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Posts Tagged ‘prostate cancer’

Dehydrated tomatoes show promise for preventing prostate cancer

New research suggests that the form of tomato product one eats could be the key to unlocking its prostate cancer-fighting potential, according to a report in the June 1 issue of Cancer Research, a journal of the American Association for Cancer Research.

“Processing of many edible plants through heating, grinding, mixing or drying dramatically increases their nutrition value, including their cancer prevention potential. It appears that the greatest protective effect from tomatoes comes by rehydrating tomato powder into tomato paste,” said Valeri V. Mossine, Ph.D., research assistant professor of biochemistry at the University of Missouri.

The protective effect of tomato products against prostate cancer has been suggested in many studies, but researchers remain uncertain about the exact mechanisms. Mossine and colleagues demonstrated that FruHis, an organic carbohydrate present in dehydrated tomato products, exerts a strong protective effect.

Researchers divided rats into groups of 20 and fed them a control diet or a diet that included tomato paste, tomato powder or tomato paste plus additional FruHis. All animals were then injected with prostate cancer-causing chemicals.

Animals fed the tomato paste plus FruHis diet had the longest survival from cancer at 51 weeks compared with 50 weeks in the tomato powder group, 45 weeks in the tomato paste alone group and 40 weeks in the control group.

On post-mortem exam, prostate tumors were found in 10 percent of the rats that had been given a combination of tomato paste and FruHis, compared with 30 percent of animals in the tomato powder group, 25 percent in the tomato paste alone group and 60 percent in the control group.

Mossine said the protective effect of tomato-based products was restricted to prostate tumors, which is consistent with other research on tomatoes and cancer. Incidence of other tumors was too small to examine.

In vitro, Mossine and colleagues evaluated the anti-cancer properties of FruHis and 14 other D-fructose amino acids and found that FruHis in a concentrated form protected against DNA damage known to lead to prostate cancer. When combined with lycopene, FruHis stopped cancerous cell growth more than 98 percent of the time.

“Before this study, researchers attributed the protective effect of tomatoes to ascorbic acid, carotenoids, or phenolic compounds,” Mossine said. “FruHis may represent a novel type of potential dietary antioxidant. Experiments like these suggest that a combination of FruHis and lycopene should be investigated as a potential therapeutic anti-tumor agent, not just a prevention strategy.”

Although Mossine cautioned against drawing broad conclusions from this animal study, he said, “the result may introduce an additional intrigue into an ongoing dispute over the beneficial effects of dietary lycopene and tomato products in lowering the risk of prostate cancer. Human trials are certainly warranted.”

Source: American Association for Cancer Research

Josh says:

The paper is not currently available. I wonder how long it will take for FruHis to be available as a supplement or added to multivitamins. It certainly should be easy enough to mass produce.

Estrogen helps drive distinct, aggressive form of prostate cancer

Using a breakthrough technology, researchers led by a Weill Cornell Medical College scientist have pinpointed the hormone estrogen as a key player in about half of all prostate cancers.

Estrogen-linked signaling helps drive a discrete and aggressive form of the disease caused by a chromosomal translocation, which in turn results in the fusion of two genes.

“Fifty percent of prostate cancers harbor a common recurrent gene fusion, and we believe that this confers a more aggressive nature to these tumors,” explains study senior author Dr. Mark A. Rubin, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College. Dr. Rubin is also attending pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

“Interfering with this gene fusion — or its downstream molecular pathways — will be crucial in the search for drugs that fight the disease. Based on our new data, we now believe that inhibiting estrogen may be one way of doing so,” he says.

The findings are published in the May 27 online edition of the Journal of the National Cancer Institute. Dr. Rubin conducted the study while at the Brigham and Women’s Hospital and in collaboration with Dr. Todd Golub and other members of the Broad Institute of MIT and Harvard, in Cambridge, Mass. His team is now continuing this line of research at Weill Cornell.

Dr. Rubin, along with researchers at the University of Michigan, first discovered and described the common fusions between the TMPRSS2 and ETS family member genes subset of prostate cancer in the journal Science in 2005. “The discovery showed that these malignancies occur after an androgen (male hormone)-dependent gene fuses with an oncogene — a type of gene that causes cancer,” he explains.

Experts have long understood that male hormones help spur prostate cancer — in fact, androgen-deprivation therapy is a first-line treatment against the disease. And yet the disease can progress despite androgen reduction, suggesting that other pathways might be at work.

“So, we wanted to learn more — what is the genetic and molecular ‘fingerprint’ of this aggressive subset of prostate tumor”" Dr. Rubin says.

Answering that question required the analysis of 455 prostate cancer samples from trials in Sweden and the United States that were conducted as far back as the mid-1970s.

“These samples were placed in fixative and not frozen, so we needed new methods of retrieving the genetic information,” Dr. Rubin says. To do so, his team led by co-lead authors Dr. Sunita Setlur and Dr. Kirsten Mertz developed an innovative technology for effectively “reading” the gene transcription profiles hidden in the samples.

“That led us to perform the largest gene-expression microarray analysis yet conducted in prostate cancer research, amassing information on more than 6,000 genes,” Dr. Rubin says. “This allowed us to obtain a robust, 87-gene expression ‘signature’ that distinguishes fusion-positive TMPRSS2-ERG cancers from other prostate malignancies.”

A close analysis of the signature yielded a surprise: that estrogen-dependent molecular pathways appear to play a crucial role in regulating (and encouraging) this aggressive subset of prostate cancer.

While estrogen is typically thought of as a “female” hormone, men produce it as well.

“Now, we show for the first time that this natural estrogen can stimulate the production of the cancer-linked TMPRSS2-ERG transcript, via the estrogen receptor (ER)-alpha and ER-beta. These receptors are found on the surface of some prostate cancer cells,” Dr. Rubin explains.

The finding could have implications for prostate cancer research, including drug development. According to Dr. Rubin, “We now believe that agents that dampen estrogen activity (ER-beta antagonists) could inhibit fusion-positive prostate cancers. Alternatively, any intervention that boosts estrogen activity (ER-alpha) might also give a boost to these aggressive malignancies.”

Research into just why fusion-positive prostate cancers are so aggressive — and potential molecular drug targets to help curb that aggression — will continue under Dr. Rubin’s direction at Weill Cornell, in collaboration with members of his group and with computational biologist Dr. Francesca Demichelis.

“The technological achievement of using fixed samples that were up to 30 years old is significant,” Dr. Rubin says. “In the future, we hope to explore banked tissues from clinical trials to help understand why they failed. This should lead to insight for designing the next trial.”

Source: New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College

Sunita R. Setlur, Kirsten D. Mertz, Yujin Hoshida, Francesca Demichelis, Mathieu Lupien, Sven Perner, Andrea Sboner, Yudi Pawitan, Ove Andrén, Laura A. Johnson, Jeff Tang, Hans-Olov Adami, Stefano Calza, Arul M. Chinnaiyan, Daniel Rhodes, Scott Tomlins, Katja Fall, Lorelei A. Mucci, Philip W. Kantoff, Meir J. Stampfer, Swen-Olof Andersson, Eberhard Varenhorst, Jan-Erik Johansson, Myles Brown, Todd R. Golub, and Mark A. Rubin. Estrogen-Dependent Signaling in a Molecularly Distinct Subclass of Aggressive Prostate Cancer. Journal of the National Cancer Institute Advance Access published on May 27, 2008. doi:10.1093/jnci/djn150

Josh says:

This has a lot of potential to help prostate cancer patients. Knowing that we should also try to inhibit estrogen and estrogen production in these patients is a novel strategy and hopefully will help save a lot of lives.

Major collaboration uncovers surprising new genetic clues to diabetes

An international team that included scientists from the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health (NIH), today reported it has identified six more genetic variants involved in type 2 diabetes, boosting to 16 the total number of genetic risk factors associated with increased risk of the disease. None of the genetic variants uncovered by the new study had previously been suspected of playing a role in type 2 diabetes. Intriguingly, the new variant most strongly associated with type 2 diabetes also was recently implicated in a very different condition: prostate cancer.

The unprecedented analysis, published today in the advance online edition of Nature Genetics, combined genetic data from more than 70,000 people. The work was carried out through the collaborative efforts of more than 90 researchers at more than 40 centers in Europe and North America.

“None of the genes we have found was previously on the radar screen of diabetes researchers,” said one of the paper’s senior authors, Mark McCarthy, M.D., of the University of Oxford in England. “Each of these genes, therefore, provides new clues to the processes that go wrong when diabetes develops, and each provides an opportunity for the generation of new approaches for treating or preventing this condition.” … Continue Reading »