Barbara Brenner, Former Executive Director
Note: Abstract numbers listed here are available for viewing online at www.sabcs.org.
Today this Symposium started in earnest. Actually, I had physical evidence last night that the real thing was about to start, when I got back to my hotel room to find a plastic bag attached to my door knob. The text on the bag said it contained “important announcements for meeting attendees.” Turned out that in that bag were no fewer than 13 different (and expensive to produce) drug company promotions. Pharma is very present, as always, at this meeting.
Causes and Prevention: the epi perspective at San Antonio
It was intriguing to see that the title of the first plenary presentation at this meeting was “an epidemiological perspective on the causes and prevention of breast cancer.” Since I’ve been coming to this meeting for years, I didn’t hold high hopes for hearing about environmental toxins or radiation, and I wasn’t disappointed; neither was mentioned.
Dr. Valerie Beral focused her presentation on the protective effects of childbearing, breast feeding and, to some degree on the risks posed by HT, obesity and alcohol use.
So there was nothing new in terms of what might be contributing to breast cancer incidence in this talk. There was, however, and interesting approach to presenting the information. Dr. Beral based her talk on the difference in breast cancer incidence between the industrialized world and rural, developing areas. She noted that there is a 6 to 7 fold difference in incidence between developed and developing countries. It was interesting to get this perspective coming off of my trip to India.
Beral’s view is that reproductive factors account for these differences. She referred to and agreed with the early 20th century view that breast cancer was the result of “not using breasts for their natural purposes” of reproduction and breast feeding.
Beral also noted that not all hormonal factors that she sees as important operate in the same way. For example, despite the thought that breast cancer takes years to develop, both oral contraceptives and hormone therapy (with or without progestin) cause transient increases in breast cancer risk that rapidly disappear when the drugs stopped being used.
Discussing other other modifiable factors, Beral pointed out that there were issues of nutrition, but not diet. She referred specifically to obesity and alcohol use, stating that there would be 40,000 fewer cases of breast cancer in the US if no woman was obese or drank alcohol or used HT. That’s a 20% reduction in incidence in the US. Beral noted that this doesn’t mean there would be no breast cancer, since some breast cancer is just “bad luck.” She failed to say anything about the use of science to try to illuminate the facts behind “bad luck.”
One statement that Beral made that wasn’t explained by her or by her information on reproductive factors and life-style factors was that the incidence of breast cancer is rising rapidly in urban areas of developing countries. That phenomenon is almost certainly not the result of changes in birth or breast-feeding patterns since the migration to urban areas in developing countries is happening faster than reproductive patterns are presumably changing.
And there was a lot missing from Beral’s presentation. There was no discussion of the increase in breast cancer in industrialized countries that results from breast cancer screening, despite the current brouhaha about this topic in the US. There was no mention of medical radiation exposures in developed countries. And there was no mention of the hormone-mimicking substances in the food of developed countries or the body care products in use. (On this topic, see a letter to the Journal of Clinical Oncology from Adrienne Olson and others titled “Breast Cancer Patients Unknowingly Dosing Themselves with Estrogen By Using Topical Mosturizers,” Vol 27, Number 26, 9/10/2009, e103-104.)
And, while Beral acknowledged that it would not be good social policy to encourage women in the developed world to have many offspring, or to start having babies in the teen years to reduce the incidence of breast cancer, she did endorse the development of a “vaccine” that would provide short term exposure in early adulthood to the hormones of late pregnancy and lactation, providing what she called “lifelong protection against breast cancer.” There was no mention of what risk this sort of vaccine might impose over the long term.
While it didn’t redeem her proposal for preventing breast cancer in my eyes, Dr Beral ended her talk with gratitude to the US for electing Barack Obama as its President.
Exemestane (Aromasin) Updates: The AI Drum Beat Goes On
In several presentations this morning, we heard the good news about exemestane studies in the adjuvant setting. Exemestane is a Pfizer drug, and the first two presentations discussed below were funded by the company.
Daniel Rea presented (Abstract 11) information on the TEAM trial, a prospective, randomized Phase III trial comparing 5 years of exemestane to tamoxifen followed by exemestane for a total of 5 years in post-menopausal hormone positive women. There was no difference in disease free survival (DFS), overall survival (OS), or time to recurrence (TTR) between the two groups at a median of 5.5 years of follow up. While there were fewer uterine effects with exemestane, there was more hypertension with exemestane, as well as more osteoporosis. Rea concluded that either exemestane alone, or tamoxifen followed by exemestane would be appropriate.
Sounds to me like recommending a change in practice based on a single trial.
The presentation of Abstract 12 by Judith Bliss looked at the updated information from the Intergroup exemestane study in which all patients were given tamoxifen, and half were randomly switched to exemestane. She noted that exemestane modestly improves overall survival, and improves disease free survival compared to tamoxifen alone. She focused on breast cancer-free survival as a way of looking at the treatment of effect of exemestane, and showed that exemestane extends breast cancer-free survival by 4% over tamoxifen after 8 years of follow up.
Bliss also noted that, where distant recurrences occurred in the patients in the trial, they were more often to bone with exemestane, for reasons that are unclear. There was also a lower incidence of second primary cancers with exemestane, which may be related to increasing age of patients at randomization. Her conclusion was that switching patients to exemestane improves outcomes as far out as 9 years.
The studies on switching patients from tamoxifen to an AI all seem to be pointing in the same direction, so these two presentations were not surprising.
More interesting was the presentation of Abstract 14 looking at the question of whether having worse symptoms from an AI predicts better outcomes with the drug, as suggested by a study release earlier this year. The conclusion of Vared Stearns in presenting this study was that the answer is no. She concluded that doctors should not use emerging symptoms as basis for recommendations regarding continuing treatment or switching
The final presentation on AI’s that I heard today was about how to adjust for cross-over that occurred in the letrozole (Femara) v. tamoxifen trial, BIG 1-98. (Abstract 15.)
Meredith Reagan explained that selective cross-over, in which patients in the control arm are given the opportunity to take the treatment being tested, disturbs randomization and the conclusions that can be drawn from the trial.
She argued for the use of inverse probability of censoring weighted analysis (IPCW) to adjust results to get the best adjustment to control for cross-over. Using this approach still shows a statistically significant advantage for letrozole over 5 years.
Heard in the Halls
Needless to say, there’s a lot that goes on at meetings like this that isn’t about the presentations, since so much goes on in the breast cancer field.
Today, I heard to things that I thought others might want to know. One is that some members of Congress are so upset about the new USPSTF recommendations on mammography screening, that they are trying to initiate an investigation of the Task Force. When did the members of Congress become scientists and doctors? Why do they think that intimidating researchers will help advance scientific inquiry (click here for BCA’s take on the new guidelines)?
The other news is that Nancy Brinker is back as CEO of the Komen for the Cure Foundation. Seems that the most recently hired chief honcho – Hala Moddelmog has been shown the door, and the Foundation is going back to old leadership. This should be interesting, though many people think that Brinker, founder of the organization, has always called the shots.
And I heard something last night at the dinner for advocates hosted by the Alamo Breast Cancer Foundation that warmed my heart. Dr. Charles Coltman, a founder of SABCS, talked about the earliest days of this meeting, and the involvement of Rose Kushner, a fantastic activist. He described how she demanded changes in how patients were treated, and how she would sit in the front row at the meeting, and ask questions of the presenters. That spirit is largely gone from this meeting, but I remain ever hopeful that it might be regained.