Dogs with osteosarcoma most commonly exhibit lameness or pain at the metaphyseal sites, and radiographs often reveal bone lesions.

Large and giant breed dogs are more likely to be affected, possibly because of the rapid growth that occurs in young larger breed dogs.

Previous bony fractures are also thought to possibly cause osteosarcoma, because of chronic bone irritation sometimes associated with injury.

Osteosarcomas are most likely to be found on the distal radius and the proximal humerus of the forelimb.

A key indication of osteosarcoma is a bone lesion not crossing a joint space that has evidence of bone lysis.

Radiographs may reveal lung metastases, which occur only in late stages of this tumor. If they are present, the dog has a poor prognosis.

90% of dogs will die of metastatic disease, even though metastasis may not be initially evident on radiographs.

Metastasis to the lungs often becomes evident after surgical removal of the primary osteosarcoma.

High-detail radiographs of the lesions and radiographs of the thorax are the first step towards diagnosing osteosarcoma in dogs.

The diagnosis is confirmed through a biopsy, taken at the time of limb amputation. Multiple biopsies are often taken from the middle of the tumor to confirm diagnosis.

Treatment of Osteosarcoma in dogs

Amputation of the limb affected by the osteosarcoma is the most common treatment for this disease.

This aggressive treatment is often results in a reasonable quality of life for the dog and offers a good prognosis.

In some cases, the affected limb may be spared, especially in dogs with a preexisting orthopedic or neurological condition, where limb loss would prove severely debilitating.

In such situations, radiation therapy is often used to treat osteosarcoma, along with surgical excision of the tumor along with a large section of the bone.

Chemotherapy is recommended after surgery in order to attack remaining cancer cells that may not have been removed.

Though tumor excision may salvage the limb, there are potential complications associated with this option.

The two most common are:

1) recurrent local disease; and

2) allograft infection (since bone allografts are often necessary to replace some of the excised bone).

Even after limb amputation, osteosarcoma often recurs as metastases to the lungs. The reason for this recurrence is thought to be due to cancer cells which had already seeded the lungs, but which were unable to grow when the primary, or first, tumor was present on the limb.

Primary tumors are known to produce certain angiogenesis inhibitors, such as angiostatin and endostatin, which circulate in the bloodstream and act to suppress the growth of cancer cells in distant organs.

When the primary tumor is removed by amputation, the presence of these inhibitors is reduced, allowing those distant cancer cells to grow.

Dogs with osteosarcoma were recently shown to secrete angiostatin in their urine, which disappears once their tumor is removed.

Hence, antiangiogenic therapy may prove to be useful to treat osteosarcoma in the limb, as well as to prevent metastases.

In animal studies, various angiogenesis inhibitors have been shown to reduce osteosarcoma growth, including anti-VEGF antibody, AGM-1470, and vitamin D3. These agents have not yet been formally studied in formal canine trials.

Harimaya K, Tanaka K, Matsumoto Y, Sato H, Matsuda S, Iwamoto Y.

Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Osteosarcoma is the most frequent malignant bone tumor in children. It is highly invasive, however, the mechanisms behind osteosarcoma cell invasion are as yet still unknown.

In the present study, treatment with TNFalpha enhanced the invasiveness of two human osteosarcoma cell lines, OST and MNNG.

TNFalpha treatment also induced tumor cell motility, adhesion to laminin, the expression of matrix metalloproteinase 9 (MMP9), and the nuclear translocation of nuclear factor kappaB (NFkappaB) in the osteosarcoma cells.

Moreover, antioxidants inhibited TNFalpha-induced osteosarcoma cell invasion, motility and NFkappaB nuclear translocation, but not adhesion to laminin or MMP9 expression.

NFkappaB decoy, another NFkappaB inhibitor, also inhibited TNFalpha-induced osteosarcoma cell invasion and motility.

Therefore, motility and NFkappaB activation were possibly related to TNFalpha-induced osteosarcoma cell invasion.

However, adhesion to laminin or MMP did not demonstrate any correlation with TNFalpha-induced osteosarcoma cell invasion.

Although NFkappaB is known to regulate TNFalpha-induced phenotypes, it may influence only motility and invasion, but not the MMP or laminin-mediated adhesion of these osteosarcoma cells.

Artemisinin Blocks Prostate Cancer Growth and Cell Cycle Progression by Disrupting Sp1 Interactions with the Cyclin-dependent Kinase-4 (CDK4) Promoter and Inhibiting CDK4 Gene Expression^*

Todesco A, Carli M, Iacona I, Frascella E, Ninfo V, Rosolen A.

Clinica di Oncoematologia Pediatrica, Azienda Ospedaliera-Universita di Padova, Padova, Italy.

BACKGROUND: A boy age 14 years who was in complete remission from Stage IIB small cell osteosarcoma, which was misdiagnosed as Ewing sarcoma and consequently was treated, developed inoperable lung metastases when he was off therapy.

He received second-line treatment for recurrent Ewing sarcoma, including chemotherapy and radiotherapy, and obtained only a temporary response.

A compassionate treatment with all-trans retinoic acid (ATRA) and interferon-alpha (IFNalpha) was then undertaken.

METHODS: The patient initially was treated according to the national SE91 protocol for nonmetastatic Ewing sarcoma. After a bilateral pulmonary recurrence, he received second-line chemotherapy and irradiation of the largest metastasis, with a temporary partial response.

The patient was then treated with a combination of oral ATRA (All-trans retinoic acid
) (90 mg/m(2) for 3 days per week) and subcutaneous IFNalpha (3 x 10(6) U/m(2) 5 days per week) for 4 months.

The same therapy also was administered for the control of residual disease after surgery for a total duration of 1 year of ATRA/IFN treatment. During the first 3 weeks of therapy, ATRA pharmacokinetics were studied.

RESULTS:

After progression of the patient’s disease, despite the administration of first-line and second-line chemotherapy, combined treatment with ATRA/IFNalpha yielded a partial remission, which allowed surgical resection of the largest metastasis.

The same therapy was effective in preventing tumor recurrence after incomplete removal of the remaining metastases.

Treatment was well tolerated, and the patient is in stable complete remission 14 months after the end of therapy.

The pharmacokinetics results confirmed the indication of an intermittent schedule for oral ATRA therapy.

CONCLUSIONS:

ATRA/IFNalpha treatment may be considered as an alternative approach in the treatment of patients with metastatic osteosarcoma who have disease that is resistant to conventional chemotherapy and in the treatment of patients with minimal tumor residue.

Copyright 2000 American Cancer Society.

He proposes worldwide policy changes regarding people’s vitamin D daily intake amount in order to maximize the vitamin’s contribution to reducing the frequency of many diseases, including childhood rickets, adult osteomalacia, cancer, autoimmune type-1 diabetes, hypertension, cardiovascular disease, obesity and muscle weakness, according to an August 9, 2010 news release, “Biochemist proposes worldwide policy change to step up daily vitamin D intake.”

“A reduction in the frequency of these diseases would increase the quality and longevity of life and significantly reduce the cost of medical care worldwide,” Norman explained in the news release. He added, “It is high time that worldwide vitamin D nutritional policy, now at a crossroads, reflects current scientific knowledge about the vitamin’s many benefits and develops a sound vision for the future.”

Currently, the recommended daily intake of vitamin D in the United States is 200 international units (IU) for people up to 50 years old; 400 IU for people 51 to 70 years old; and 600 IU for people over 70 years old. Today there is a wide consensus among scientists that the relative daily intake of vitamin D should be increased to 2,000 to 4,000 IU for most adults.

“Worldwide public health is best served by a recommendation of higher daily intakes of vitamin D,” Norman said in the news release. “Currently, more than half the world’s population gets insufficient amounts of this vitamin. At present about half of elderly North Americans and Western Europeans and probably also of the rest of the world are not receiving enough vitamin D to maintain healthy bone.”

Reporting in a review paper in the July 28, 2010, issue of Experimental Biology and Medicine, Norman and Roger Bouillon of the Laboratory of Experimental Medicine and Endocrinology at the Katholieke Universiteit Leuven, Belgium, warn that if the current nutritional guidelines for vitamin D remain unchanged, rickets and osteomalacia, which could be easily prevented, will continue to occur.

They add that if the present guidelines for vitamin D intake are strictly implemented and applied worldwide to pregnant or lactating women, newborns and children, the occurrence of rickets in infants could be effectively eradicated.

Norman, the first author of the review paper, and Bouillon note that if the daily dietary intake of vitamin D is increased by 600-1000 IU in all adults above their present supply, it would bring beneficial effects on bone health in the elderly and on all major human diseases (for example, cancer, cardiovascular, metabolic and immune diseases).

The researchers add, however, that if the vitamin D dietary intake were increased to 2000 IU per day and even more for subgroups of the world population with the poorest vitamin D status, it could favorably impact multiple sclerosis, type-1 diabetes, tuberculosis, metabolic syndrome, cardiovascular risk factors and most cancers. Interestingly, there are theories (not related to this study) that multiple sclerosis is somehow related to a type of herpes virus. More research needs to be done on this topic.

About vitamin D:

Also known as the “sunshine vitamin,” vitamin D was discovered 90 years ago as a dietary agent that prevented the bone disease rickets. Exposure to the sun is the body’s natural way of producing the vitamin. Skin exposed to solar UVB radiation can produce significant quantities of vitamin D. But this vitamin D synthesis is reliably available year-round only at latitudes between 40 degrees north and 40 degrees south. A combination of sunshine, food, supplements, and possibly even limited tanning exposure can raise the daily intake of the vitamin to 2000 IU.

Vitamin D is itself biologically inert. Its biological effects result only after it is metabolized first in the liver and then in the kidney – a process that converts the vitamin into a steroid hormone. The best sources of unfortified foods naturally containing vitamin D are animal products and fatty fish and liver extracts like salmon or sardines and cod liver oil. Vitamin D-fortified food sources in the United States (the fortification levels aim at about 400 IU per day) include milk and milk products, orange juice, breakfast cereals and bars, grain products, pastas, infant formulas and margarines.

Watch Out for Vitamin D Excess

Vitamin D excess can cause health problems such as hypercalcemia, vomiting, thirst and tissue damage. The precise upper limit for daily vitamin D intake is not well defined. Just who is researching vitamin D excess or genetic problems of some people who don’t do well on too much vitamin D?

The University of California, Riverside campus is planning a medical school. Locally, in the Sacramento-Davis regional area, UC Davis also is researching the effects of vitamin D on humans.

UC Davis Researches the Effects of Vitamin D on Humans

University of California, Davis studies the effects of vitamin K-2 on human health. Check out the research of Dr. Paul Davis, a nutritionist in the Department of Nutrition and Food Science, UC Davis, and a researcher with the UC Davis Cancer Center. Dr. Davis´ research focuses on the interaction of dietary constituents (macronutrients and nonnutritional components) with processes/risk factors for chronic human diseases (i.e. coronary vascular disease and cancer). He also studies the effects of dietary fiber and other components (dietary lipids particularly) on control of food intake and processes of nutrient absorption and packaging/secretion in the gastrointestinal tract.

Many current reports in nutrition-oriented literature refer to nutrient retentions for processing, storage and cooking that were compiled more than 25 years ago. So it’s necessary for scientists to keep doing current studies.

Walnut Consumption Slows Prostrate Cancer Growth in Mice

A few months ago in March, 2010, a study at UC Davis reported that walnut consumption slows the growth of prostate cancer in mice and has beneficial effects on multiple genes related to the control of tumor growth and metabolism, according to researchers at UC Davis and the U.S. Department of Agriculture Western Regional Research Center in Albany, Calif. have found.

The study, by Paul Davis announced the findings March 22, 2010 at the annual national meeting of the American Chemical Society in San Francisco. Davis explained at the conference that the research findings provide additional evidence that walnuts, although high in fat, are healthful.

“This study shows that when mice with prostate tumors consume an amount of walnuts that could easily be eaten by a man, tumor growth is controlled,” he reported to Science Daily, published online March 23, 2010 in the article, Walnuts Slow Prostate Tumors in Mice, Study Finds. “This leaves me very hopeful that it could be beneficial in patients,” Dr. Davis explained to Science Daily.

Vitamin D Health Benefits Study

Also see the study, Effects Of Vitamin D Deficiency Amplified By Shortage Of Estrogen,17 November 2009. Researchers at Johns Hopkins reported what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone.

How Does Vitamin D work in the human body?

What does vitamin D actually do? It plays an important role in calcium balance so you get normal bone strength. The major function of vitamin D is to improve the efficiency of calcium absorption from the small intestine, according to Dr. Ray Sahelian’s newsletter and nutrition information sites. Can taking too much vitamin D calcify your aorta? What are the risks? And do you have to inherit a specific gene variation for vitamin D to calify your coronary arteries? What does the research show?

What happens to the way your body handles, absorbs, or builds up vitamin D after menopause when the estrogen level plummets? And were you born with or without the gene variation that takes the vitamin D3 you eat along with the calcium and calcifies your arteries with it instead of putting it into your bones where it belongs? How do you find a genetics/DNA test to tell you whether you have inherited that genetic mutation or variation?

Epidemiological data show low levels of vitamin D lead to a higher incidence of breast cancer, colon cancer, prostate cancer, ovarian cancer, as well as multiple myeloma, according to Dr.Sahelian’s site. Patients with Crohn’s disease are known to have low levels. Vitamin D supplementation may even improve mood during the winter months, according to Dr. Sahelian. But you’d be better off taking less than more until you know how much you’ll really need of vitamin D.

Scientists repeatedly warn vitamin consumers of the danger regarding excessive intake. Vitamin D taken in high amounts can cause excessive calcification of bone, calcification of soft tissue, kidney stones, headaches, weakness, nausea, and vomiting.

There answer right now is that no one knows exactly the long-term effects of high dose daily use of vitamin D. Find out whether or not you need to supplement at all. Research is ongoing. In the meantime, are you taking a teaspoon full of cod liver oil that already has 400 units of vitamin D in it along with some vitamin A? Look at the label and see whether it tell you the vitamin content of the oil. How do you compare the different answers given by your various heathcare professionals?

When you take all those vitamin D3 supplements that are recommended in so many articles in the media, how do you know whether your body will use it to protect your organs against bone loss or use it to send calcium deposits into your organs, heart valves, and arteries?

Find out from your doctor whether or not your blood test tell you that you may or may not need to supplement. Does your diet have plenty of vitamin D? Do you get enough sun exposure?

Most people may benefit from taking 400 units a day either as part of a multivitamin product and a balanced diet. A few people without much sun exposure and a poorer diet, or if you live in latitudes where there’s not much sun, might benefit from 600-800 units of vitamin D3.

The only questions scientists have is that over a long term, we don’t know what the risks are. You’re doctor should talk with you if you have chronic medical conditions whether you need up to 1,000 units daily. But the question is for how long without posing a risk of calcifying your arteries from too high a dose for too long a time of taking supplements of vitamin D.

When you do take a supplement, be sure it’s natural vitamin D3, not synthetic vitamin D2. The conclusion is the final word is not yet in on the danger of calcifying your brain and arteries with too much vitamin D supplementation.

Why take the risk when you can keep your supplementation, if any, to a dose related to what your body needs. You can find out what vitamin deficiencies you have by taking a test to see what’s actually absorbed into your cells and what’s just floating in your bloodstream.

What needs to be evaluated right now is whether other genes that control calcium homeostasis are involved in the pathogenesis of this disorder. In plain language, how many gene variations control the way calcium and vitamin D3 are processed in your own body? And how can you find out? Are there genetic tests that show you how your body handles vitamin D3?

The media is full of articles saying that the 400 mg of vitamin D3 is too little to protect you against cardiovascular problems, that you probably need 1,000 mg. But what happens if you have a genetic variation or mutation that communicates to your body in a different way, where when you take vitamin D3 and calcium in supplements or at high food intakes, that the calcium doesn’t go into your bones, but into the arteries and valves around your heart? Will vitamin K2 in the MK-7 form protect you from calcification if you have this genetic variation? And where can you find out if it will?

Another article at BioMed Experts, Osteoporosis and calcification of the aorta, Bone and Mineral, 1992;19(2):185-94,1992: Frye M A; Melton L J; Bryant S C; Fitzpatrick L A; Wahner H W; Schwartz R S; Riggs B L, notes, “Aortic calcification was not associated with any measures of calcium metabolism, after adjusting for age, except for a slight negative association between linear aortic calcifications and 25(OH) vitamin D levels (P < 0.05).”

Another abstract of a 2003 article, “Influence of sex and estrogen on vitamin D-induced arterial calcification in rats” notes, “It is known that the process of arteriosclerosis is affected by sex and estrogen. The present study was thus undertaken to examine the effects of these factors on arterial calcification, a form of arteriosclerosis, using a rat model of vitamin D toxicity.

The article concludes with, “These results suggest that sex and estrogen can modify the process of arterial calcification. The mechanisms remain to be determined, although the effects were independent of serum calcium level.”

Food for Bones

What other vitamin works along with vitamin D3? An extract of natto, a fermented soy food from Japan, is particularly rich in the highly bioavailable form of vitamin K2 called menaquinone-7 (MK-7), linked to greater bone health and reduction in risk factors. PL Thomas & Co. Inc. (PLT) announced the launch of Natural Vitamin K2 as a newly available proprietary extract under the trademark MenaQ7™.

Natural Vitamin K2 helps keep calcium in the bones and out of the arteries, providing significant potential health benefits. Natural Vitamin K2 also may provide significant benefit to cardiovascular health due to its roles in calcium utilization. Also see the UC Davis study, Temporary reversal of anticoagulation using oral vitamin K.

Scientists also study vitamin K-2 along with vitamin D. For further information, see page 253 in the book titled, The Cholesterol Hoax, by Sherry Rogers, M.D. where the physician explains the potent protection of vitamin K2. She reports that, “Folks who have higher levels of vitamin K2 have a 57% reduction in heart disease (Geleijnse).” The reason is that Vitamin K2 controls calcium regulation and “specifically inhibits arterial vascular calcifications” (Vermeer, Shearer, Schugers.).” The physician also notes that “Vitamin K decreases circulating cholesterol. (Kawashima).”

Of course you need vitamin D3 to absorb calcium as well, and you also need magnesium in balance. So check out these references to research studies. There’s an excellent article on what vitamin K2 does for the body, especially an aging one, in the July 2008 issues of the Total Wellness newsletter.  And in the January 2009 issue, it’s packed with information on vitamin D3 and what it does for bones and arteries along with vitamin K2. Don’t exceed a daily dose of 100 mgs. of K2 in the MK-7 form with natto.

Investigators from Complutense University in Madrid assessed the anti-tumor potential of THC and JWH-133, a non-psychotropic CB2 receptor-selective agonist, in the treatment of ErbB2-positive breast tumors – a highly aggressive form of breast cancer that is typically unresponsive to standard therapies.

Researchers reported, “[B]oth Delta-9-tetrahydrocannabinol … and JWH-133 …reduce tumor growth [and] tumor number [in mice]. … [T]hese results provide a strong preclinical evidence for the use of cannabinoid-based therapies for the management of ErbB2-positive breast cancer.”

In 2007, investigators at the California Pacific Medical Center Research Institute reported that the administration of the nonpsychoactive cannabinoid CBD limited breast cancer metastasis in a manner that was superior to comparable synthesized agents.

Previous preclinical studies assessing the anticancer properties of cannabinoids have shown that they inhibit the proliferation of a wide range of cancers, including brain cancer, prostate cancer, oral cancers, lung cancer, skin cancer, pancreatic cancer, biliary tract cancers, and lymphoma.

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.

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