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    Originally posted by doofaloofa View Post
    why Chi of coarse!

    killer rabits v's diarrhea bees



      I've been researching Hydrogen Peroxide for a while now. I've found some interesting stuff pertaining to cancer through all of the research.

      Dr. Otto Warburg was a biochemist who did alot of breakthrough in cancer research. Alot of his works were "locked" when he died. Someone had access to some of his work and his partners work and was able to piece together some of it.

      These are just a couple links. Interesting finds.

      I also found something that claimed that cooked vegitables caused a propensity for cancer. Supposedly that cooked vegitables caused blood cells to "clump" together creating an oxygen deficiency in certain areas.

      I wish I had more time and more resources. This seems very interesting.


        Warburg's hypothesis has led to quite a few attempts to develop anti-cancer drugs. There were some relatively recent studies done that utilized drugs like bromopyruvic acid and dichloroacetic acid to interfere with glycolytic metabolism. Some of these were quite successful from an in vitro point of view.

        Originally posted by webstank
        The issue in curing cancer with hydrogen peroxide boils down to getting enough hydrogen peroxide inside the cancer cells.
        Excellent! Now that that's solved, if only I could drink enough bleach to....oh snap!

        Speaking of enzymes, did you know that catalase, the enzyme responsible for H2O2 removal, has one of the highest functional activities knwon? It's something like 50 million molecules per second.


          Though, Warburg's hypothesis still has its proponents and it most definitely illuminates some interesting points, but since it doesn't describe the genetic portion of the issue, it is kind of a side show to more important issues at hand. In other words, yes the metabolism of cancer cells changes, but the underlying cause of what caused these changes is the root of the issue.


            Originally posted by Sorekara View Post
            I wish I had more time and more resources. This seems very interesting.
            So, got any more cancer related articles that you wish you could read if only you had more time and resources?

            As exciting as drinking bleach is, I have to say that I was hoping for more. I mean in the past bullshido did have quite a few characters.

            If you want to talk Warburg, here you go one of the most important papers using DCA to induce apoptosis:

            A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth

            The unique metabolic profile of cancer (aerobic glycolysis) might confer apoptosis resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential (DJm) and low expression of the K+ channel Kv1.5, both contributing to apoptosis resistance. Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DJm, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity.Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is
            a promising selective anticancer agent.


              Originally posted by jubei33 View Post
              So, got any more cancer related articles that you wish you could read if only you had more time and resources?

              As exciting as drinking bleach is, I have to say that I was hoping for more. I mean in the past bullshido did have quite a few characters.

              If you want to talk Warburg, here you go one of the most important papers using DCA to induce apoptosis:

              A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth

              (originally published in Cancer Cell 11, 37–51, January 2007)
              Too bad I don't understand any of that. I appreciate your efforts sincerely.


                Learn about this motherfuckaaas!!!

                Characterization of microRNA expression levels and their biological correlates in human cancer cell lines.
                Gaur A, Jewell DA, Liang Y, Ridzon D, Moore JH, Chen C, Ambros VR, Israel MA.

                Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire 03755, USA.

                MicroRNAs are small noncoding RNAs that function by regulating target gene expression posttranscriptionally. They play a critical role in developmental and physiologic processes and are implicated in the pathogenesis of several human diseases including cancer. We examined the expression profiles of 241 human microRNAs in normal tissues and the NCI-60 panel of human tumor-derived cell lines. To quantify microRNA expression, we employed a highly sensitive technique that uses stem-loop primers for reverse transcription followed by real-time PCR. Most microRNAs were expressed at lower levels in tumor-derived cell lines compared with the corresponding normal tissue. Agglomerative hierarchical clustering analysis of microRNA expression revealed four groups among the NCI-60 cell lines consisting of hematologic, colon, central nervous system, and melanoma tumor-derived cell lines clustered in a manner that reflected their tissue of origin. We identified specific subsets of microRNAs that provide candidate molecular signatures characteristic of the tumor-derived cell lines belonging to these four clusters. We also identified specific microRNA expression patterns that correlated with the proliferation indices of the NCI-60 cell lines, and we developed evidence for the identification of specific microRNAs as candidate oncogenes and tumor suppressor genes in different tumor types. Our results provide evidence that microRNA expression patterns may mark specific biological characteristics of tumors and/or mediate biological activities important for the pathobiology of malignant tumors. These findings call attention to the potential of microRNAs to provide etiologic insights as well as to serve as both diagnostic markers and therapeutic targets for many different tumor types.
                then go drink some booze!


                  Uh oh--NOW YOU IN FORIT ! I got into the liquor cabinet again:

                  Efficacy of Gefitinib, an Inhibitor of the Epidermal Growth Factor Receptor Tyrosine Kinase, in Symptomatic Patients With Non–Small Cell Lung Cancer: A Randomized Trial


                  Context: More persons in the United States die from non–small cell lung cancer (NSCLC) than from breast, colorectal, and prostate cancer combined. In preclinical testing, oral gefitinib inhibited the growth of NSCLC tumors that express the epidermal growth factor receptor (EGFR), a mediator of cell signaling, and phase 1 trials have demonstrated that a fraction of patients with NSCLC progressing after chemotherapy experience both a decrease in lung cancer symptoms and radiographic tumor shrinkages with gefitinib.

                  Objective To assess differences in symptomatic and radiographic response among patients with NSCLC receiving 250-mg and 500-mg daily doses of gefitinib.

                  Design, Setting, and Patients Double-blind, randomized phase 2 trial conducted from November 2000 to April 2001 in 30 US academic and community oncology centers. Patients (N = 221) had either stage IIIB or IV NSCLC for which they had received at least 2 chemotherapy regimens.

                  Intervention Daily oral gefitinib, either 500 mg (administered as two 250-mg gefitinib tablets) or 250 mg (administered as one 250-mg gefitinib tablet and 1 matching placebo).

                  Main Outcome Measures Improvement of NSCLC symptoms (2-point or greater increase in score on the summed lung cancer subscale of the Functional Assessment of Cancer Therapy-Lung [FACT-L] instrument) and tumor regression (>50% decrease in lesion size on imaging studies).

                  Results Of 221 patients enrolled, 216 received gefitinib as randomized. Symptoms of NSCLC improved in 43% (95% confidence interval [CI], 33%-53%) of patients receiving 250 mg of gefitinib and in 35% (95% CI, 26%-45%) of patients receiving 500 mg. These benefits were observed within 3 weeks in 75% of patients. Partial radiographic responses occurred in 12% (95% CI, 6%-20%) of individuals receiving 250 mg of gefitinib and in 9% (95% CI, 4%-16%) of those receiving 500 mg. Symptoms improved in 96% of patients with partial radiographic responses. The overall survival at 1 year was 25%. There were no significant differences between the 250-mg and 500-mg doses in rates of symptom improvement (P = .26), radiographic tumor regression (P = .51), and projected 1-year survival (P = .54). The 500-mg dose was associated more frequently with transient acne-like rash (P = .04) and diarrhea (P = .006).

                  Conclusions Gefitinib, a well-tolerated oral EGFR-tyrosine kinase inhibitor, improved disease-related symptoms and induced radiographic tumor regressions in patients with NSCLC persisting after chemotherapy.
                  Gefitnib is of a new class of tyrosine kinase inhibitors, which were developed out of a clearer understanding of molecular biology.


                    and while we're on the subject:

                    Epidermal growth factor receptor in relation to tumor development: EGFR-targeted anticancer therapy


                    epidermal growth factor receptor (EGFR) mutation;
                    KRAS mutation;
                    monoclonal antibodies;
                    tyrosine kinase inhibitor

                    The discovery that signaling by the epidermal growth factor receptor (EGFR) plays a key role in tumorigenesis prompted efforts to target this receptor in anticancer therapy. Two different types of EGFR-targeted therapeutic agents were subsequently developed: mAbs, such as cetuximab and panitumumab, which target the extracellular domain of the receptor, thereby inhibiting ligand-dependent EGFR signal transduction; and small-molecule tyrosine kinase inhibitors, such as gefitinib and erlotinib, which target the intracellular tyrosine kinase domain of the EGFR. Furthermore, recent clinical and laboratory studies have identified molecular markers that have the potential to improve the clinical effectiveness of EGFR-targeted therapies. This minireview summarizes the emerging role of molecular profiling in guiding the clinical use of anti-EGFR therapeutic agents.


                      piR-823, a novel non-coding small RNA, demonstrates in vitro and in vivo tumor suppressive activity in human gastric cancer cells.

                      Cheng J, Deng H, Xiao B, Zhou H, Zhou F, Shen Z, Guo J.

                      Ningbo University School of Medicine, Ningbo 315211, China.

                      Piwi-interacting RNAs (piRNAs), new non-coding small RNAs, are association with chromatin organization, messenger RNA stability and genome structure. However, the roles of piRNA in carcinogenesis are not clearly defined. By using real-time reverse transcription-polymerase chain reaction technology, we found that the expression level of piR-823 in gastric cancer tissues was significant lower than that in non-cancerous tissues. After increase the level of piR-823 in gastric cancer cells, cell growth was inhibited. The results of xenograft nude mice model confirmed its tumor suppressive properties. All of the evidences indicated that piR-823 play a crucial role in the occult of gastric cancer.


                        I'm going to ask in this thread, as some people here seem to demonstrate a tad more understanding of cancer than I.

                        Is cancer cured?
                        Snopes says no. Also it links to this which I scanned then somehow got an immediate headache.


                          I vote no, too. At least until human trials and clear evidence of positive results.

                          Dichloroacetate was discussed earlier on page 3 or 4. I can't remember which one, but we were talking about the Warburg hypothesis, which is an interesting discussion by itself.

                          Cancer is just a complicated beast, one that affects us at the core (our genes).

                          edit: I'll give you a better, more in depth answer when I'm not at work.
                          Last edited by jubei33; 12/08/2011 12:51am, .


                            Ok, this is the paper in question. It was research done by Evangelos D. Michelakis at the University of Alberta in Canada and its quite interesting. The problem is mostly the hysteria and conspiracy attached to it. These kind of things, (meaning: early successful experiments) often dredge up the nutcases enmasse.

                            The tests were conducted in rats and in vitro tests, which aren't the same as or equivalent to tests in humans. Though animals are a judicious choice for early testing, they cannot adequately substitute for the human factor.

                            Many of our current cancer drugs have had similarly successful in vitro tests. There's kind of a long history of cancer cure false positives in this theme, where early results are touted as fantastic and the end of cancer!!, but these haven't run the distance to date. Often the results they get when tested in humans are less dramatic, though still quite useful. I'm thinking of Imatinib, I think, which is a tyrosine kinase inhibitor and is first line for chronic myelogenic leukemia. (it might have been an earlier monoclonal antibody that received all the hype, though..but oh well.)

                            12/9 edit: I started this yesterday with the mindset of "Oh, this again", but now that I re-read it. It sounds quite negative. I don't want to give the impression that his work is at fault. That's not it at all, its a very good start. All the spin, you can blame that on half of the nutcases out there with their conspiracy mindset. In this way, this work is more of a sideshow to all these grandstanding bozos, they take away the depth and importance of this guy's efforts.
                            Last edited by jubei33; 12/08/2011 3:58pm, .


                              Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg).
                              Nimptsch K, Rohrmann S, Linseisen J.

                              Division of Cancer Epidemiology, German Cancer Research Centre, Heidelberg, Germany.

                              Anticarcinogenic activities of vitamin K have been observed in various cancer cell lines, including prostate cancer cells. Epidemiologic studies linking dietary intake of vitamin K with the development of prostate cancer have not yet been conducted.

                              We evaluated the association between dietary intake of phylloquinone (vitamin K1) and menaquinones (vitamin K2) and total and advanced prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition.

                              At baseline, habitual dietary intake was assessed by means of a food-frequency questionnaire. Dietary intake of phylloquinone and menaquinones (MK-4-14) was estimated by using previously published HPLC-based food-content data. Multivariate-adjusted relative risks of total and advanced prostate cancer in relation to intakes of phylloquinone and menaquinones were calculated in 11 319 men by means of Cox proportional hazards regression.

                              During a mean follow-up time of 8.6 y, 268 incident cases of prostate cancer, including 113 advanced cases, were identified. We observed a nonsignificant inverse association between total prostate cancer and total menaquinone intake [multivariate relative risk (highest compared with lowest quartile): 0.65; 95% CI: 0.39, 1.06]. The association was stronger for advanced prostate cancer (0.37; 0.16, 0.88; P for trend = 0.03). Menaquinones from dairy products had a stronger inverse association with advanced prostate cancer than did menaquinones from meat. Phylloquinone intake was unrelated to prostate cancer incidence (1.02; 0.70, 1.48).

                              Our results suggest an inverse association between the intake of menaquinones, but not that of phylloquinone, and prostate cancer. Further studies of dietary vitamin K and prostate cancer are warranted.
                              Pyruvate kinase M2 (PKM2) is a rate-limiting enzyme of aerobic glycolysis in cancer cells and plays important roles in cancer metabolism and growth. Here we show that vitamin K3 and K5 (VK3 and VK5) are relatively specific PKM2 inhibitors. VK3 and VK5 showed a significantly stronger potency to inhibit PKM2 than to inhibit PKM1 and PKL, 2 other isoforms of PK dominantly expressed in most adult tissues and liver. This study combined with previous reports supports that VK3 and VK5 have potential as adjuvant for cancer chemotherapy.
                              and it can save your ass if you get poisoned by warfarin. (Keep in mind these are a bit early.)


                                Different kinds of cancers develop resistances to the drugs used to treat them. Its interesting that in many cases these are very similar to bacterial resistances against antibiotics. Take for example, the classic cancer drug methotrexate. Methotrexate is the first of a class of drugs called anti-folates that are used to starve dividing cells of the purine and pyramidine nitrogenous bases needed DNA replication. It blocks the enzyme dihydrofolate reductase that eventually produces the folate necessary for this. Without the ability to produce more, dividing cells are limited in their ability to replicate DNA, a step necessary in cell division. Since cancer cells are promiscuous towards cell division, it affects them more than the normal cells of a given tissue.

                                However, cancer cells can resist this kind of treatment. In response to methotrexate exposure some cancer cells can amplify the DHFR gene, producing more of the enzyme. This requires more of the drug to overcome the resistant strain, but this may not practical in terms of toxicity for the patient.

                                Other resistance methods change the ability of the cell to acquire or retain the drug. Drugs like methotrexate (and others) utilize a drug transport receptor called the Reduced Folate carrier (RFC) for transport into the cell. Mutations have been recognized in this carrier in resistant cells, such that there is less methotrexate accumulation into the cell. Furthermore, some cancers have been noted to produce less of this receptor all together. The opposite strategy, in this case, is also true of cancer cells: they increase their ability to remove toxic drugs as well. Cancer cells are know to express drug transporters known as the ABC transporters. Perhaps these are best known for providing the safety net for the brain (and gonads): the' blood brain barrier'. These export chemicals from a cell, yielding resistance to a wide selection of drugs. In the case of cancer, proteins identified of note are the breast cancer resistance protein (BCRP) and the multi-drug resistance protein (MDR), both often found in cancer cell phenotypes that were less responsive to chemotherapies.



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