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Mice injected with cancer cells experienced significantly elevated levels of C-reactive protein, white blood cells, and lipid peroxidation compared with control mice. These levels were reduced in animals that received cisplatin and/or DHA. While treatment with 125 mg/kg DHA inhibited tumor growth by 38 percent compared to untreated animals, 250 mg/kg suppressed tumor growth by 79 percent, which was a greater effect than that of cisplatin alone (which was associated with a 55 percent reduction). The combination of DHA and cisplatin resulted in an 81 percent inhibition of growth, while reducing elevated white blood cell levels (leukocytosis) to normal levels. Treatment with the higher dose of DHA alone was associated with a similar reduction in white blood cells, which, when elevated, are associated with tumor growth. A strong relationship was observed between tumor growth and white blood cell levels as well as C-reactive protein levels. In another experiment with rats treated with cisplatin, the addition of 250 mg/kg DHA prevented lethal kidney toxicity in 88 percent of the animals that received it, while none of the rats that received cisplatin alone survived.

DURHAM, N.C. -- Restricting carbohydrates, regardless of weight loss, appears to slow the growth of prostate tumors, according to an animal study being published this week by researchers in the Duke Prostate Center. "Previous work here and elsewhere has shown that a diet light in carbohydrates could slow tumor growth, but the animals in those studies also lost weight, and because we know that weight loss can restrict the amount of energy feeding tumors, we weren't able to tell just how big an impact the pure carbohydrate restriction was having, until now," said Stephen Freedland, M.D., a urologist in the Duke Prostate Center and lead investigator on this study. The researchers believe that insulin and insulin-like growth factor contribute to the growth and proliferation of prostate cancer, and that a diet devoid of carbohydrates lowers serum insulin levels in the bodies of the mice, thereby slowing tumor growth, Freedland said.

Scientists in Japan recently studied some of the glyconutrients from spinach and found they inhibited destruction of DNA, cancer cell growth, and tumor growth. They used the nutrients to suppress the growth of colon adenocarcinoma in mice. After a two week period of ingesting the nutrients, a 56.1% decrease in solid tumor volume occurred without any side effects. And the nutrients reduced the ability of tumors to supply themselves with blood which they need to fuel their growth. Markers of cell proliferation were drastically reduced. (Lipids, August, 2008)

Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xenograft model. Ho YT, Yang JS, Lu CC, Chiang JH, Li TC, Lin JJ, Lai KC, Liao CL, Lin JG, Chung JG. Phytomedicine. 2009 Sep;16(9):887-90. Epub 2009 Mar 20. PMID: 19303753 Our primary studies showed that berberine induced apoptosis in human tongue cancer SCC-4 cells in vitro. But there is no report to show berberine inhibited SCC-4 cancer cells in vivo on a murine xenograft animal model. SCC-4 tumor cells were implanted into mice and groups of mice were treated with vehicle, berberine (10mg/kg of body weight) and doxorubicin (4mg/kg of body weight). The tested agents were injected once per four days intraperitoneally (i.p.), with treatment starting 4 weeks prior to cells inoculation. Treatment with 4mg/kg of doxorubicin or with 10mg/kg of berberine resulted in a reduction in tumor incidence. Tumor size in xenograft mice treated with 10mg/kg berberine was significantly smaller than that in the control group. Our findings indicated that berbeirne inhibits tumor growth in a xenograft animal model. Therefore, berberine may represent a tongue cancer preventive agent and can be used in clinic.

PHILADELPHIA - Researchers at Amgen are testing a fully human monoclonal antibody that inhibits the activity of insulin-like growth factors (IGF-1 and IGF-2) and appears to reduce pancreatic cancer cells in early testing, according to a report in Molecular Cancer Therapeutics, a journal of the American Association for Cancer Research.

Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP. Mantena SK, Sharma SD, Katiyar SK. Carcinogenesis. 2006 Oct;27(10):2018-27. Epub 2006 Apr 18. PMID: 16621886 doi:10.1093/carcin/bgl043 In the present investigation, we show that berberine, which is present abundantly in Berberis plant species, significantly inhibits the viability, proliferation and induces cell death in human epidermoid carcinoma A431 cells (Figure 1), but this effect was not found in normal human epidermal keratinocytes under the identical conditions, except for a non-significant reduction in cell viability at higher concentrations of berberine (50 and 75 µM) and treatment of cells for a longer period of time (72 h). These data suggested that berberine may be examined as an effective chemotherapeutic agent against non-melanoma skin cancers. In conclusion, our study indicates that berberine inhibits growth, induces G1 arrest and apoptotic cell death of human epidermoid carcinoma A431 cells. We also provide mechanistic evidences that berberine-induced apoptosis in human epidermoid carcinoma cells is mediated through disruption of mitochondrial membrane potential and activation of caspase 3 pathway, although other pathways may have a role and that require further investigation. Moreover, further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the prevention of non-melanoma skin cancers.

A type of drug designed to stunt tumour growth has actually been found to fuel cancer if given at too low a dose. UK scientists were investigating a kind of drug called an anti-angiogenesis, still under development, which hampers the growth of tumour blood vessels.

Low doses of the active form of vitamin D and non-steroidal anti-inflammatory drugs act as a powerful combination to halt the growth of prostate cancer cells, say US scientists. Writing in Cancer Research, a team from Stanford University says it discovered that the amount of both activated vitamin D, or calcitriol, and NSAIDs could be reduced by half to one-tenth the dosage to thwart prostate cancer cell growth in cell lines and primary tissue culture

ScienceDaily (Sep. 1, 2005) - STANFORD, Calif. - The growth of prostate cancer cells can be halted by combining a form of vitamin D, available only by prescription, with low doses of an over-the-counter painkiller, researchers at the Stanford University School of Medicine have found. The combination reduced prostate cancer cell growth in a laboratory dish by up to 70 percent, according to the findings, published in the Sept. 1 issue of Cancer Research.

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

ScienceDaily (June 11, 2009) - University of Florida researchers have come up with a new gene therapy method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply. In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated.

The active compound in marijuana, THC, can slow the growth of lung tumours and reduce the spread of the cancer in mice, a preliminary study reveals. Human lung cancer tumours grew less than half as fast in mice that received moderate doses of the compound, the researchers reveal. They hope that drugs mimicking the apparent anti-cancer effects of tetrahydrocanabinol (THC) could one day help treat patients. The team strongly discourage people from self-medicating by smoking marijuana, noting that doing so could potentially encourage tumour growth.

A signalling pathway that influences how sensitive cancer cells are to the beneficial effects of dietary restriction is described in this week's Nature. Dietary restriction - eating less calories while maintaining essential vitamins and minerals - can extend lifespan, and reduce cancer incidence and growth. But some types of cancer cell are more sensitive to the anti-growth effects of dietary restriction than others, Nada Kalaany and David Sabatini report. The effect hinges on the activity of the phosphatidylinositol-3-kinase (PI3K) pathway. If the pathway is active, dietary restriction has no effect on cancer cells. However, if the pathway is inactive, tumours are sensitive to dietary restriction.

Flaig TW, Su LJ, Harrison G, Agarwal R, Glode LM. Silibinin synergizes with mitoxantrone to inhibit cell growth and induce apoptosis in human prostate cancer cells. Int J Cancer. 2007 Jan 17; [Epub ahead of print] PMID: 17230508 [PubMed - as supplied

Scheper MA, Nikitakis NG, Chaisuparat R, Montaner S, Sauk JJ. Sulindac Induces Apoptosis and Inhibits Tumor Growth in vivo in Head and Neck Squamous Cell Carcinoma. Neoplasia. 2007 Mar;9(3):192-9. PMID: 17401459 [PubMed - in process]

If angiogenesis controls cancer growth, what controls angiogenesis? Researchers at the University of Michigan and the University of South Florida believe that the copper status is critical to the function growth factors.

Q. Pan, C. G. Kleer, K. L. van Golen, J. Irani, K. M. Bottema, C. Bias, M. De Carvalho, E. A. Mesri, D. M. Robins, R. D. Dick, G. J. Brewer, and S. D. Merajver Copper Deficiency Induced by Tetrathiomolybdate Suppresses Tumor Growth and Angiogenesis Canc

C. Cox, S. D. Merajver, S. Yoo, R. D. Dick, G. J. Brewer, J. S.-J. Lee, and T. N. Teknos Inhibition of the Growth of Squamous Cell Carcinoma by Tetrathiomolybdate-Induced Copper Suppression in a Murine Model Arch Otolaryngol Head Neck Surg, July 1, 200

"NOTTINGHAM, England, Dec. 29 (UPI) -- A drug derived from a mushroom -- cordycepin -- may be used to treat some cancers, British researchers say. Dr. Cornelia de Moor of The University of Nottingham in England and colleagues are investigating the drug originally extracted from a rare parasitic mushroom called cordyceps that grows on caterpillars. The researchers say low-dose cordycepin seems to inhibit the uncontrolled growth and division of cells and at high doses it also inhibits growth by stopping cells from sticking together. Both of these effects, they say, probably have the same underlying mechanism -- interfering with the production of cell proteins.

White button mushroom (Agaricus bisporus) exhibits antiproliferative and proapoptotic properties and inhibits prostate tumor growth in athymic mice. Adams LS, Phung S, Wu X, Ki L, Chen S. Nutr Cancer. 2008;60(6):744-56. PMID: 19005974