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Matti Narkia

Anticancer Properties of Ganoderma Lucidum Methanol Extracts In Vitro and In Vivo - Nut... - 0 views

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    Anticancer properties of Ganoderma lucidum methanol extracts in vitro and in vivo.
    Harhaji Trajković LM, Mijatović SA, Maksimović-Ivanić DD, Stojanović ID, Momcilović MB, Tufegdzić SJ, Maksimović VM, Marjanović ZS, Stosić-Grujicić SD.
    Nutr Cancer. 2009;61(5):696-707.
    PMID: 19838944
    DOI: 10.1080/01635580902898743

    Anticancer activities of various extracts of the medicinal mushroom, Ganoderma lucidum, have been widely demonstrated and are mainly associated with the presence of different bioactive polysaccharides and triterpenoids. We have evaluated and compared in vitro and in vivo the antitumor effects of two preparations from Ganoderma lucidum: a methanol extract containing total terpenoids (GLme) and a purified methanol extract containing mainly acidic terpenoids (GLpme). Both extracts inhibited tumor growth of B16 mouse melanoma cells inoculated subcutaneously into syngeneic C57BL/6 mice and reduced viability of B16 cells in vitro, whereby GLme exhibited stronger effect. Furthermore, anticancer activity of GLme was demonstrated for the first time against two other rodent tumor cell lines, L929-mouse fibrosarcoma and C6-rat astrocytoma. The mechanism of antitumor activity of GLme comprised inhibition of cell proliferation and induction of caspase-dependent apoptotic cell death mediated by upregulated p53 and inhibited Bcl-2 expression. Moreover, the antitumor effect of the GLme was associated with intensified production of reactive oxygen species, whereas their neutralization by the antioxidant, N-acetyl cysteine, resulted in partial recovery of cell viability. Thus, our results suggest that GLme might be a good candidate for treatment of diverse forms of cancers.
Matti Narkia

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth... - 1 views

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    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.
Matti Narkia

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer - British J... - 1 views

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    Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer.
    Michelakis ED, Webster L, Mackey JR.
    Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review.
    PMID: 18766181
    doi:10.1038/sj.bjc.6604554

    The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials

    More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res
Matti Narkia

JAMA -- Soy Food Intake and Breast Cancer Survival, December 9, 2009, Shu et al. 302 (2... - 0 views

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    Soy Food Intake and Breast Cancer Survival.
    Xiao Ou Shu et al.
    JAMA Vol. 302 No. 22, December 9, 2009; 302(22):2437-2443.

    Results During the median follow-up of 3.9 years (range, 0.5-6.2 years), 444 deaths and 534 recurrences or breast cancer-related deaths were documented in 5033 surgically treated breast cancer patients. Soy food intake, as measured by either soy protein or soy isoflavone intake, was inversely associated with mortality and recurrence. The hazard ratio associated with the highest quartile of soy protein intake was 0.71 (95% confidence interval [CI], 0.54-0.92) for total mortality and 0.68 (95% CI, 0.54-0.87) for recurrence compared with the lowest quartile of intake. The multivariate-adjusted 4-year mortality rates were 10.3% and 7.4%, and the 4-year recurrence rates were 11.2% and 8.0%, respectively, for women in the lowest and highest quartiles of soy protein intake. The inverse association was evident among women with either estrogen receptor-positive or -negative breast cancer and was present in both users and nonusers of tamoxifen.

    Conclusion Among women with breast cancer, soy food consumption was significantly associated with decreased risk of death and recurrence.
Matti Narkia

Combination of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates cumul... - 0 views

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    Combination of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates cumulative recurrence of hepatocellular carcinoma.
    Yoshiji H, Noguchi R, Toyohara M, Ikenaka Y, Kitade M, Kaji K, Yamazaki M, Yamao J, Mitoro A, Sawai M, Yoshida M, Fujimoto M, Tsujimoto T, Kawaratani H, Uemura M, Fukui H.
    J Hepatol. 2009 Aug;51(2):315-21. Epub 2009 May 15.
    PMID: 19501932

    CONCLUSIONS: The combination treatment of VK and ACE-I may suppress the cumulative recurrence of HCC after the curative therapy, at least partly through suppression of the VEGF-mediated neovascularization.
Matti Narkia

A systematic review of the anticancer properties of berberine, a natural product from C... - 0 views

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    A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs.
    Sun Y, Xun K, Wang Y, Chen X.
    Anticancer Drugs. 2009 Oct;20(9):757-69.
    PMID: 19704371
Matti Narkia

Vitamin D for cancer prevention: global perspective. Garland CF et al. -Ann Epidemiol. ... - 0 views

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    Vitamin D for cancer prevention: global perspective.
    Garland CF, Gorham ED, Mohr SB, Garland FC.
    Ann Epidemiol. 2009 Jul;19(7):468-83. Review.
    PMID: 19523595
Matti Narkia

Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xeno... - 0 views

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    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.
Matti Narkia

Induction of Ovarian Cancer Cell Apoptosis by 1,25-Dihydroxyvitamin D3 through the Down... - 0 views

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    Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase.
    Jiang F, Bao J, Li P, Nicosia SV, Bai W.
    J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12.
    PMID: 15485861
    doi: 10.1074/jbc.M410395200

    Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression.

    Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene.

    It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro
Matti Narkia

Developmental toxicity evaluation of berberine in rats and mice. Gloria D. Jahnke. 2006... - 0 views

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    Developmental toxicity evaluation of berberine in rats and mice.
    Jahnke GD, Price CJ, Marr MC, Myers CB, George JD.
    Birth Defects Res B Dev Reprod Toxicol. 2006 Jun;77(3):195-206.
    PMID: 16634078
    DOI: 10.1002/bdrb.20075

    BACKGROUND: Berberine, a plant alkaloid, is found in some herbal teas and health-related products. It is a component of goldenseal, an herbal supplement. Berberine chloride dihydrate (BCD) was evaluated for developmental toxicity in rats and mice.
    METHODS: Berberine chloride dihydrate was administered in the feed to timed-mated Sprague-Dawley (CD) rats (0, 3625, 7250, or 14,500 ppm; on gestational days [GD] 6-20), and Swiss Albino (CD-1) mice (0, 3500, 5250, or 7000 ppm; on GD 6-17). Ingested doses were 0, 282, 531, and 1313 mg/kg/day (rats) and 0, 569, 841, and 1155 mg/kg/day (mice).
    RESULTS:There were no maternal deaths. The rat maternal lowest observed adverse effect level (LOAEL), based on reduced maternal weight gain, was 7250 ppm. The rat developmental toxicity LOAEL, based on reduced fetal body weight per litter, was 14,500 ppm. In the mouse study, equivocal maternal and developmental toxicity LOAELs were 5250 ppm. Due to scattering of feed in the high dose groups, a gavage study at 1000 mg/kg/day was conducted in both species.
    CONCLUSIONS: In rats, maternal, but not fetal adverse effects were noted. The maternal toxicity LOAEL remained at 7250 ppm (531 mg/kg/day) based on the feed study and the developmental toxicity NOAEL was raised to 1000 mg/kg/day BCD based on the gavage study. In the mouse, 33% of the treated females died. Surviving animals had increased relative water intake, and average fetal body weight per litter decreased 5-6% with no change in live litter size. The maternal toxicity LOAEL remained at 5250 ppm (841 mg/kg/day) BCD, based on increased water consumption. The developmental toxicity LOAEL was raised to 1000 mg/kg/day BCD based on decreased fetal body weight.
Matti Narkia

Mechanisms of Berberine (Natural Yellow 18)-Induced Mitochondrial Dysfunction: Interact... - 0 views

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    Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator.
    Pereira CV, Machado NG, Oliveira PJ.
    Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3.
    PMID: 18599498
    doi: 10.1124/jpet.107.128017

    The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study.

    Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs.

    In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.
Matti Narkia

Mitochondrially Targeted Effects of Berberine [Natural Yellow 18, 5,6-dihydro-9,10-dime... - 0 views

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    Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions.
    Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ.
    J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17.
    PMID: 17704354
    doi: 10.1124/jpet.107.128017

    The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.
Matti Narkia

Berberine Inhibits Metastasis of Nasopharyngeal Carcinoma 5-8F Cells by Targeting Rho K... - 0 views

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    Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567.
    Tang F, Wang D, Duan C, Huang D, Wu Y, Chen Y, Wang W, Xie C, Meng J, Wang L, Wu B, Liu S, Tian D, Zhu F, He Z, Deng F, Cao Y.
    J Biol Chem. 2009 Oct 2;284(40):27456-66. Epub 2009 Aug 3.
    PMID: 19651779
Matti Narkia

Berberine suppresses in vitro migration and invasion of human SCC-4 tongue sq... - 0 views

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    Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-kappaB, u-PA and MMP-2 and -9.
    Ho YT, Yang JS, Li TC, Lin JJ, Lin JG, Lai KC, Ma CY, Wood WG, Chung JG.
    Cancer Lett. 2009 Jul 8;279(2):155-62. Epub 2009 Feb 28.
    PMID: 19251361
    doi:10.1016/j.canlet.2009.01.033

    There is increasing evidence that urokinase-type plasminogen activator (u-PA) and matrix metalloproteinases (MMPs) play an important role in cancer metastasis and angiogenesis. Inhibition of u-PA and MMPs could suppress migration and invasion of cancer cells. Berberine, one of the main constituents of the plant Rhizoma coptidis, is a type of isoquinoline alkaloid, reported to have anti-cancer effects in different human cancer cell lines. There is however, no available information on effects of berberine on migration and invasion of human tongue cancer cells. Here, we report that berberine inhibited migration and invasion of human SCC-4 tongue squamous carcinoma cells. This action was mediated by the p-JNK, p-ERK, p-p38, IκK and NF-κB signaling pathways resulting in inhibition of MMP-2 and -9 in human SCC-4 tongue squamous carcinoma cells. Our Western blowing analysis also showed that berberine inhibited the levels of urokinase-plasminogen activator (u-PA). These results suggest that berberine down-regulates u-PA, MMP-2 and -9 expressions in SCC-4 cells through the FAK, IKK and NF-κB mediated pathways and a novel function of berberine is to inhibit the invasive capacity of malignant cells.
Matti Narkia

A phase 2 trial exploring the effects of high-dose (10,000 IU/day) vitamin D(3) in brea... - 0 views

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    A phase 2 trial exploring the effects of high-dose (10,000 IU/day) vitamin D(3) in breast cancer patients with bone metastases.
    Amir E, Simmons CE, Freedman OC, Dranitsaris G, Cole DE, Vieth R, Ooi WS, Clemons M.
    Cancer. 2009 Nov 13. [Epub ahead of print]
    PMID: 19918922
    DOI: 10.1002/cncr.24749

    METHODS:
    Patients with bone metastases treated with bisphosphonates were enrolled into this single-arm phase 2 study. Patients received 10,000 IU of vitamin D3 and 1000 mg of calcium supplementation each day for 4 months. The effect of this treatment on palliation, bone resorption markers, calcium metabolism, and toxicity were evaluated at baseline and monthly thereafter.


    CONCLUSIONS:
    Daily doses of 10,000 IU vitamin D3 for 4 months appear safe in patients without comorbid conditions causing hypersensitivity to vitamin D. Treatment reduced inappropriately elevated parathyroid hormone levels, presumably caused by long-term bisphosphonate use. There did not appear to be a significant palliative benefit nor any significant change in bone resorption. Cancer 2010. © 2009 American Cancer Society.
Matti Narkia

JAMA -- Abstract: Cancer Incidence and Mortality After Treatment With Folic Acid and Vi... - 0 views

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    Cancer Incidence and Mortality After Treatment With Folic Acid and Vitamin B12.
    Ebbing M, Bønaa KH, Nygård O, Arnesen E, Ueland PM, Nordrehaug JE, Rasmussen K, Njølstad I, Refsum H, Nilsen DW, Tverdal A, Meyer K, Vollset SE.
    JAMA. 2009 Nov 18;302(19):2119-2126. v
    PMID: 19920236

    Conclusion Treatment with folic acid plus vitamin B12 was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods.
Matti Narkia

Inverse association between serum 25(OH) vitamin D levels and non-melanoma skin cancer ... - 0 views

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    Inverse association between serum 25(OH) vitamin D levels and non-melanoma skin cancer in elderly men.
    Tang JY, Parimi N, Wu A, John Boscardin W, Shikany JM, Chren MM, Cummings SR, Epstein EH Jr, Bauer DC; for the Osteoporotic Fractures in Men (MrOS) Study Group.
    Cancer Causes Control. 2009 Nov 18. [Epub ahead of print]
    PMID: 19921445

    Our results suggest that a diagnosis of NMSC is not a surrogate for adequate 25(OH)D levels or increased UV exposure, and high 25(OH)D levels may be associated with a reduced risk of NMSC.
Matti Narkia

Meta-analysis of vitamin D, calcium and the prevention of breast cancer. - [Breast Canc... - 0 views

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    Meta-analysis of vitamin D, calcium and the prevention of breast cancer.
    Chen P, Hu P, Xie D, Qin Y, Wang F, Wang H.
    Breast Cancer Res Treat. 2009 Oct 23. [Epub ahead of print]
    PMID: 19851861

    These results provide strong evidence that vitamin D and calcium have a chemopreventive effect against breast cancer.
Matti Narkia

Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids - Journal... - 0 views

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    Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids.
    Berquin IM, Min Y, Wu R, Wu J, Perry D, Cline JM, Thomas MJ, Thornburg T, Kulik G, Smith A, Edwards IJ, D'Agostino R, Zhang H, Wu H, Kang JX, Chen YQ.
    J Clin Invest. 2007 Jul;117(7):1866-75.
    PMID: 17607361

    Our data suggest that modulation of prostate cancer development by polyunsaturated fatty acids is mediated in part through Bad-dependent apoptosis. This study highlights the importance of gene-diet interactions in prostate cancer.
Matti Narkia

Israeli 'cancer shift' over heart disease mortality may be led by greater risk in women... - 0 views

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    Israeli 'cancer shift' over heart disease mortality may be led by greater risk in women with high intake of n-6 fatty acids.
    Shapira N.
    Eur J Cancer Prev. 2007 Oct;16(5):486-94.
    PMID: 17923822
    doi: 10.1097/CEJ.0b013e3280145b6d

    Population studies of Israeli Jews, Arabs, and women support the association of high n-6 polyunsaturated fatty acid intake with increased cancer risk and higher female sensitivity. Research findings suggest that gender and sex hormones may influence n-6 polyunsaturated fatty acid metabolism and carcinogenesis. This appears to be the first time gender has been proposed to modulate national cancer epidemiology, suggesting implications for differential nutritional prevention, warranting further research.
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