Archive for February, 2013
22 February 2013
A new generation of anti-caner therapies are truly marvels of science and engineering, with a hefty price tag.
As reported today by the New York Times, a new anti-breast cancer drug was approved today by the United States FDA. T-DM1 (Kadcyla) is a monoclonal antibody (Herceptin) attached to a toxic payload of mertansine (DM-1).
I could go on for a long time about the technological achievements that have gone into creating monoclonal antibody-based drugs, such as the 1984 Nobel Prize in Medicine, but the bottom line is that, in general, monoclonal antibody-based drugs:
Pro: Highly specific (i.e. it’s possible to have few side effects if the target and patients are chosen wisely)
Con: Must be administered intravenously, must be stored and transported with extreme care, and are extremely EXPENSIVE
The NY Times reports:
“Genentech, which developed the drug, said it would cost about $9,800 a month, or $94,000 for a typical course of treatment. That is about twice the price of Herceptin itself, which is also made by Genentech, but it is similar to the price of some other new cancer drugs. It is approved for patients with HER2-positive breast cancer, about 20 percent of cases.”
There are many more monoclonal antibody-based cancer therapies in the works. In May the NY Times reported that:
“About 25 such drugs from a variety of companies are in clinical trials, according to Alain Beck, a French pharmaceutical researcher who closely tracks the field. Genentech alone has eight in clinical trials besides T-DM1, and another 17 in earlier stages of development.”
The good news is that technological advances like these are slowly making cancer treatable, but I can’t help but wonder if the high price tag of these therapies will put them out of reach for all but society’s wealthiest.
Imagine the dilemma of a family faced with living with crippling disease or crippling debt. I will spare you my diatribe about our for-profit health system and the ethics of profiting off of society’s most sick and disenfranchised. But, this is a discussion that EVERYONE should be having now. Because, sooner or later, most of us WILL have to face this dilemma, either individually or within our families.
Wouldn’t it be nice if we could prevent more cancer in the first place? It’s something I spend a lot of time thinking about…
Ok, back to the research bench. Have a nice weekend! (hopefully with exercise and sunscreen!)
21 February 2013
My Cancer for Dummies blog turned two years old. How time flies!
Cancer for Dummies started as an experiment in science communication for public education. My readers have consistently challenged me to challenge my own ideas and concepts, and lo and behold it is I who have also become more educated in the process as well!
I’ve averaged three articles per month (75 to date), and look forward to many more. Though as of late I’ve also branched out and started writing more about original research and emerging ideas and paradigms in cancer research, I still enjoy the “dumb” questions sent in by curious minds.
If you haven’t already, please “like” the Cancer for Dummies facebook page, and if you feel so inclined, please “share” it as well.
Thanks for reading!
15 February 2013
Original Research Commentary
It’s been anecdotally said that when it comes to fighting cancer, attitude affects outcome. The other day I became aware of a randomly controlled clinical trial (hard science golden standard) that tested this hypothesis.
Lead by Barbara Andersen, a group of 227 breast cancer patients were treated with standard therapy (surgery, chemotherapy) until their disease was in remission, then split into two groups: a control group and an intervention group.
“The intervention was conducted in groups of 8 to 12 patients with two clinical psychologist leaders. It included relaxation training, positive ways to cope with stress and cancer-related difficulties (e.g., fatigue), methods to maximize social support, and strategies for improving health behaviors (diet, exercise) and adherence to cancer treatments. A total of 26 sessions (39 therapy hours) were delivered over 12 months.”
The patients were were then followed for 11 years, and monitored to see how often their cancer came back. The intervention group had statistically better outcomes; the patients receiving stress management therapy (whose cancer came back) lived an average of six months longer, and at time of publication, 15% more patients in the intervention group remained in remission and disease free, compared to the control group that did not receive the psychological support.
Follow-up articles have implicated the role of stress hormones in promoting cancer growth, further establishing causation to the stress-cancer connection.
The take away message is this: there IS a psychological component that influences cancer patient outcomes, shown here with hard science.
8 February 2013
Ok ok, So Jared Diamond did not produce a book about cancer (though I think it would most certainly be interesting). But in a recent NY Times commentary he brings up an interesting point about small, repetitive risks we take:
“Studies have compared Americans’ perceived ranking of dangers with the rankings of real dangers, measured either by actual accident figures or by estimated numbers of averted accidents. It turns out that we exaggerate the risks of events that are beyond our control, that cause many deaths at once or that kill in spectacular ways — crazy gunmen, terrorists, plane crashes, nuclear radiation, genetically modified crops. At the same time, we underestimate the risks of events that we can control (“That would never happen to me — I’m careful”) and of events that kill just one person in a mundane way.”
(See the full article)
In many ways this parallels cancer risk; some things are indeed completely out of our control (for the time being with current science and technology) and these days most cancer “awareness” in my opinion simply plucks the tune of fear with the visceral chords of mortality and comes short of real education about cancer risk. Instead, many people are left with lingering anxiety and fear about the big, bad “C” and pin their hopes on researchers like myself to save them when the Emperor Of All Maladies comes knocking at the door.
I have previously described cancer risk as a bit like an umbrella (and apparently the National Cancer Institute has recently as well, see image):
“Can an umbrella save your life? Maybe. If you go out into the rain, you get wet. Get wet or stay wet often enough, and you’ll get sick. An umbrella won’t stop you from getting wet, but it will prevent you from getting too wet. And maybe it will keep you from getting so wet that you catch a chill and get sick. Cancer risk is a little like rain. It’s all around us, and it’s nearly impossible to be a living, breathing human being without getting wet from the rain from time to time. But, there are choices you can make and things you can do to create your umbrella against cancer. It cannot prevent you from ever getting cancer, just like an umbrella can’t prevent you from getting wet. But both can lessen your risk of getting sick, and leave you in a much healthier and happier state of being.”
Cancer prevention has been a previous topic in my blog, and aside from abstaining from smoking, too much UV exposure, radon exposure, HPV, Hepatitis, obesity, or untreated stomach ulcers, the one thing that I have seen convincing evidence in positively preventing cancer is habitual aerobic exercise.
But, tanning salons are still as popular as ever, and many young people in the US still take up smoking every year, despite monumentally better awareness of the lung cancer connection. Obesity is a tantalizingly complex personal and political issue, but the same concept applies: we all make many, many small decisions on a daily basis that affect our health. Cancer risk is just one of them. Embrace the sunscreen! Take the stairs instead of the elevator. Start cycling to work. Avoid the sweets. Salads make great lunches too. Avoid second hand smoke (or find a way to quit if you’re a smoker!). Develop a dialogue with your doctor about cancer prevention. Help your friends and family do the aforementioned as well!
We must be conscious of the effects of the little decisions we make every day as part of our individual, personal roadmap to living longer and happier. Understanding and mitigating these small risks can add up to big prevention. And maybe more healthy years for you, dear reader! In the meantime, feel free to send me your cancer prevention queries!
A seldom-mentioned caveat biasing a great deal of cancer research? Tumor heterogeneity in mouse models of cancer?
5 February 2013
I’ve been writing often on the topic of tumor heterogeneity as of late, and today I became curious about the level of tumor heterogeneity in mouse models of human cancer vs. the amount seen in the clinic, and how this seldom-mentioned caveat might have biased a huge amount of cancer research and therapy development to date.
This morning a labmate presented a really neat, compact paper from Cancer Research in Journal Club: “Synthetic Lethal Interaction of Combined BCL-XL
and MEK Inhibition Promotes Tumor Regressions in KRAS Mutant Cancer Models” by Cororan et al. our of Massachusetts General Hospital Cancer Center. Journal Club is an activity we do once a week where scientists and clinicians from all over the Moores Cancer Center get together and go over a recently published original research paper. We discuss the techniques, the data, the implications, and how we can best apply this to our own research and treating cancer on a weekly basis over coffee and bagels. It’s one of my favorite times of the week.
Anyway, this morning the above paper was presented, which illustrates a very elegant model for combining two different drugs to target cancers driven by KRAS mutations, like many pancreatic and colorectal cancers. In a nutshell, one drug targets the fast growth of the cells, another takes the lock off the cancer cells’ self destruct switch.
Dr. Stupack pointed out a caveat of the study, in which cell lines isolated from tumors have likely undergone artificial selection to enhance these anti-cell-suicide traits; a type of selection that might not necessarily reflect that which occurs in patients, and may bias the cancer cells used in the model to be homogenous in a way that would promote response to the authors’ hypothesis. Not good.
However, the authors of the paper did complement their studies with a spontaneous model of pancreatic cancer driven by KRAS, which was argued to not be subject to the same caveats. Perhaps the cancer cells developed by the mice are not going to be selected for in the same capacity as human cells in artificial culturing conditions for years on end, but the course of the disease model itself is less than a year, which is not likely to have the time to develop the same heterogeneity as, say, a human cancer that takes decades to develop and undergoes many, many more rounds of cell division and selection for diverse pockets of meaner, hardier, of cancer cells.
In short, how could one engineer a mouse model of cancer to better reflect human cancers in terms of genetic heterogeneity? Mice only live about two years, and experimental cancer studies lasting decades are impractical on many fronts. Is there some way to engineer enhanced tumor heterogeneity into existing mouse models of human cancer?
Again, I will leave this article with an open question for researchers and collaborating curious minds (like yourself, dear reader!). I offer it as another short glimpse into my stream of thoughts on enhancing targeted cancer therapies.