Thread: Cancer Gift
9/10/2011 8:01pm, #31
9/11/2011 7:11pm, #32
- Join Date
- Jul 2011
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.
9/12/2011 4:24am, #33
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
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.
9/12/2011 6:17am, #34
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.
9/14/2011 3:57pm, #35
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.
9/16/2011 8:38pm, #36
- Join Date
- Jul 2011
11/22/2011 8:53am, #37
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.
11/25/2011 5:13pm, #38
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.
11/25/2011 5:17pm, #39
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;
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.
11/30/2011 4:41pm, #40
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.