has tried a new investigational drug—one that is not specifically geared
to treat breast cancer. Rather, it targets cancers with a mutation in a gene called
PIK3CA—which Doerner has. Because the mutation developed in her tumor and
was not inherited or present in her normal cells, it created an opportunity to
intervene with a treatment that is quite specific.
The human genome is the instruction manual for assembling all the molecules
that keep cells alive. It’s a biochemical code, and sometimes the coding ends up
with its own bad autocorrect. Often these glitches don’t matter, but sometimes,
like writing “one” when you mean “none,” a slight change makes a big difference.
A malformed molecule comes off the factory line, and like paper airplanes, the
proteins of life won’t work if they’re not folded just right. When a cell collects too
many misshapen molecules from bad instructions, the normal checks and
balances on growth can go offline. These errors manifest in two main ways. In one
instance, certain genes, called oncogenes, get switched on and can lead to cancer
growth. In another situation, genes, called tumor suppressor genes, are switched
off. Either way, these errors can be inherited or develop in the body over time.
This is why cancer is ultimately a genetic disease, and why, in Doerner’s case,
genetics were not on her side.