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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

"Língzhī (traditional Chinese: 靈芝; simplified Chinese: 灵芝; Japanese: reishi; Korean: yeongji, hangul: 영지) is the name for one form of the mushroom Ganoderma lucidum, and its close relative Ganoderma tsugae. Ganoderma lucidum enjoys special veneration in Asia, where it has been used as a medicinal mushroom in traditional Chinese medicine for more than 4,000 years, making it one of the oldest mushrooms known to have been used in medicine. Lingzhi may possess anti-tumor, immunomodulatory and immunotherapeutic activities, supported by studies on polysaccharides, terpenes, and other bioactive compounds isolated from fruiting bodies and mycelia of this fungus (reviewed by R. R. Paterson[4] and Lindequist et al.[7]). It has also been found to inhibit platelet aggregation, and to lower blood pressure (via inhibition of angiotensin-converting enzyme[8]), cholesterol and blood sugar.[9] Laboratory studies have shown anti-neoplastic effects of fungal extracts or isolated compounds against some types of cancer. In an animal model, Ganoderma has been reported to prevent cancer metastasis,[10] with potency comparable to Lentinan from Shiitake mushrooms.[11] The mechanisms by which G. lucidum may affect cancer are unknown and they may target different stages of cancer development: inhibition of angiogenesis (formation of new, tumor-induced blood vessels, created to supply nutrients to the tumor) mediated by cytokines, cytoxicity, inhibiting migration of the cancer cells and metastasis, and inducing and enhancing apoptosis of tumor cells

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.

Ursolic acid is a pentacyclic triterpene acid, used in cosmetics,[2] that is also capable of inhibiting various types of cancer cells by inhibiting the STAT3 activation pathway[3][4] and human fibrosarcoma cells by reducing the expression of matrix metalloproteinase-9 by acting through the glucocorticoid receptor. Ursolic acid is present in many plants, including apples, basil, bilberries, cranberries, elder flower, peppermint, rosemary, lavender, oregano, thyme, hawthorn, prunes. Apple peels contain high quantity of ursolic acid and related compounds which are responsible for the anti-cancer activity of apple. Ursolic acid can also serve as a starting material for synthesis of more potent bioactive derivatives, such as anti-tumor agents

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.

CancerGuide is a cancer information page written by Steve Dunn, a fellow patient. I strongly believe, and indeed I know from personal experience, that information can save your life. This page is dedicated to helping cancer patients find the best treatment for their disease by finding, and understanding, the best and latest information on their disease. The focus here is on technical information. While this page does offer links to the best cancer information sources on the net, what makes this page special is no holds barred help and information about things on and off the net from someone who's been been where you are now. The information on this page is information with a point of view, not information sanitized by committee!

Lysis of tumor cells by natural killer cells in mice is impeded by platelets. Nieswandt B, Hafner M, Echtenacher B, Männel DN. Cancer Res. 1999 Mar 15;59(6):1295-300. PMID: 10096562

Serum 25-hydroxyvitamin D and colon cancer: eight-year prospective study. Garland CF, Comstock GW, Garland FC, Helsing KJ, Shaw EK, Gorham ED. Lancet. 1989 Nov 18;2(8673):1176-8. PMID: 2572900 Blood samples taken in 1974 in Washington County, Maryland, from 25 620 volunteers were used to investigate the relation of serum 25-hydroxyvitamin D (25-OHD) with subsequent risk of getting colon cancer. 34 cases of colon cancer diagnosed between August, 1975, and January, 1983, were matched to 67 controls by age, race, sex, and month blood was taken. Risk of colon cancer was reduced by 75% in the third quintile (27-32 ng/ml) and by 80% in the fourth quintile (33-41 ng/ml) of serum 25-OHD. Risk of getting colon cancer decreased three-fold in people with a serum 25-OHD concentration of 20 ng/ml or more. The results are consistent with a protective effect of serum 25-OHD on colon cancer.

In this video Dr. Ramakant Deshpande explaining the 6 Myths and facts of Lung cancer. Dr. Ramakant Deshpande MS; FICS; FAIS; DHA having experience of 31+ years and is a Chief of Thoracic Surgical Oncology, Asian Institute of Oncology. - Padmashree award by the President of India in 2014 - Lifetime Achievement Award at the Indian National Critical Care Society Annual Meet at Jaipur 2014 - Lifetime Achievement Award by Zee Maaza TV in 2019 - Senior of Robotic surgery at the Asian Cancer Institute - Established the Minimally Invasive method of Thoracoscopy - President of the Indian Society of Oncology - Director - Asian Cancer Institute - Ex Tata Memorial Doctor This video is under the "My Health My Right" Initiative of MedicoExperts - A Global Virtual Hospital. For inquiry Call/WhatsApp us at +91 9769516280 #Lungcancer​ #MyHealthMyRight​ #lunghealth​ #lungtreatment​ #lungcancermyths​ #lungcancerfacts​ #MedicoExperts​ #DrRamakantDeshpande​ #oncology​ #cancer

Inhibition of suppressor T lymphocytes (Ts) by cimetidine. Sahasrabudhe DM, McCune CS, O'Donnell RW, Henshaw EC. J Immunol. 1987 May 1;138(9):2760-3. PMID: 2952721 Cyclophosphamide (CY) is the most extensively studied inhibitor of suppressor T lymphocyte (Ts) function. However, repeated administration of CY can abrogate sensitization. Therefore, we were interested in identifying noncytotoxic inhibitors of Ts function as adjuncts in the immunotherapy of Ts-inducing murine tumors. The effect of cimetidine (a histamine type 2 receptor antagonist) and diphenhydramine (a histamine type 1 receptor antagonist) on the Ts mediating tolerance to 2,4-dinitrofluorobenzene was studied. We report our data regarding the specific inhibition of Ts by cimetidine.

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.

A recently published study in Nutrition and Cancer (60(5), 643-651) by researchers at Kansai Medical University in Osaka, Japan has shown that AHCC (Active Hexose Correlated Compound) enhances immune function by increasing the number of dendritic cells (DCs). DCs are a key part of the immune system responsible for presenting foreign substances to other immune system cells. The study was conducted in a double-blind randomized fashion where twenty-one healthy subjects received a placebo or AHCC at 3.0 g/day for 4 weeks. Blood samples were obtained and measured at baseline and at 4 weeks. The number of circulating types of DCs was measured which included CD 11c+ DCs (myeloid DC population; DC1) and CD11c- DCs (lymphoid DC population; DC2). Other parameters measured included mixed-leukocyte reaction (MLR), natural killer (NK) cell activity, the proliferative response of T lymphocytes toward mitogen (phytohemagglutinin [PHA]) and cytokine production of interleukin (IL)-2, IL-4, IL-6, IL-10, interferon gamma-gamma, and (alpha)-tumor necrosis factor.

San Diego, CA (PRWEB) May 25, 2009 -- Coming on the heels of the publishing in the Annals of Epidemiology of a new study led by Dr. Cedric Garland, on the preventive measures of vitamin D, GrassrootsHealth D*action Project is calling on physicians, health clinics and groups throughout the country to recognize the need for determining vitamin D levels and to ensure the public have their blood levels of vitamin D tested. According to research from the newly published study by Cedric F. Garland, Dr. P.H., FACE, Department of Family and Preventive Medicine and Moores Cancer Center of the University of California, San Diego (UCSD), "It is projected that raising the minimum year-around serum 25(OH)D level to 40-60 ng/ml (100-150 nmol/L) would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three quarters of deaths from these diseases, in the US and Canada."

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.

Maintaining adequate levels of vitamin D during winter months requires a daily dose of 20 micrograms, four times the current recommended dose, says a new study. The study, led by Susan Sullivan from the University of Maine, has important implications for ongoing consultations on vitamin D recommendations, with the current level of five micrograms (200 International Units) seen by many as insufficient.

A new study showing a reduction in the toxic side effects of ROS-generating chemotherapies with concurrent antioxidant supplementation will be presented at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO) that takes place June 1-5 at McCormick Place in Chicago. According to the study's authors, mitigating chemotherapy toxicity by supplementing with antioxidants may improve survival rates and tumor response by helping patients complete their prescribed treatment cycles.

DCA is an organic compound, and a byproduct of TCE (trichloroethylene), a chemical that has been a concern in the development of cancer. In January 2007, researchers at the University of Alberta published a study in the journal Cancer Cell suggesting that DCA showed promise in shrinking tumors in lab rats as well as inhibiting growth of cultured human cancer cells. They hypothesized that DCA may be able to change cancer cells back to normal ones by switching them from the aberrant energy pathways they rely on to those used by normal cells.

One way tumors fly under the radar of the immune system is by using IDO, an enzyme used by fetuses to help avoid rejection, to recruit powerful regulatory T cells that turn down the immune response, researchers say.

Tetrathiomolybdate promotes tumor necrosis and prevents distant metastases by suppressing angiogenesis in head and neck cancer -- Hassouneh et al. 6 (3): 1039 -- Molecular Cancer Therapeutics

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