LITTLE FALLS, N.J., June 8 -- Multivitamin supplementation during pregnancy may improve a baby's birth weight more than iron-folic acid supplementation alone, a meta-analysis showed.

In an analysis of 13 studies, women who received a multivitamin had a 17% greater reduction in the risk of having a baby with low birth weight (RR 0.83, 95% CI 0.74 to 0.93), Prakesh Shah, M.D., of Mount Sinai Hospital in Toronto, and colleagues reported in the June 9 Canadian Medical Association Journal. The number needed to benefit was 50 (95% CI 33 to 100). The World Health Organization recommends iron-folic acid supplementation alone for all pregnant women, but this strategy "needs to be challenged in light of the evidence from our review," according to the researchers. They said their findings indicate that multivitamin supplementation could prevent about 1.5 million babies worldwide from being born with low birth weight each year. Dr. Shah and colleagues identified 13 high-quality randomized or quasi-randomized (group assignments by identifiers such as date of birth or day of the week) trials evaluating the effect of multivitamin supplementation at any time during pregnancy. These included four cluster-randomized trials. The multivitamins used in the various studies contained eight to 28 micronutrients. For the prevention of low birth weight (less than 2,500 grams), multivitamins yielded a benefit against both iron-folic acid supplementation and placebo (RR 0.81, 95% CI 0.73 to 0.91). Overall birth weight was significantly higher in the multivitamin group than in the iron-folic acid group (difference 54 g), but there was no significant difference compared with placebo. There were no significant differences between the three study groups in the risk of preterm birth, small-for-gestational-age birth, or gestational age. The researchers noted that the meta-analysis was limited by variability among the studies in terms of the timing and duration of supplementation, the composition of the micronutrients, and the characteristics of the study populations. But they said "the practice in most developed countries of giving multivitamins along with iron and folic acid to pregnant women needs to be adopted in developing countries." They acknowledged the difficulty in determining which components of the multivitamins were responsible for the beneficial effects. "Therefore," they said, "it is not unreasonable to recommend a composite of micronutrients for supplementation because it would be impossible to identify and target individual deficiencies in every pregnant woman." In an accompanying editorial, Zulfiqar Bhutta, M.B.B.S., Ph.D., and Batool Azra Haider, M.B.B.S., of the Aga Khan University in Karachi, Pakistan, urged caution when interpreting the results. Drs. Bhutta and Haider had previously concluded that there was not enough evidence to justify replacing iron-folic acid supplementation with a multivitamin strategy. They said the authors of the current meta-analysis should arguably have adjusted for the cluster-randomized trials. In addition, they said, Dr. Shah and colleagues did not stratify the results by maternal nutritional status and stature and omitted several outcomes such as perinatal mortality. Considering these limitations, though, "if proven effective and safe in representative healthcare systems, multimicronutrient supplementation should replace iron-folic acid supplementation in susceptible populations." The study was funded by a Knowledge Synthesis/Translation grant from the Canadian Institutes of Health Research. Neither the study authors nor the editorialists reported any conflicts of interest.

Primary source: Canadian Medical Association Journal Source reference: Shah P, et al "Effects of prenatal multimicronutrient supplementation on pregnancy outcomes: a meta-analysis" CMAJ 2009; 180: E99-E108. Additional source: Canadian Medical Association Journal Source reference: Bhutta Z, Haider B "Prenatal micronutrient supplementation: Are we there yet?" CMAJ 2009; 180: 1188-89.

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coronary atherosclerosis in women in early menopause but poor specificity and no correlation with lab parameters, preliminary data from an ongoing study showed.

As verified by coronary angiography, contrast stress echocardiography had a sensitivity of 80% for coronary disease, but specificity was less than half that, Sharon Mulvagh, M.D., of the Mayo Clinic in Rochester, Minn., reported at the American Society of Echocardiography meeting. Newer laboratory tests for coronary disease, such as high-sensitivity C-reactive protein (hs-CRP) and brain natriuretic peptide (BNP), had no correlation with contrast stress echo, nor did coronary calcification. Predictors of a positive echo test were body mass index, family history of premature coronary artery disease (CAD), and a positive stress ECG. "This is the first large prospective trial of early or recently menopausal women at low to intermediate risk for coronary artery disease undergoing contrast stress echo, stress ECG, electron-beam computed tomography, and novel serologies," said Dr. Mulvagh. "Contrast stress echo detected angiographically significant CAD twice as often as stress ECG, but was less specific. "These are the preliminary results, and data from two- and five-year follow-up are pending," she added. Little progress has been made in the development of diagnostic strategies for women in early menopause who have cardiovascular risk factors and chest pain. But technologic advances in contrast stress echo have improved image quality, visualization of wall segments, and diagnostic confidence, said Dr. Mulvagh. Whether contrast echo enhanced the utility of other indicators of CAD had not been carefully studied, she said. So, the Stress Echo in Menopausal Women at risk for Coronary Artery Disease Trial (SMART) was designed to address some of the unanswered questions about the role of contrast stress echo in evaluating early menopausal women. SMART has a twofold primary objective: (1) Determine the prognostic value of contrast stress echo for predicting coronary events; (2) Explore the relationship between wall motion abnormalities identified by contrast stress echo and stress ECG, coronary calcium score, and novel serum biomarkers. The secondary objective is to evaluate the diagnostic accuracy of contrast stress echo and stress ECG in a subset of SMART participants undergoing clinically indicated coronary angiography. Investigators at Mayo campuses in Rochester, Scottsdale, Ariz., and Jacksonville, Fla., enrolled 400 perimenopausal, early menopausal, and surgically menopausal women referred for contrast stress echo. All were judged to have a low to moderate likelihood of CAD. Ultimately, 389 patients underwent a contrast stress echo -- 366 had exercise tests and 23 had dobutamine assessments. Patients also had assessment of BNP, atrial natriuretic peptide (ANP), endothelin, and hs-CRP. A subset of patients had quantification of coronary calcification by electron beam CT. Patients were monitored continuously by 12-lead ECG during contrast stress echo evaluation. An abnormal stress echo result was defined as new or worsening of wall motion abnormalities during peak stress. An abnormal ECG was defined as 1 mm or greater horizontal or downsloping ST-segment depression or ST-segment elevation for at least 80 milliseconds. The mean age of the study group was 54.4, the mean BMI was 31.5, and 95.5% of the women were white. A quarter of the women were current or former smokers, 16.5% were diabetic, 60% had a family history of CAD, 63% were hypertensive, 80% were dyslipidemic, and 57% were obese. Dr. Mulvagh reported that 42 women (11.5%) had abnormal contrast stress echo tests. Additionally, 22 participants (6%) had positive ECG tests, and 23 (6.2%) had indeterminate or inadequate ECG results. Stress ECG had poor correlation with a positive contrast stress echo result. Of the 42 patients who had positive echo tests, only seven (16.7%) were positive by stress ECG. Of 308 women who had measurement of hs-CRP, 72 had values less than 1 mg/dL (low risk), 113 had values of 1.0 to 3.0 mg/dL (average risk), and 123 had values greater than 3.0 mg/dL (high risk). Neither a positive nor a negative contrast stress echo result correlated with hs-CRP values associated with the tests. ANP and endothelin levels also had no correlation with contrast stress echo results. The only statistically significant association involved BNP, which increased during peak wall motion score index (WMSI) (P<0.001),> A subset of 124 patients had EBCT assessment of coronary calcium. Values did not correlate with contrast stress echo results. Of the 124, 14 had abnormal contrast stress echo tests, and their coronary calcium score averaged 37.3. In the remaining 110 patients with normal contrast stress echo tests, the coronary calcium score averaged 48.4. A subset of 48 patients had coronary angiography for suspected CAD. Compared with angiography, contrast stress echo had a sensitivity of 80% but a specificity of 37%, resulting in an overall accuracy of 46%. Stress ECG had a 40% sensitivity, 79% specificity, and overall accuracy of 71%. In a multivariate analysis, only conventional CAD risk factors correlated with as positive contrast stress echo test (BMI, diabetes, family history of premature CAD, and positive stress ECG). The patients will continue to be followed for five years, and an interim analysis will be performed after two years, Dr. Mulvagh said. The authors reported no potential conflicts of interest.

Primary source: American Society of Echocardiography Source reference: Abdelmoneim S, et al "Initial results from the 'Stress echo in Menopausal women at risk for coronary ARTery Disease (SMART) Trial:' An outcomes study evaluating the diagnostic and prognostic value of noninvasive testing for cardiovascular disease" J Am Soc Echocardiogr 2009; 22(5): Abstract P1-57.

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NEW ORLEANS, June 8 -- A head-to-head trial of two GLP-1 analogs and the possibility of predicting a diabetes diagnosis five years before the patient exhibits standard clinical markers are the focus of this exclusive MedPage Today InFocus discussion.

Sue Kirkman, M.D., vice president of clinical affairs for the American Diabetes Association, examines the results of those two studies with staff writer Kristina Fiore.

The beauty of the trial comparing liraglutide and exenatide, Dr. Kirkman said, is that two drugs in a relatively new class of drugs are being compared to each other rather than to one of the well-established treatments.

Dr. Kirkman also touches on the potential implications for very early screening in diabetes based on findings from the Whitehall study.

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NEW ORLEANS, June 8 -- Insulin sensitivity, beta-cell function, and blood glucose may provide telltale signs of impending type 2 diabetes up to five years before onset, researchers affirmed.

The traditional marker for diabetes and prediabetes diagnosis -- fasting blood glucose -- shot up in the three years prior to diabetes onset, Adam G. Tabák, M.D., of University College London, and colleagues found in a 13-year study of British civil servants.

But beta-cell function abnormalities emerged three to four years before onset and insulin sensitivity fell sharply over the five years before diagnosis, they reported here at the American Diabetes Association meeting and simultaneously online in The Lancet.

These biomarker trajectories, determined at regular check-ups over time, could improve the accuracy of risk prediction models to allow for earlier prevention efforts, the researchers said.

The models typically use only the most recent blood glucose measurements, with prevention then focusing on patients who meet glucose-based prediabetes criteria, they noted, However, waiting to intervene until prediabetes may be too late, since they are "already on the steep part of the glucose trajectory," the researchers said. "We hypothesize that prevention would be more effective before this unstable period, but more research is needed," they said. "If a person could be kept on the linear part of the fasting glucose (or postload glucose) trajectory, the onset of diabetes might be substantially delayed," they said. The results provide "unique longitudinal data illuminating what had long been suspected from cross-sectional data," said David R. Matthews, M.D., and Jonathan C. Levy, M.D., both of the Oxford Centre for Diabetes at the University of Oxford in Oxford, England, in an accompanying editorial. Although they expressed skepticism that the results could be used for earlier screening because the predictions would have poor sensitivity and specificity, they said beta-cell function and insulin resistance could be valuable additions to risk prediction. "We know that we have proven advice and therapies that we can give," they said. "Now the hunt has to be intensified for the pathology that causes the decompensation that precipitates diabetes." M. Sue Kirkman, M.D., ADA vice-president of clinical affairs, agreed that the findings might not be immediately applicable to clinical practice. A trial to compare early screening versus usual screening practice would be required, she said. Dr. Tabák's group examined the Whitehall II study for a "high-resolution" look at changing glucose metabolism over time in 6,538 British civil servants (71% male, 91% white) without baseline diabetes who were followed with repeated serum glucose measurements and oral glucose tolerance tests. Over up to 13 years of follow-up (median 9.7 years), 505 participants were diagnosed with diabetes. Among those who did not develop the disease, metabolic changes were fairly gradual. Insulin secretion changed little. Modest, linear rises occurred in fasting glucose (mean 0.004 mmol/L per year) and slight falls for insulin sensitivity -- a decline of about 15% over 13 years, which Drs. Matthews and Levy called "doubtless the effect of progressive inactivity and middle-age spread." For incident diabetes cases, fasting plasma glucose also declined linearly until three years before diagnosis, although with a 0.028-mmol/L-per-year steeper slope than seen in nondiabetics. But the last three years leading up to diagnosis showed a rapid drop in fasting glucose levels following a quadratic trajectory. For postload glucose levels, the rate of increase up until six years prior to the end of follow-up was not significantly different between study participants who would go on to develop incident diabetes and those who would not. Again, though, diabetes cases showed 1.5-fold higher postload glucose concentrations that rose in a cubic trajectory during the six years before diagnosis to the end of follow-up. In the two years before diagnosis, cases had a rapid increase in glucose concentrations from 7.60 to 11.90 mmol/L. Insulin sensitivity declined identically between groups (1.11% per year) until five years before diagnosis. After that point, the slope was an absolute 2.76% steeper among diabetes cases to reach 86.7% by the end of the 13-year follow-up. Beta-cell function measured by calculated insulin secretion averaged 10.4% higher in individuals who would develop diabetes up until the four years prior to diagnosis, which the editorialists explained as a compensatory effort to "maintain normoglycemia in a prevailing climate of insulin resistance." Then roughly three years before diabetes onset, beta-cell function revealed "a further last-ditch increase" with a quadratic increase before crashing to 62.4% of normal. Sensitivity analyses, including body mass index adjustment, had little impact on difference in trajectory of metabolic changes between groups. Although the largely white, male study population could limit generalizability, Dr. Kirkman noted that the findings match those of other studies, such as beta-cell results in a study of Pima Indians. The researchers said their findings supported a multistage model of diabetes development with a long compensatory period, then a stable adaptation, and finally "a transient unstable period with a rapid rise of glucose to overt diabetes." The Whitehall II study was supported by the Medical Research Council, Economic and Social Research Council, British Heart Foundation, Health and Safety Executive, and U.K. Department of Health, the National Heart Lung and Blood Institute, National Institute on Aging, Agency for Health Care Policy Research, and The John D. and Catherine T. MacArthur Foundation. The researchers reported no conflicts of interest. Drs. Matthews and Levy reported no conflicts of interest. Dr. Kirkman reported no conflicts of interest.

Primary source: The Lancet Source reference: Tabák AG, et al "Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study" Lancet 2009. Additional source: The Lancet Source reference: Matthews DR, Levy JC "Impending type 2 diabetes" Lancet 2009.

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WASHINGTON, June 8 -- A new draft of a healthcare reform bill from the Senate Health, Education, Labor and Pensions (HELP) Committee proposes reimbursing physicians at rates similar to those in Medicare as part of a public insurance plan option.

Not surprisingly, the bill would create a new government-sponsored insurance program -- which has been the most divisive component of healthcare reform.

While the bill offers few specifics of its "affordable access plan," such as who would be eligible, it does propose to reimburse physicians and hospitals at Medicare rates, plus an additional 10%.

The 170-page draft bill, written by HELP Chairman Sen. Edward Kennedy (D-Mass.), is a working draft, complete with committee notes and blank spots where pertinent details would be filled in. But it is a concrete proposal from one of the two committees responsible for healthcare reform.

Kennedy has not been working full time in Washington since he was diagnosed with malignant glioma in his left parietal lobe almost 13 months ago, but he has been working remotely to make good on his longtime promise of healthcare reform. (See Kennedy Diagnosed with Glioma)

The other committee of jurisdiction is the Senate Finance Committee, which has said it would mark up a bill in the next few weeks but hasn't unveiled a draft so far.

Kennedy's bill would require all individuals to have insurance and would require all employers to provider insurance or else pay their employees to purchase a plan elsewhere.

While President Barack Obama and Sen. Max Baucus (D-Mont.), chairman of the Senate Finance Committee, have endorsed an employer-mandate, they have largely stayed away from promoting an individual mandate -- something that was not politically popular during the failed reform efforts in the 1990s.

Under the bill, the government would provide credits to help eligible businesses pay for covering their employees, and certain small businesses and employees would be exempt.

Kennedy's bill would also establish an insurance exchange, called the "Affordable Health Benefits Gateway," which would be modeled after the "Connector" in Massachusetts.

The Gateway would be a state-run, one-stop shop for insurance-seekers to compare the benefits and costs of "qualified" insurance plans.

A new "Medical Advisory Council" would decide what services are "essential healthcare benefits" that all health plans would be required to cover.

The council would issue payment recommendations each year for medical and surgical care, mental health services, maternity care, and other specific services. They would take effect automatically unless rejected by Congress.

The bill would drastically change how insurance companies operate by requiring them to account for exactly what policy-holders' premiums paid for, and to provide a partial rebate to patients from portions of their premiums that didn't go toward paying for the medical expenses.

In affect, the bill would put a cap on insurance company profits.

The bill would also require plans to provide a bare minimum of basic services, provide coverage to dependents through age 26, and make it illegal for insurance plans to deny coverage based on pre-existing conditions -- something insurance groups have already pledged to do. (See Health Insurers Back Coverage for All Regardless of Current Health)

It would also require insurers to cover preventive medical services, including all recommended immunizations, and prohibit private insurers from setting annual or lifetime limits on benefits.

The bill would also:

• Expand Medicaid to cover those with incomes up to 150% of the federal poverty level, and help defray costs for states that have already expanded their Medicaid programs
• Establish an insurance plan for people with disabilities to help cover the costs of receiving community-based care

The draft bill does not contain any cost figures. The Senate Finance Committee's plan is expected to focus more heavily on cost estimates.

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LITTLE FALLS, N.J., May 22 -- Researchers attempting to clarify the debate over intense glucose control through meta-analysis concluded that it does reduce cardiovascular risk among type 2 diabetes patients, but not overall mortality.

Their meta-analysis of five studies found that the approach reduces the risk of nonfatal myocardial infarction by 17%, and coronary heart disease events by 15%, according to Kaushik K. Ray, M.D., of Strangeways Research Lab in Cambridge, England, and colleagues.

But the treatment had no effect on stroke or all-cause mortality, the group reported in the May 23 issue of The Lancet.

"Intensive glucose-lowering treatment has cardiovascular benefit compared with standard treatment for individuals with type 2 diabetes," the researchers concluded. But it appears considerably less significant than controlling blood pressure and cholesterol, they said.

There have been conflicting reports on the effectiveness of intensive glucose control in reducing macrovascular events and all-cause mortality in patients with type 2 diabetes. But the researchers said many trials have been underpowered to show clinical benefit.

So they conducted a meta-analysis of five prospective trials -- including ADVANCE and ACCORD -- involving a total of 33,040 patients.

Over 163,000 person-years of follow-up, there were 1,497 nonfatal myocardial infarction events, 2,318 coronary heart disease events, 1,127 fatal and nonfatal stroke events, and 2,892 deaths from any cause.

The researchers found that there were 2.3 fewer myocardial infarctions and 2.9 fewer coronary heart disease events for every 200 patients on intensive glucose control treatment for five years.

That translates to a number-needed-to-treat of 87 and 69, respectively.

"This benefit is much more modest than is that from a per-mmol/L reduction in LDL cholesterol or from a 4-mm Hg lower blood pressure," the researchers said.

Intensive glycemic control resulted in a 17% reduction in events of nonfatal myocardial infarction (OR 0.83, 95% CI 0.75 to 0.93) and a 15% reduction in coronary heart disease events (OR 0.85, 95% CI 0.77 to 0.93).

There was no significant effect on stroke or all-cause mortality.

Additionally, almost twice as many patients on intensive glycemic control had a hypoglycemic episode as those on standard treatment.

Therefore, a practical clinical approach "might be to reduce HbA1c concentration steadily with care taken to avoid severe hypoglycemia," the researchers said.

Those on intensive control also gained more weight -- an average of 2.5 kg more than those on standard treatment.

The meta-analysis was limited by the methodological rigor of the assessed studies, as well as the possibility of publication bias. Also, the researchers could not assess the effects of intensive glycemic control among different patient subgroups.

An additional limitation was the inability to assess different treatment regimens.

Still, they concluded that their "quantitative analysis of randomized controlled trials provides reliable large-scale evidence of a consistent beneficial effect of intensive treatment on nonfatal myocardial infarction and coronary heart disease, without increased risk of all-cause mortality."

In an accompanying editorial, Theodore Mazzone, M.D., of the University of Illinois at Chicago, said the findings suggest a need for additional clinical trial data about the effect of controlling blood sugar on coronary heart disease risk in patients with type 2 diabetes.

Dr. Mazzone said that intensive glucose-control efforts "might need to be started sooner after onset of diabetes, and extended follow-up could be required."

He noted that tight glucose control does not have as great an impact as blood pressure and cholesterol control. But he said that given an "urgent need to address residual risk of coronary heart disease in a rapidly expanding population with type 2 diabetes, it is premature to conclude that glucose control has no part to play."

Some of the researchers reported receiving honoraria from Novartis, Merck, GlaxoSmithKline, Merck, and Novo Nordisk.

Primary source: The Lancet
Source reference:
Ray KK, et al "Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomized controlled trials" Lancet 2009; 373: 765-72.

Additional source: The Lancet
Source reference:
Mazzone T "Hyperglycemia and coronary heart disease: the meta picture" Lancet 2009; 373: 1737-38.

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Breast Cancer Risk Factors Vary by Tumor Subtype
RIDGEWOOD, N.J., May 22 -- Risk factors for the development of invasive breast cancer vary depending on whether the tumor is luminal A, luminal B, triple negative, orWomen with the luminal B breast cancer subtype, for instance, were likely to be younger at diagnosis than those with luminal A (OR before age 50 of 1.83, 95% CI 1.32 to 2.55, P=0.0001), Marilyn L. Kwan, Ph.D., of Kaiser Permanente in Oakland, Calif., and colleagues reported online in Breast Cancer Research.

Luminal B patients also were less likely to use hormone replacement therapy (OR 0.66, 95% CI 0.46 to 0.94) and oral contraceptives (OR 0.73, 95% CI 0.55 to 0.96), or to consume alcohol (OR 0.74, 95% CI 0.56 to 0.98), the investigators found.

Luminal A tumors are estrogen receptor and/or progesterone receptor positive and human epidermal growth factor receptor 2 (Her2) negative. Luminal B tumors are estrogen receptor and/or progesterone receptor positive, as well as Her2 positive.

These two subtypes have been associated with improved prognoses compared with the subtypes referred to as Her2 overexpressing and "triple negative" (basal-like in 70% of cases).

Her2-overexpressing tumors are estrogen receptor and progesterone receptor negative but Her2 positive, and triple negative tumors, as the name implies, are negative for all three, but positive for cytokeratin 5/6 and/or epidermal growth factor receptor in the majority of cases.

Previous studies have examined associations between breast cancer risk factors, race, and hormone receptor status, but few studies have investigated the relationship between risk factors and molecular subtypes.

To address this, the researchers examined data from two large, prospective breast cancer survivorship studies, the Life After Cancer Epidemiology (LACE) Study and the Pathways Study.

LACE involved 2,280 women diagnosed with early-stage invasive breast cancer between 1997 and 2000, recruited primarily from the Kaiser Permanente Northern California Cancer Registry and the Utah Cancer Registry.

Patients were 18 to 70 years old, had completed treatment other than adjuvant hormonal therapy, and were free of recurrence.

The Pathways Study is an ongoing prospective cohort study that began recruiting in January 2006 and currently includes 2,212 women.

Patients in this study were at least 21 years old at the time of diagnosis, have primary invasive breast cancer of any stage, and no prior history of any cancer.

The current analysis includes all patients in LACE and the first 723 women in the Pathways Study whose cancers corresponded with those in LACE (stage I ≥ 1 cm, II, or IIIA) and for whom molecular subtype data were available.

Demographically, the pool of cohorts was relatively heterogeneous.

Among the 2,544 cases of invasive breast cancers included in the study:

* 1,868 (73%) were classified as luminal A
* 294 (12%) were luminal B
* 288 (11% were triple negative
* 94 (4%) were Her2-overexpressing

Compared with luminal A cases, triple negative cases tended to be younger, (OR before age 50 of 2.78, 95% CI 1.99 to 3.90, P
Her2-overexpressing cases were more likely to be younger than luminal A cases (P=0.03) and less likely to use HRT (OR 0.49, 95% CI 0.26 to 0.79).

Women with the Her2-overexpressing subtype also were more likely to be Hispanic (OR 2.19, 95% CI 1.16 to 4.13) or Asian (OR 2.02, 95% CI 1.05 to 3.88).

Premenopausal women with the triple-negative subtype were more likely to be overweight (OR 1.82, 95% CI 1.03 to 3.24) or obese (OR 1.97, 95% CI 1.03 to 3.77).

Women with the triple-negative subtype and parity of three or more also were more likely to have not breastfed their children (OR 1.68, 95% CI 1.00 to 2.81).

The "significant heterogeneity of associations by tumor subtype . . . lend[s] further support to the growing evidence base that breast cancer is a heterogeneous disease defined by estrogen receptor, progesterone receptor, and Her2 expression with distinct etiologic pathways and prognoses," the researchers concluded.

They cited study limitations that include the small number of Her2-overexpressing tumors, the case-case comparison design, and the fact that the associations reported are all in reference to risk of having the luminal A subtype "and should not be extended to risk of having invasive breast cancer."

Triple negative cases could not be further classified as basal-like or unclassified due to absence of data on CK 5/6 and EGFR markers.

These findings suggest that "public health programs aimed towards achieving a healthy weight and promoting breastfeeding might reduce the number of poor prognostic triple negative tumors among all breast cancer cases, especially the high-risk African American group," they concluded.

The LACE Study was funded by the National Cancer Institute, the Utah Cancer Registry, and the State of Utah Department of Health.

The Pathways Study was funded by the National Cancer Institute, the Department of Defense, and the American Cancer Society.

The authors declared that they have no competing interests.

Primary source: Breast Cancer Research
Source reference:
Kwan M, et al "Epidemiology of breast cancer subtypes in two prospective cohort studies of breast cancer survivors" Breast Cancer Res 2009: 11:R31.

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