Posted On:12/08/2011 12:34am
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.
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Posted On:12/08/2011 1:46am
Style: Boxing, Solar Ray Attack
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 1:51am at .
He was punching him like the collective karmic debt he'd accrued was coming to collections, mostly on his face.
Posted On:12/08/2011 4:50pm
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 4:58pm at .
Posted On:1/25/2012 6:25am
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.)
Posted On:2/10/2012 7:07pm
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.
Posted On:3/05/2012 9:23pm
Here's a pic of the two compounds in question. Notice the key differences in red and their very close similarity. It was developed in the 40s for cancer treatment and is used even today. This drug was first developed by a little known Indian scientist named Yellapragada Subbarao, who did a lot of very important work in early biochemistry, but sadly went mostly unnoticed.
Rectify this injustice mofos! Tell others of this sorrowful tale.
Posted On:3/24/2012 12:27am
One of the most recent advances in cancer therapy has been the development of new drugs inhibiting a class of enzymes called tyrosine kinases. Normally, these enzymes are involved with the transduction of signals involving the growth and proliferation of a cell. In cancer cells, however, their activity is greatly increased such that they gain increased ability to proliferate and spread general nastiness, in contrast to the ordered and regulated growth of normal cells. In 2005, one of the first drugs of the class, imatinib, was lauded by time magazine and the New York Times as a great leap forward in cancer treatment and "converted a fatal cancer into a manageable chronic condition." [NYtimes] With few treatment options besides a bone marrow transplant, chronic myelogenous leukemia and was one of the more fatal kinds of cancer. However, with these new therapies researchers have shown that “after 60 months of Gleevec (imatinib’s brand name) therapy, 98% of patients had shown a complete hematologic response. Also at 60 months, the estimated overall survival rate for patients was 89%, with a relapse rate of only about 17%.” 
However, a word of caution must be spread. These drugs are not the often sought after ‘cure for cancer,’ as patients still run the risk of relapse and mutation fueled resistance to the therapies, as well as the controversy considering the incredible cost of treatment (imatinib costs $32-98K per year for CML). That said, their development is still a milestone in our understanding of cancer pathology and its treatment. Much of the class was developed out of what is called 'rational design' methodology, that is to say by using deductive means based upon knowledge of the shape and function of the principal components of the systems. This is opposed to drug screening strategies, used during much of the earlier history of drug discovery, of finding a lucky diamond in the rough and modifying it to fit certain 'structural activity relationships'. Direct knowledge of the target areas and their effects has allowed medicinal chemists to design new approaches from the ground up to develop more effective treatments for disease. Perhaps, as the knowledge base becomes deeper and more comprehensive, we might be able to attack the real root of the issue in this terrible disease, but for the time being we must be patient with the fruits that our limited knowledge provides.
What exactly is a tyrosine kinases and what does it do?
Read more here....
Posted On:3/24/2012 1:03am
I've avoided joining this thread because I feel it is way over my head, but as a Radiation Therapist I feel have more of a grasp on the subject than most people. This thread has mainly focused on chemo treatments but what does the OP think about radiation treatments for caner and other therapies? Often times chemo is used with radiation and surgery to treat cancer but I don't recall seeing it mentioned much here.
In addition diseases such as leukemia were once frequently treated with radiation but are now less commonly treated. Does the OP think other forms of radiation therapy will ultimately be replaced by chemo?
Posted On:3/24/2012 1:19am
Yes, I feel they will ultimately be replaced with more effective and target specific chemo therapies designed from knowledge gleaned from molecular biology. Perhaps in the future these will then be replaced with RNA-DNA based therapies that target the broken genes in question and then, rather than remission, we could be looking at a specific cure as its thought of in the common parlance. On that note, we should be on the lookout for micro RNA based diagnostics and, if we're so lucky, therapies very soon.
Posted On:3/27/2012 8:37am
As a radiation therapist, what do you feel are the major challenges of your profession in the next 10 years? How are the current best practices changing with the times and how are they improving the treatment of patients?
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