ACS’s Michael J. Thun on Cancer: Progress, But a Long Way to Go
Science Watch Newsletter Interview: July/August 2010 (Page 3 of 3)
What’s the causal link between obesity and cancer risk? Is that understood?
Obesity affects cancer risk a few different ways. One is through direct chronic trauma. For example, reflux esophagitis, from acid and bile repeatedly bathing the lower esophagus, causes adenocarcinoma of the lower esophagus in a small percentage of people. Another example would be gallstones causing chronic inflammation and grinding inside the gall bladder, leading to gall bladder cancer.
"Per-capita cigarette sales in the U.S. have decreased by almost two-thirds since the Surgeon General’s Report on smoking in 1964. This represents the greatest public health achievement with respect to chronic disease in the last 60 years."
Other mechanisms are mediated by hormones. Adipose tissue is the main source of estrogens in postmenopausal women, and estrogens drive the promotion of breast cancer. Obesity and excess adiposity also increase circulating insulin-like growth factor, IGF, which promotes cancer growth, and it does it in two ways: one, it decreases the amount of the carrier protein around, making IGF more available to cells, and, two, it increases the synthesis of IGF. Adipose cells also release a lot of free radicals that cause oxidative, pro-inflammatory damage.
What should we expect to see in cancer trends in the future, and what should we be doing about it now that we’re not?
With the aging of the population, the number of incident cancers will roughly double from 2000 to 2050 in the U.S., assuming that incidence rates remain the same. In terms of limiting the number of people affected by cancer, interventions that would make the biggest difference would be to better implement what we already know about tobacco control, and to identify politically acceptable policy measures that could help people maintain a healthier body weight.
With tobacco control, we know that increasing the price of cigarettes is very effective at reducing consumption, particularly in kids and poor people. It’s politically doable, because only 20% of the population smokes. With obesity, where two-thirds of the population is overweight or obese, there may be much greater political resistance to taxes.
Then there’s the whole issue of what can be done to make physical activity more a part of people’s lives. That’s a complicated matter that has to do with how we design communities and the availability and requirement for walking in our daily lives.
In terms of treatment, one important advance that could soon come out of laboratory and clinical research would be methods to distinguish tumors that need aggressive treatment from those don’t. If we can provide better predictions of both prognosis and response to various therapies, it will allow us to implement much more effective therapies and to improve the clinical management of cancers—particularly prostate cancer and, to a lesser extent, breast cancer—where overtreatment is currently a significant problem.
There have been reports of breast cancer rates decreasing recently. How do you account for that? Is that because of public health messages or interventions?
Breast cancer rates have decreased in the past five years, and one key question is whether they will continue to go down. The news about hormone-replacement treatment and breast cancer really erupted with the Women’s Health Initiative back in 2002, and that led to a decrease in postmenopausal hormone treatment.
The rapid downturn is thought to reflect withdrawal of the late-stage promoting effect of hormones on breast tumors. But now mammography is also slipping, and it remains to be seen whether the decrease in breast cancer incidence continues. There’s also the question of how much of the decrease in breast cancer is real and how much is a function of less screening, and we don’t know the answer.
What’s the hardest message to communicate to the public in cancer epidemiology?
The hardest message to communicate invariably relates to prevention. Nobody makes money off it, and when it works, nothing happens. And it’s particularly hard because there are all kinds of obstacles in the way. In the case of tobacco addiction, for instance, the fact that kids start smoking before they realize they’re mortal makes them less susceptible to standard prevention messages.
At what age do kids realize they’re mortal?
It’s an incremental thing.
Selected Highly Cited Papers by Michael J. Thun and
Colleagues, Published Since 1998 (Ranked by citations) |
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Rank | Paper | Ciations |
1 | A. Jemal, et al., "Cancer statistics, 2007," CA – A Cancer J. for Clinicians, 57(1): 43-66, 2007. | 2,823 |
2 | A. Jemal, et al., "Cancer statistics, 2008," CA – A Cancer J. for Clinicians, 58(2): 71-96, 2008. | 2,800 |
3 | E.E. Calle, et al., "Overweight, obesity, and mortality from cancer in a prospectively studied cohort of US adults," New Engl. J. Med., 348(17): 1625-38, 2003. | 1,348 |
4 | C.A. Pope, et al., "Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution," JAMA, 287(9): 1132-41, 2002. | 1,286 |
5 | J. Stevens, et al., "The effect of age on the association between body-mass index and mortality," New Engl. J. Med., 338(1): 1-7, 1998. | 675 |
6 | M.J. Thun, et al., "Nonsteroidal anti-inflammatory drugs as anticancer agents: Mechanistic, pharmacologic, and clinical issues," J. Natl. Cancer Inst., 94(4): 252-66, 2002. | 520 |
SOURCE: Thomson Reuters Web of Science®. |
KEYWORDS: MICHAEL J. THUN, AMERICAN CANCER SOCIETY, ACS, CANCER, CANCER EPIDEMIOLOGY, CIGARETTES, TAR AND NICOTINE, OBESITY AND CANCER.
Citing URL: http://sciencewatch.com/inter/aut/2010/10-jul/10junThun/