The American Institute for Cancer Research (AICR) is launching a new campaign in partnership with Giant Food. The campaign, called Shop for Health, Eat for Life, will run in all Giant food stores from June 19 to July 2, 2009.

Shop for Health, Eat for Life aims to help individuals and families reduce their risk of cancer, encourage a healthy diet and raise funds for cancer research and education. The campaign encourages Giant customers to purchase specially marked products and offers several in-store promotions and recipes, free nutrition educational materials and product giveaways in select stores. Two to three cents per Shop for Health, Eat for Life item sold will be donated to the AICR, with a goal of contributing up to $150,000 for cancer research.

The campaign was announced at AICR’s Washington D.C. headquarters on Wednesday, June 10. Event participants included Kelly Browning, Executive Vice President and CEO of AICR; Robin Michel, Executive Vice President and General Manager of Giant Food; Susan Higginbotham, Ph.D. RD, Director of Research for AICR; and Gerard van der Wulp, Deputy Head of Mission for the Royal Netherlands Embassy.

Products included in Shop for Health, Eat for Life are:

- Nature’s Promise Whole Wheat Spaghetti 16 oz.
- Nature’s Promise Whole Wheat Linguini 16 oz.
- Nature’s Promise Premium Organic Spinach 16 oz.
- Nature’s Promise Premium Organic Peas 16 oz.
- Nature’s Promise Organic Black Beans 15.5 oz.
- Nature’s Promise Premium Organic Frozen Strawberries 10 oz.
- KRAFT 2% Shredded Cheese
- KRAFT Triscuit Baked Whole Grain Wheat Reduced Fat Crackers
- KRAFT Planters 16 oz. Dry Roasted Peanuts
- KRAFT Caprisun 100% Juices
- KRAFT 2% and non-fat Breakstone 16 oz. Cottage Cheese

“AICR provides Americans with practical information they can trust — information that will help them make the everyday choices that lower cancer risk,”said AICR’s Browning. “But they still have to make those choices for themselves, and that’s why we’re so pleased to be a part of this campaign with Giant Food.

“Shop for Health, Eat for Life puts AICR’s science-based advice where it can do the most good - right in the grocery aisle, where those all-important choices are actually made every day.”

A new campaign, Shop for Health, Eat for Life, an initiative of Giant Food and the American Institute of Cancer Research, was announced on Wednesday, June 10, 2009. Kelly Browning, Executive Vice President and CEO of AICR; Robin Michel, Executive Vice President and General Manager of Giant Food and Gerard van der Wulp, Deputy Head of Mission for the Royal Netherlands Embassy, spoke about the relevance of healthy diet and nutritious food choices with cancer prevention. The Shop for Health, Eat for Life program will be in all Giant Food stores from June 19 to July 2, 2009.

Giant Chef Mike Reed prepares delicious healthy food options for guests at the Shop for Health, Eat for Life launch event, Wednesday, June 10, 2009 at the American Institute of Cancer Research (AICR). Shop for Health, Eat for Life is a program designed by Giant Food and AICR to educate consumers about cancer prevention and raise funds for research. The program will be in all Giant Food stores from June 19 to July 2, 2009.

About Giant Food

Giant Food LLC, headquartered in Landover, MD, operates 182 supermarkets in Virginia, Maryland, Delaware and the District of Columbia, and employs approximately 22,000 associates. Included within the 182 stores are 164 full-service pharmacies. For more on Giant visit http://www.giantfood.com.

Source
American Institute for Cancer Research

WHEELING, W.Va., June 23 — Excess body weight during young adulthood both increases the likelihood of eventually developing pancreatic cancer and reduces the average age of disease onset, researchers said.

Compared with individuals with a body mass index (BMI) less than 25 before age 39, those considered overweight (BMI 25 to 29.9) had an odds ratio of 1.67 for developing pancreatic cancer (95% CI 1.20 to 2.34), according to Donghui Li, PhD, of the M.D. Anderson Cancer Center in Houston, and colleagues.

Participants who were obese (BMI greater than 30) from the age of 20 to 49 had an odds ratio of 2.58 for pancreatic cancer (95% CI 1.70 to 3.90), they wrote in the June 24 issue of the Journal of the American Medical Association.

Earlier research had implicated obesity as a risk factor for pancreatic cancer, but their case-control study of some 1,600 people is the first to show that fatness at an early age may be especially dangerous, the researchers said.

• Explain to interested patients that pancreatic cancer is among the least treatable and most often fatal malignancies.
• Explain that excess weight and obesity are linked to a wide range of health problems.
• Note that the study used a case-control design, a weaker form of evidence than a prospective approach that follows patients over a long period of time.

Their study also indicated that obese and overweight individuals past the age of 30 with pancreatic cancer had reduced survival rates, irrespective of other prognostic factors such as disease stage.

Dr. Li and colleagues matched 841 patients with pancreatic adenocarcinoma with 754 healthy people for age, sex, and race. Participants were interviewed about their history of height and weight starting in their teen years.

Median follow-up for calculations of pancreatic cancer survival was 22.1 months, covering 609 of the patients for whom at least one year of follow-up was available.

Dr. Li and colleagues said the strongest associations were seen in participants who were overweight or obese during their 30s, and even more so in those who had gained at least five BMI units since their teens.

“Even though the prevalence of overweight and obesity continued to increase until ages 70 to 79 years, the increased risk of pancreatic cancer with weight gain leveled off for gains coming after ages 40 to 49 years,” the researchers noted.

History of smoking and male gender appeared to magnify the effect of excess weight.

Dr. Li and colleagues estimated the population-attributable risk of pancreatic cancer associated with BMI at 10.3% for lifetime nonsmokers and 21.3% for those who had smoked at some point.

Additionally, BMI of 25 or more before age 50 was associated with receiving a pancreatic cancer diagnosis from two to six years earlier than normal-weight patients.

Median age of disease onset for normal-weight, overweight, and obese patients was 64, 61, and 59, respectively (P<0.05).

And, excess weight from the ages of 30 to 79, or in the year before study entry, significantly increased the risk of death from pancreatic cancer after controlling for disease stage and tumor resection status.

Hazard ratio for death among overweight patients was 1.26 (P=0.04); for obese patients, it was 1.86 (P<0.001).

“While our observations require confirmation, they provide support for a role of excess body weight in the development and progression of pancreatic cancer,” Dr. Li and colleagues concluded.

“These observations have great public health implications because it implies that weight gain in young adults is associated with a greater risk of pancreatic cancer than in older adults,” they said.

The researchers speculated that insulin dysregulation associated with excess weight could be a mechanistic factor underlying the relationship.

They noted, though, that the case-control approach has inherent weaknesses, and said a further limitation was that participants were drawn from a single institution. The study also relied on participants’ self-reports of past weight.

In an accompanying editorial, Robert McWilliams, MD, and Gloria M. Petersen, PhD, both of the Mayo Clinic in Rochester, Minn., agreed that the implications of the study are important.

“The additional evidence of knowing that obesity could contribute to earlier onset of disease and worsened survival adds further to the call for interventions at the public health level to stem the increasing rates of obesity at all ages in the U.S. population,” they wrote.

Drs. McWilliams and Petersen added that the findings that increased weight may affect all aspects of the pancreatic cancer process from initial development to final outcome “may provide biological insight into why pancreatic cancer portends such a poor prognosis.”

The study was supported by the National Institutes of Health. No potential conflicts of interest were reported by study authors or the editorialists.

Primary source: Journal of the American Medical Association

Source reference:

Li D, et al “Body mass index and risk, age of onset, and survival in patients with pancreatic cancer” JAMA 2009; 301: 2553-62.

Additional source: Journal of the American Medical Association

Source reference:

McWilliams R, et al “Overweight, obesity, and pancreatic cancer: beyond risk alone” JAMA 2009; 301: 2592-93.

HOUSTON, June 24 — An investigational cancer therapy demonstrated significant antitumor activity in patients with BRCA1/2 mutations, according to the investigators in the most recent string of favorable studies.

• Explain to patients that an investigational drug showed activity in tumors that have certain types of genetic mutations.
• Emphasize that the drug is not yet available.

Almost two-thirds of mutation carriers had a clinical benefit from treatment with olaparib, Johann S. de Bono, MD, PhD, of the Royal Marsden Hospital in London, and colleagues reported in the June 24 issue of the New England Journal of Medicine.

In fact, only mutation carriers had responses to the oral inhibitor of poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP). However, the agent demonstrated activity in patients with breast, ovarian, and prostate cancer.

The drug was well tolerated, and analysis of patient blood, hair, and tissue samples confirmed PARP inhibition.

The findings point to a need to rethink the drug approval process to accelerate development of anticancer therapies, the authors concluded.

“This study raises the possibility that for some anticancer drugs, the traditional processes of clinical development and registration need to be altered,” they said.

“Due consideration must now be given to developing rationally designed molecularly targeted therapies for patients whose tumors have the same molecular defect but different origins, such as the ovary, breast, or prostate. Such a radical change in drug evaluation and registration may be key to accelerating the development of anticancer drugs.”

PARPs have a major role in DNA repair mechanisms, including the repair pathway for the tumor-suppressor proteins BRCA1 and BRCA2. Mutations in the proteins disrupt normal repair processes and allow emergence of a tumor with aberrant DNA repair not found in normal tissues.

“This tumor-specific defect can be exploited by using PARP inhibitors to induce selective tumor cytotoxicity, sparing normal cells,” the authors said. “PARP inhibition in these tumor cells with deficient homologous-recombination repair generates unrepaired DNA single-strand breaks that are likely to cause the accumulation of DNA double-strand breaks and collapsed replication forks.”

In vitro studies showed that BRCA1/2-deficient cells were as much as 1,000-fold more sensitive to PARP inhibition compared with wild-type cells. Moreover, PARP inhibition prevented the growth of BRCA2-deficient tumor xenografts.

Success in the laboratory led to a phase I clinical trial reported by Dr. de Bono and colleagues. The trial involved 60 patients with solid tumors that had proved refractory to standard therapy or for which no suitable therapies existed. By design, the trial was enriched with 21 patients with BRCA-deficient tumors and one patient who had a strong BRCA-positive family history but refused testing.

Treatment with olaparib started at a dose of 10 mg a day for two of every three weeks. The dose subsequently was increased to 600 mg or more twice a day, given continuously for three weeks in four-week cycles.

Dose-limiting toxicity was defined as a grade 3 or 4 adverse effect occurring in the first cycle of treatment with a given dose of olaparib.

That occurred in patients who received 400 or 600 mg bid. The observations established 400 mg bid as the maximum tolerated dose.

Adverse effects possibly related to the study drug were primarily grade 1 or 2 in severity and included nausea (in 32% of patients), fatigue (30%), vomiting (20%), taste alteration (13%), and anorexia (12%). Three patients had anemia and two developed grade 4 thrombocytopenia.

Two patients died during the study: one with advanced non-small cell lung cancer and a history of lower respiratory tract infections and one with ovarian cancer, who died of septicemia. Neither death seemed related to treatment with olaparib.

Two patients had rapidly progressive disease. Both had tumors usually not associated with BRCA mutations: small-cell lung cancer and vaginal adenocarcinoma.

Of 19 BRCA carriers evaluable for tumor response, 12 (63%) had either radiologic or tumor-marker responses or disease stabilization for at least four months. Nine of the 12 met RECIST criteria for tumor response, one of which was sustained for 76 weeks. Two other patients had responses that persisted for a year or longer.

No tumor responses occurred in patients who did not have known BRCA mutations.

“These data indicate that using PARP inhibition to target a specific DNA-repair pathway has the necessary selectivity profile and a wide therapeutic window for BRCA-deficient cells, supporting the clinical relevance of the hypothesis that BRCA mutation-associated cancers are susceptible to a synthetic lethal therapeutic approach,” the authors said.

The positive results follow those from two breast cancer studies reported in May at the American Society of Clinical Oncology meeting. One study involved only patients with triple-negative disease, and the other was limited to patients with BRCA mutations. (See New Drug Class Promising in Breast Cancer)

The study was supported by KuDOS Pharmaceuticals, a subsidiary of AstraZeneca. Additional support was provided by Cancer Research U.K., the Experimental Cancer Medicine Center, the National Institute for Health Research Biomedical Research Center, and Breakthrough Breast Cancer. Co-authors Andrew Tutt, Mark J. O’Connor, Alan Ashworth, and Stan B. Kaye reported financial relationships with KuDOS or AstraZeneca. Co-authors included employees of KuDOS and AstraZeneca.

Primary source: New England Journal of Medicine

Source reference:
Fong PC, et al “Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers” N Engl J Med 2009; 361(2): DOI: 10.1056/NEJMoa0900212.

Related Article(s):

• ASCO: New Drug Class Promising in Breast Cancer