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Matti Narkia

Changes of terminal cancer patients' health-related quality of life after high dose vit... - 0 views

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    Changes of terminal cancer patients' health-related quality of life after high dose vitamin C administration.\nYeom CH, Jung GC, Song KJ.\nJ Korean Med Sci. 2007 Feb;22(1):7-11.\nPMID: 17297243
Matti Narkia

A pilot clinical study of continuous intravenous a...[P R Health Sci J. 2005] - PubMed ... - 0 views

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    A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA. P R Health Sci J. 2005 Dec;24(4):269-76. PMID: 16570523
fifthseason financial

Loans for terminally ill - 0 views

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    Fifth Season provides loans for late-stage cancer patients, secured by their existing life insurance policy. Apply now for a cancer loan or financial support at Fifth Season Financial.
Matti Narkia

The DCA Site - Updating You on DCA and Cancer - Dichloroacetic acid and Dichloroacetate - 0 views

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    After the news story in the Belgium press of two terminally ill cancer patients who used DCA and are now on the road to recovery, the Belgium people are asking questions. "It has brought a lot commotion in Belgium. All the people are wondering why they haven't heard from DCA any sooner! And they wonder why it isn't recognized yet as an official medicine for cancer!
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

DCA or dichloroacetate drug used by dying cancer patients as a last resort - 0 views

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    30 April,2007: Terminally ill patients with incurable cancers are increasingly using a compound via Internet trade that is not yet approved, reports Nature. The 'drug' in question -- dichloroacetate (DCA) - has been but found shrinking tumours in rats but yet to put on studies to ascertain its safety in human use.
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
Final Duties

Flower found that can kill tumors in 1 hit! - 1 views

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    proven to kill cancer tumors in mice in 1 hit, They have said 18 months in the daily mail to start clinical trials, Why then fecikn wait that long!Its a bloody flower!! The government have no intention on curing cancer and never will have! ''conspiracy'' how much money would they lose if the cured it! billions, greedy wankers... why give people hope just another load of bollocks.. Just like that guy on the run who proved that cannabis cures cancer in oil form, why's he on the run? from curing people of cancer,......... after watching my dad the last 6 months suffer going through endless chemo sessions i get so angry when i see stuff like this say 18 months before clinical trials start and 7-8 years b4 it comes out!! although it has proven results! 100's of thousands of terminal cancer patients will be dead before they pull there greedy fat cat fingers out there arses, sorry rant over just makes me so angry! my dad and my best friend both suffering and they say 7-8 years b4 it will even be realised with a proven record of killing 90% of most tumors !
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