Pomegranates have made headlines in the past for being helpful in fighting prostate cancer and benefiting the heart. Now researchers find that eating the fruit may reduce the incidence of hormone-dependent breast cancer.
Pomegranates are a rich source of a type of phytonutrient (plant-based nutrient) called ellagic acid, which belongs to a larger group of compounds known as ellagitannins. Ellagitannins are water-soluble, which makes them easy for the body to absorb. When naturally occurring ellagitannins (found in fruits such as pomegranates, raspberries, and others), they are broken down into ellagic acid, glucose, and other substances.
The principal investigator of the new study, Shiuan Chen, PhD, director of the Division of Tumor Cell Biology and co-leader of the Breast Cancer Research Program at City of Hope in Durante, California, noted in the news release from the American Association for Cancer Research (AACR) that phytonutrients have the ability to “suppress estrogen production that prevents the proliferation of breast cancer cells and the growth of estrogen responsive tumors.”
The ellagic acid found in pomegranates inhibits aromatase, an enzyme that transforms androgen to estrogen. Because aromatase has a major role in breast cancer, the ability of pomegranates to suppress this enzyme means they have the potential to inhibit the growth of breast cancer.
Dr. Chen and his colleagues evaluated whether the phytonutrients in pomegranates can inhibit aromatase and ultimately cancer growth. From a group of ten ellagitannin-derived compounds in pomegranates, they found that the fruit has the potential to prevent estrogen-responsive breast cancers. A metabolite of ellagic acid, called urolithin B, significantly inhibited breast cancer cell growth.
Gary Stoner, PhD, professor in the Department of Internal Medicine at Ohio State University, who was not associated with the study, noted that the results are promising enough to warrant further experiments with pomegranate in both animals and humans. Powel Brown, MD, PhD, a medical oncologist and chairman of the Clinical Cancer Prevention Department at the University of Texas MD Anderson Cancer Center, concurred with Stoner’s assessment and suggested that future research focus on testing pomegranate juice for its impact on estrogen levels, menopausal symptoms, and as a cancer preventive agent.
Pomegranates have been the subject of much research in the fight against prostate cancer as well. One example is a recent study published in October 2009 in which scientists found that pomegranate extract induced the death of prostate cancer cells. A subsequent study noted that the ellagic acid in pomegranate juice may be responsible for its benefits against prostate cancer.
In an Oklahoma State University review, researchers noted that pomegranate juice has been shown to significantly reduce atherosclerotic lesions in mice and intima media thickness in cardiac patients, and to reduce both serum angiotensin converting enzyme activity and systolic blood pressure in hypertensive patients, all of which benefit the heart.
Stoner suggests that individuals “might consider consuming more pomegranates to protect against cancer development in the breast and perhaps in other tissues and organs.” Given that research indicates that pomegranates may help fight prostate cancer, benefit the heart, and also fight serious infections such as MRSA, it seems like good advice.
SOURCES:
American Association for Cancer Research, news release Jan. 5, 2010
Basu A, Penugonda K. Nutrition Reviews 2009 Jan; 67(1): 49-56
Kasimsetty SG et al. Journal of Agricultural and Food Chemistry 2009 Nov 25; 57(22): 10636-44
Koyama S et al. Growth Hormone & IGF Research 2009 Oct 21
Full Article at eMaxHealth
Three proteins may be used to diagnose ovarian cancer, according to a new study released on Wednesday.
Researchers analyzed blood samples from 34 women with ovarian cancer and 70 women without the disease to evaluate six proteins identified as potential indicators of ovarian cancers.
Garnet Anderson of the Fred Hutchinson Cancer Research Center in Seattle and colleagues found that levels of three of the six proteins began to increase slightly in patients with ovarian cancer three years before diagnosis.
Anderson wrote in the Journal of the National Cancer Institute that the elevated levels aren't really what we'd probably define as abnormal until within the last year before diagnosis of ovarian cancer.
Ovarian cancer is rare, but can be deadly. There is no simple and reliable screening program to test for the medical condition in women who do not have symptoms.
When the cancer id diagnosed in its early stage, the five-year survival rate can be as high as 93 percent, according to the American Cancer Society.
Therefore, a screening method that can detect ovarian cancer in its early stage is desired.
The researchers wanted a screening method just that can be used like the PSA test
for prostate cancer. However, the prostate specific antigen is by itself not a reliable indicator.
Reference: http://www.foodconsumer.org
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Study finds that imetelstat targets mechanism that allows cancer cells to divide
MONDAY, Jan. 4 (HealthDay News) -- An experimental drug called imetelstat shows promise in treating glioblastoma brain cancer and
prostate cancer, according to the results of preclinical studies in which the drug was tested on human prostate cancer cells and in rodents with glioblastoma.
Researchers from the University of Texas Southwestern Medical Center found that the drug had an effect on most tumor cells, as well as cancer stem cells believed to cause most of a cancer's growth. Tests in mice with glioblastoma also showed that the drug was able to cross from the bloodstream into the brain. Most drugs cannot cross the blood-brain barrier.
The glioblastoma study is published in the January issue of Clinical Cancer Research, and the prostate cancer study was published online in the International Journal of Cancer.
Imetelstat (also called GRN163L) is being tested in clinical trials as a treatment for breast cancer, lung cancer and lymphocytic leukemia. The drug targets a mechanism that allows cancer cells to continue dividing.
"Because it attacks a mechanism that's active in most cancers, it might prove to be widely useful, especially when combined with other therapies," Dr. Jerry Shay, a professor of cell biology at the university and senior co-author of both studies, said in a university news release.
More information
The U.S. National Cancer Institute has more about brain tumors.
-- Robert Preidt
SOURCE: University of Texas Southwestern Medical Center, news release, Jan. 4, 2010
German Cancer Research Center, Heidelberg, Germany.
To review and summarize evidence from longitudinal studies on the association between serum 25-hydroxyvitamin D (25(OH)D) and the risk of prostate cancer (PC).
Relevant prospective cohort studies and nested case-control studies published until July 2009 were identified by systematically searching Ovid Medline, EMBASE, and ISI Web of Knowledge databases and by cross-referencing. The following data were extracted in a standardized manner from eligible studies: first author, publication year, country, study design, characteristics of the study population, duration of follow-up, PC incidence/PC mortality according to serum vitamin D status and the respective risk ratios, and covariates adjusted for in the analysis. Due to the heterogeneity of studies in categorizing serum vitamin D levels, all results were recalculated for an increase in serum 25(OH)D by 10ng/ml. Summary odds ratios (ORs) were calculated using meta-analysis methods.
Overall, eleven original articles were included, ten of which reported on the association between serum vitamin D levels and PC incidence and one article reported on the association with PC mortality. Meta-analysis of studies on PC incidence resulted in a summary OR (95% confidence interval, CI) of 1.03 (0.96-1.11) associated with an increase of 25(OH)D by 10ng/ml (P=0.362). No indication for heterogeneity and publication bias was found.
According to available evidence from longitudinal studies, serum 25(OH)D is not associated with PC incidence.
UroToday.com Prostate Cancer Section
Inhibiting TNF-receptor associated protein-1 (TRAP-1) may prevent cancer cell death, according to investigators at the University of Massachusetts Medical School. They also note that TRAP-1 is a marker of localized and metastatic prostate cancer and is required for prostate cancer cell viability.
The report will appear in the January 2010 issue of the American Journal of Pathology in a paper titled “Cytoprotective Mitochondrial Chaperone TRAP-1 as a Novel Molecular Target in Localized and Metastatic Prostate Cancer.”
Since TRAP-1 is known to regulate cell death, the researchers decided to study its role in prostate cancer. They found that the protein was highly expressed in both high-grade human prostate cancer lesions and mouse models of prostate cancer but not in benign or normal prostate tissue.
In addition, TRAP-1 overexpression in noncancer prostate cells inhibited cell death, whereas TRAP-1-deficient prostate cancer cells had enhanced levels of cell death. Moreover, treatment with gamitrinibs, a class of small molecules that inhibit TRAP-1, resulted in prostate cancer cell death but not death of noncancerous prostate cells.
Dario C. Altieri, M.D., who led this research, reported in February on the synthesis and properties of gamitrinib as a treatment for prostate cancer in The Journal of Clinical Investigation. He designed gamitrinibs to selectively target Hsp90 in human tumor mitochondria. TRAP-1 is a mitochondria-localized Hsp90 chaperone. Therefore, Dr. Altieri believes that based on his research, targeting TRAP-1 via gamitrinib may be a viable therapeutic strategy for patients with advanced prostate cancer.
Dr. Altieri’s experiments also found that TRAP-1 was differentially expressed in localized and metastatic prostate cancer compared with normal prostate.
A similar approach may be also suitable for other types of cancer, as TRAP-1 is broadly expressed in disparate human malignancies, Dr. Altieri continues. He plans to “further dissect the biology of TRAP-1 cytoprotection in cancer cells and test whether disabling its function may overcome drug resistance, the most common reason of treatment failure and dismal outcome in patients with advanced prostate cancer.”
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