Archive for the ‘Natural Therapies’ Category

Garden-variety berries provide about the same cancer-fighting punch as more exotic ones

Posted 16 Jun 2010 — by James Street
Category Natural Therapies

By Nathan Seppa, Science News

Garden-variety berries provide about the same cancer-fighting punch as more exotic ones, a study of rats with esophageal cancer shows. A separate study finds a potentially protective effect against breast cancer as well.
Click here to find out more!

Cancer biologist Gary Stoner of Ohio State University in Columbus and his colleagues tested seven berry types against cancer of the esophagus in rats —black raspberries, red raspberries, blueberries, strawberries, noni berries, açai berries and wolfberries (also called goji berries).

The scientists injected the animals with a carcinogenic chemical and gave some of the rats normal food, while others got similar chow containing 5 percent of one of the berries in dehydrated form.

While nearly all of the rats fed normal chow developed tumors rapidly, only about two-thirds of the berry-supplemented rats did. Overall, these rats had about half as many tumors as the others, the researchers report in the June Pharmaceutical Research. The berry-fed rats also had lower concentrations of interleukin-5 and a rat version of interleukin-8, inflammatory proteins implicated in esophageal cancer.

Earlier work by Stoner’s group found that black raspberries contain ample amounts of the two cancer-fighting compounds ellagitannin and anthocyanin. Ellagitannins also show up in nuts, pomegranates and other berries, while anthocyanins give many berries a red, purple or blue color.

But the new work shows that a berry need not have large concentrations of either compound to be a cancer fighter. For example, blueberries and açai berries are high in anthocyanins but low in ellagitannins. And wolfberries are low in both, Stoner says.

“There may be different things in different berries that are providing these [anticancer] effects,” says Ramesh C. Gupta, a cancer biologist at the University of Louisville School of Medicine in Kentucky. “It’s a good thing,” he says, since availability varies by region.

In the other study, Gupta and his colleagues induced breast cancer in female rats by implanting estrogen in the animals. Some animals received a diet comprising 2.5 percent dehydrated blueberries or black raspberries and others got food without berries. Those getting berries showed less tumor growth, the researchers report in the June Cancer Prevention Research. The berries also decreased activation of two genes implicated in breast cancer, CYP1A1 and CYP1B1.

Although the various berries tested in these studies differ from one another in chemical composition, they have things in common, such as an anti-inflammatory effect, Stoner says. They also contain cellulose, lignin and pectin. These fibrous compounds “may be the common denominator,” he says, because in digesting these fibers, the body makes butyrate, which previous research has shown may have anticancer properties.

“It could be the presence of more conventional antioxidants such as the carotenoids, or more likely vitamin C, which was not measured in this study,” says Susan Duthie, a nutritional biochemist at the University of Aberdeen in Scotland.

In any case, the potent anticancer effect of berries shown in lab-dish and animal studies has yet to be replicated in people, she cautions. A huge European study reported earlier this year found only very modest protection against cancer from a diet high in fruits and vegetables. “There is stronger protective evidence for berries and the compounds in them against heart disease and cognitive decline in humans,” Duthie says.

Dramatically Effective New Natural Way to Starve Cancer and Obesity

Posted 14 Jun 2010 — by James Street
Category Natural Therapies, Nutrition and Cancer

The Angiogenic Foundation

Green Tea slows all cancer growth

Posted 13 Jun 2010 — by James Street
Category Natural Therapies

16/03/2004 A powerful antioxidant found in green tea may be responsible for the beverage`s heralded anticancer benefits.
New research shows that the antioxidant, known as EGCG, binds to a protein found on tumor cells and dramatically slows their growth.
Researchers say previous studies have shown that green tea helps protect against a variety of cancers, such as lung, prostate, and breast, but the mechanisms for these effects are not known.
In the study, published in the April issue of Nature Structural & Molecular Biology, researchers identified a potential target for the antitumor action of EGCG on human lung cancer cells that inhibited cancer cells` growth. By learning more about this target, researcher may be able to develop new treatments that maximize green tea`s cancer-fighting potential.
In order to better understand how the antioxidants found in green tea may protect against cancer, researchers looked at how they affected a protein found on the surface of cancer cells called laminin receptor.
The study showed that when cancer cells with this protein were treated with polyphenol EGCG, the growth of the tumor cells was significantly reduced.
Researchers say the concentration of the antioxidant required to produce these anticancer effects was equivalent to those found in the body after drinking only two to three cups of green tea.
Other components found in green tea, including caffeine, had no effect on tumor cell growth.
Researchers say the results further the understanding of how antioxidants interact with cancer cells and may one day lead to more effective cancer therapies that use green tea as a dietary cancer treatment.

Gamma-tocotrienol kills prostate tumour cells in animal model studies

Posted 10 Apr 2010 — by James Street
Category Natural Therapies, Prostate Cancer

9. April 2010 09:45

Researchers from Davos Life Science in Singapore, in collaboration with scientists at the University of Hong Kong, have shown that gamma-tocotrienol, a member of the vitamin E family, is potent in killing prostate tumour cells in animal model studies. This research was reported this week in the latest edition of Pharmacology. These findings come soon after previously published research studies that demonstrated in-vitro evidence of gamma-tocotrienol’s cancer-killing capability for breast cancer and melanoma cells.

In this latest study, immuno-compromised mice with human-grafted prostate tumours were given two weeks’ dosing of gamma-tocotrienol. Researchers saw that gamma-tocotrienol was selectively deposited in solid tumours, and this led to over 50% tumour shrinkage. Linked to this tumour shrinkage ability, gamma-tocotrienol showed two effects associated with the killing of cancer cells. Firstly, there was a decrease in the expression of two cell proteins (PCNA and Ki67) associated with cell proliferation. Secondly, there was the activation of cellular processes called caspase cascades that are associated with programmed cell death. These inhibitive properties have been previously reported in studies investigating the effect of gamma-tocotrienol on breast cancer and melanoma. Together, these data suggest a common mechanism by which gamma-tocotrienol is able to reverse the growth of cancer cells.

This study also found that the anti-tumour effect of gamma-tocotrienol was mediated by the suppression of the NF-KB cell signaling pathway. NF-B is a protein that signals to the cell to produce chemicals that promote the body’s natural inflammation response and cell survival. Over activation of NF-B is associated with chronic inflammation. There is emerging evidence that chronic inflammation contributes to carcinogenesis and the development of malignancy in various organs, including the prostate, breast and skin.

“Previous studies have established natural tocotrienol as a promising opportunity for future R&D in cancer therapy and prevention,” said Dr. Daniel Yap, Deputy Head for Tocotrienol R&D, Davos Life Science Singapore, and one of the authors of the published paper. “This research contributes further evidence to this cause, showing that natural tocotrienol can potentially reduce the risks of diseases associated with chronic inflammation, including certain cancers.”

Combining gamma-tocotrienol with other chemotherapy treatments

The inhibition of tumour growth was achieved when used in a combination treatment of gamma-tocotrienol and Docetaxel (DTX). Currently, DTX is the first-line chemotherapy treatment in patients with prostate cancer that is resistant to hormone therapy. However, DTX can only extend the patient’s overall survival by an average of 2-3 months. As the gamma-tocotrienol’s anti-tumour effects were observed using physiologically-relevant doses that do not negatively affect animal health, this may provide a new treatment strategy that can improve the therapeutic efficacy of DTX against advanced stage prostate tumours, while reducing toxicity often seen in patients treated with DTX.

Gamma-tocotrienol is one of eight forms of vitamin E. It is found in low levels in food sources such as palm fruits, cereal grains and rice bran. The amount of gamma-tocotrienol found in palm oil is relatively higher than in other sources. In previous in-vitro studies, gamma-tocotrienol was shown to be able to kill prostate, melanoma, breast and pancreatic cancer cells.

Dr. Daniel Yap added, “In addition to this prostate cancer study, we are also advancing our Phase I clinical trial in the U.S. on pancreatic cancer. We expect to accelerate our tocotrienol research for the treatment and prevention of cancers. This latest study is yet another step forward in identifying potentially-effective naturally derived treatments that might have applications for cancer patients.”

SOURCE Davos Life Science

Danish Research Confirms Rath Discovery: Enzyme Block Stops Cancer Spread

Posted 27 Feb 2010 — by James Street
Category Molecular Osteosarcoma Studies, Natural Therapies

November 28, 2004

Danish Research Confirms Rath Discovery: Enzyme Block Stops Cancer Spread

Research done at Copenhagen University and published in the International Journal of Cancer confirms a discovery made by Dr. Mathias Rath, the controversial founder of a new direction in health care called Cellular Medicine. The Danish study found that the enzyme urokinase plasminogen activator plays a critical role in the spread of cancer. Absence of the enzyme prevents the forming of metastases.

While the Danish researchers are now looking for a medication capable of eliminating the enzyme, Dr. Rath and his researchers have already found that our bodies have a natural mechanism that blocks the enzyme, which can be reinforced by abundantly supplying certain nutrients: vitamin C and the aminoacids lysine and proline.

Notorious “quackbuster” Stephen Barrett put his foot in his mouth when he cited a comment from the Swiss Study Group for Complementary and Alternative Methods in Cancer (SKAK) and the Swiss Cancer League (SCL) that Rath’s discovery was not somehing to be reckoned with, as it had “never been scientifically tested”. A very lazy way of making nothing of someone else’s discovery, to be sure, but one that is widely used by the current pharma/medical establishment when it comes to “warning” of natural cures that could significantly cut into pharma profits by using non-patentable substances such as simple nutrients to fight disease.

Matthias Rath Institute

Johns Hopkins scientists have shown that in mice at least, vitamin C – and potentially other antioxidants – can indeed inhibit the growth of some tumors

Posted 26 Feb 2010 — by James Street
Category Molecular Osteosarcoma Studies, Natural Therapies

How Vitamin C Stops Cancer

Science Daily — Nearly 30 years after Nobel laureate Linus Pauling famously and controversially suggested that vitamin C supplements can prevent cancer, a team of Johns Hopkins scientists have shown that in mice at least, vitamin C – and potentially other antioxidants – can indeed inhibit the growth of some tumors ¯ just not in the manner suggested by years of investigation.
The conventional wisdom of how antioxidants such as vitamin C help prevent cancer growth is that they grab up volatile oxygen free radical molecules and prevent the damage they are known to do to our delicate DNA. The Hopkins study, led by Chi Dang, M.D., Ph.D., professor of medicine and oncology and Johns Hopkins Family Professor in Oncology Research, unexpectedly found that the antioxidants’ actual role may be to destabilize a tumor’s ability to grow under oxygen-starved conditions. Their work is detailed this week in Cancer Cell.

“The potential anticancer benefits of antioxidants have been the driving force for many clinical and preclinical studies,” says Dang. “By uncovering the mechanism behind antioxidants, we are now better suited to maximize their therapeutic use.”

“Once again, this work demonstrates the irreplaceable value of letting researchers follow their scientific noses wherever it leads them,” Dang adds. (Yessss.)

The authors do caution that while vitamin C is still essential for good health, this study is preliminary and people should not rush out and buy bulk supplies of antioxidants as a means of cancer prevention.

The Johns Hopkins investigators discovered the surprise antioxidant mechanism while looking at mice implanted with either human lymphoma (a blood cancer) or human liver cancer cells. Both of these cancers produce high levels of free radicals that can be suppressed by feeding the mice supplements of antioxidants, either vitamin C or N-acetylcysteine (NAC).

However, when the Hopkins team examined cancer cells from cancer-implanted mice not fed the antioxidants, they noticed the absence of any significant DNA damage. “Clearly, if DNA damage was not in play as a cause of the cancer, then whatever the antioxidants were doing to help was also not related to DNA damage,” says Ping Gao, Ph.D, lead author of the paper.

That conclusion led Gao and Dang to suspect that some other mechanism was involved, such as a protein known to be dependent on free radicals called HIF-1 (hypoxia-induced factor), which was discovered over a decade ago by Hopkins researcher and co-author Gregg Semenza, M.D., Ph.D., director of the Program in Vascular Cell Engineering. Indeed, they found that while this protein was abundant in untreated cancer cells taken from the mice, it disappeared in vitamin C-treated cells taken from similar animals.

“When a cell lacks oxygen, HIF-1 helps it compensate,” explains Dang. “HIF-1 helps an oxygen-starved cell convert sugar to energy without using oxygen and also initiates the construction of new blood vessels to bring in a fresh oxygen supply.”

Some rapidly growing tumors consume enough energy to easily suck out the available oxygen in their vicinity, making HIF-1 absolutely critical for their continued survival. But HIF-1 can only operate if it has a supply of free radicals. Antioxidants remove these free radicals and stop HIF-1, and the tumor, in its tracks.

The authors confirmed the importance of this “hypoxia protein” by creating cancer cells with a genetic variant of HIF-1 that did not require free radicals to be stable. In these cells, antioxidants no longer had any cancer-fighting power.

The research was funded by the National Institutes of Health.

Authors on the paper are Dean Felsher of Stanford; and Gao, Huafeng Zhang, Ramani Dinavahi, Feng Li, Yan Xiang, Venu Raman, Zaver Bhujwalla, Linzhao Cheng, Jonathan Pevsner, Linda Lee, Gregg Semenza and Dang of Johns Hopkins.

Note: This story has been adapted from a news release issued by Johns Hopkins Medical Institutions.

Vitamin D shown to be effective in interfering with osteosarcoma metastasis biochemistry

Posted 25 Feb 2010 — by James Street
Category Human osteosarcoma research, Natural Therapies

Vitamin D’s Anti-tumorigenic Properties in Bone Involve Upregulation of MAPK and AP-1/p21waf1

Cancer Lett. 2007 Aug 28;254(1):75-86, Wei Wu, Xiaoyu Zhang, Laura P. Zanello

The molecular mechanisms underlying antiproliferative actions of the steroid 1α,25-dihydroxy vitamin D (1,25D) in human osteosarcoma cells are known only partially. To better understand the signaling involved in 1,25D anti-tumorigenic properties in bone, we stably silenced vitamin D receptor (VDR) expression in the human osteosarcoma SaOS-2 cell line. We found that 1,25D treatment reduced cell proliferation by approximately 25% after 3 days only in SaOS-2 cells expressing native levels of VDR protein, and involved activation of MAPK/AP-1/p21 pathways. Both sustained (3 days) and transient (15 min) 1,25D treatment activated JNK and ERK1/2 MAPK signaling in a nongenomic VDR-dependent manner. However, only sustained exposure to hormone led to upregulation of p21 and subsequent genomic control of the cell cycle. Specific blockade of MEK1/MEK2 cascade upstream from ERK1/2 abrogated 1,25D activation of AP-1 and p21, and subsequent antiproliferative effects, even in the presence of a nuclear VDR. We conclude that 1,25D-induced inhibition of human osteosarcoma cell proliferation occurs via sustained activation of JNK and MEK1/MEK2 pathways downstream of nongenomic VDR signaling that leads to upregulation of a c-Jun/c-Fos (AP-1) complex, which in turn modulates p21 gene expression. Our results demonstrate a cross-talk between 1,25D/VDR nongenomic and genomic signaling at the level of MAP kinase activation that leads to reduction of cell proliferation in human osteosarcoma cells.

Go to OncologySTAT for pdf file: Vitamin D Anti-tumorigenic properites in Bone