How the US Food and Drug Administration evaluates the scientific evidence for health claims.

Health claims describe the relationship between a substance (food or component of food) and a disease or health-related condition. They were first authorized through the Nutrition Labeling and Education Act of 1990. The standard set by the US Congress for the scientific evidence required to authorize a claim was the significant scientific agreement standard.

Qualified health claims for calcium and colorectal, breast, and prostate cancers: The U.S. Food and Drug Administration's evidence-based review.

In 2003, the United States Food and Drug Administration (FDA) received a health claim petition for calcium supplements and reduced risk of colorectal, breast, and prostate cancers. Health claims characterize the relationship between a substance (food or food component) and disease (e.g.

Identification of an integrated SV40 T/t-antigen cancer signature in aggressive human breast, prostate, and lung carcinomas with poor prognosis.

Understanding the genetic architecture of cancer pathways that distinguishes subsets of human cancer is critical to developing new therapies that better target tumors based on their molecular expression profiles. In this study, we identify an integrated gene signature from multiple transgenic models of epithelial cancers intrinsic to the functions of the Simian virus 40 T/t-antigens that is associated with the biological behavior and prognosis for several human epithelial tumors. This genetic signature, composed primarily of genes regulating cell replication, proliferation, DNA repair, and apoptosis, is not a general cancer signature.

The U.S. Food and Drug Administration's evidence-based review for qualified health claims: tomatoes, lycopene, and cancer.

Several studies have reported an inverse association between tomato and/or lycopene intake and the risk of some types of cancer. In 2004, the U.S.

Meat and dairy consumption and subsequent risk of prostate cancer in a US cohort study.

Objective: To evaluate the association of meat and dairy food consumption with subsequent risk of prostate cancer.

Methods: In 1989, 3,892 men 35+ years old, who participated in CLUE II study of Washington County, MD, completed an abbreviated Block food frequency questionnaire. Intake of meat and dairy related foods was calculated using consumption frequency and portion size.

Molecular mechanisms of breast cancer progression: lessons from mouse mammary cancer models and gene expression profiling.

The development of breast cancer is thought to occur through a multi-step process. The majority of breast cancers likely develop over extended periods of time arising from early, pre-invasive lesions such as atypical ductal hyperplasia (ADH) and carcinoma in situ (DCIS), progressing to invasive carcinoma and culminating in metastatic disease. However, the molecular mechanisms underlying this process are still poorly understood.

4-Hydroxybutyl(butyl)nitrosamine-induced urinary bladder cancers in mice: characterization of FHIT and survivin expression and chemopreventive effects of indomethacin.

The administration of 4-hydroxybutyl(butyl)nitrosamine (OH-BBN) to male B6D2F1 mice yielded a high incidence of large palpable urinary bladder cancers. Since prior studies demonstrated chemopreventive effects of non-steroidal anti-inflammatory drugs (NSAIDs), we further explored the efficacy of the NSAID indomethacin using different treatment regimens. OH-BBN was administered twice per week for 12 weeks (the first week of treatment was designated week 1).

Application of gene expression profiling for validating models of human breast cancer.

While classical histopathologic approaches are invaluable in classifying tumors and understanding aspects of cellular interactions, genomic approaches provide a means to molecularly dissect tumorigenesis. The relationship of gene expression to the development of neoplasia remains an area of intensive research. With the advent of large-scale genomic platforms, alterations in gene expression can be related to the morphological development of cancer.

Genomic approaches to understanding mammary tumor progression in transgenic mice and responses to therapy.

Scores of genetically engineered mice have been generated in the quest to understand mechanisms of breast cancer development and progression. More recently, there has been a growing trend for using such models for testing various therapeutic strategies and agents. The application of these mouse models for these purposes requires that they be characterized in ways that demonstrate they possess important similarities to human breast cancer.

The use of genetically altered mice for breast cancer prevention studies.

Chemoprevention through nutritional and dietary changes may offer an important means of inhibiting the development and progression of breast cancer, which would have a major impact on public health. Studies to assess the efficacy of potential chemopreventive compounds are difficult to perform in large human populations, whereas the use of genetically engineered mice (GEM) for preclinical testing offers several advantages. GEM models can be utilized to assess the inhibitory effects of nutritional and chemopreventive agents on well-defined oncogenic signaling pathways.

Comparative effects of lovastatin on mammary and prostate oncogenesis in transgenic mouse models.

The effects of lovastatin, a potent inhibitor of HMG CoA reductase, on experimental mammary and prostate oncogenesis, were studied in vitro and in vivo. Lovastatin inhibited cell growth in vitro in a dose-dependent manner for both mammary and prostate cancer cell lines, which was associated with p53-independent apoptosis. Flow cytometric analyses of lovastatin-treated mammary and prostate cancer cells demonstrated cell-cycle G(1) arrest, as well as decreases in S and G(2)/M fractions.