Some of the most interesting – on a pharmacological level – medications I’ve encountered are cancer treatments.
Take Tamoxifen, for instance. This highly effective treatment for certain types of breast cancer works because it blocks the effects of estrogen in the breast. Since estrogen plays a role in getting cells in the breast to grow, this has significant anti-cancer effect.
Yet there is a downside. Tamoxifen acts like estrogen in the uterus, which increases risk of uterine cancer over time.
I love analyzing medications and that extends to cancer treatments. But it is a more challenging interest than for other treatments.
When I look at an asthma medication, things are simpler. Does it improve breathing? Does it reduce the need to go to the emergency room? Things get thorny when common medications have black box warnings, but still not too hard.
Cancer medications are challenging on many levels, intellectually, emotionally. You are confronted with statements like “those on medication X lived 6 months on average, while those on placebo lived 4 months on average.”
The best part is finding new treatments that offer hope. Even then I am weighed down by knowledge (or, more accurately, lack of knowledge) and the challenge of grappling with exceptionally complicated information.
Take the aromatase inhibitors. Some studies say that they are a better treatment in post-menopausal woman than tamoxifen for preventing breast cancer from coming back.
The aromatase inhibitors were so much better that a study I look at was actually stopped to give participants the opportunity to switch to them.
That’s wonderful, right?
Yes. That said, one study I looked at showed superiority of the aromatase inhibitors in preventing breast cancer recurrence but showed an increased rate of other cancers.
Let me end this post with some thoughts on where cancer treatments are going.
Future Cancer Therapies
The goal of future cancer treatments is to find the molecular pathways that are deregulated in cancers and target them alone. Think doing a targeted missile strike on a house instead of carpet bombing a city.
The limitations to targeted treatments include the sheer complexity of cancers. You can knock out one pathway that leads to cancer formation only to have the tumor adopt another approach. Cancer doesn’t form when just one thing goes wrong, rather it happens when many things go wrong at once.
Resistance often arises. Cancerous cells are full of nasty tricks, like developing pumps that get rid of the medications you throw at them called Multiple Drug Resistance pumps.
New cancer treatments for the past few years have tended to fall into two categories. There are the tyrosine kinase inhibitors which are almost all named something that ends in “nib” (Lapatinib, Gefitinib, and Sunitinib). Then there are the monoclonal antibodies that have extreme specificity to some molecular target.
The tyrosine kinase inhibitors try to stop specific pathways associated with the development of cancer. Tyrosine kinases are a fairly large family of receptors and play a very large role in the regulation of cell growth. Their efficacy can range from phenomenal, Gleevec, to disappointing, Gefitinib.
The monoclonal antibodies have a variety of targets but all try to knock out some key aspect involved in the cancer. Herceptin, for instance, binds to HER2 receptors that are highly overexpressed in a significant percentage of breast cancers. Avastin binds to VEGF, a messenger that tells blood cells to grow, feeding the cancer.
There are additional areas being investigated. While unlikely to be used for at least several years, PARP inhibitors may play a role in treatment of breast cancer by increasing cells susceptibility to traditional chemotherapy.
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