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I came up with possible cancer treatments - are these feasible?

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    (Original post by Joinedup)
    what they're looking for in first year is mainly being able to find out what other people think and being able to accurately summarise and reference it properly.
    Find out if someone has had a similar thought to yours and reference it. Probably look at the primary research into these transcription factors to see if the authors mentioned anything similar... Then check for more recent publications which reference the earlier research.
    I'm transitioning into 2nd year. It's a 2nd year summer school project.
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    (Original post by susuthemusu)
    yes but instead of being a dip**** about it seeing you know very little about it, its not wise to beso critical. there is some link, it may not be the only one ofcourse, but it is a significant one.
    Oh dear, actually I know quite a lot about what you're talking about, and it just so happens I don't agree with the "evidence" in favour of it. It's actually VERY important and wise to be critical of things, especially things that don't have a lot of data to back them up.
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    (Original post by T-Toe)
    I'm doing a research project and I'm coming up with ways of how cancer cell grow could be reduced.

    Monitoring the activity of transcription factors and decipher which ones are oncogenic. Then via a series of trial and errors use various compounds which could be possible inhibitors. These inhibitors may have side effects so proper research is required.

    Like how prokaryotes have repressors ingrained in their genome e.g lacI which prevents the encoding of lac genes. Ingrain a human repressor into the human genome preventing the production of oncogenic transcription factors?

    Well?
    This has been done with Imatinib in treating chronic myeloid leukaemia, showing it is at least feasible. Imatinib is specific molecular inhibitor of a de-regulated tyrosine kinase that forms via the formation of the BCR-ABL oncogene in 95% of CML patients - so not directly related but you could at least mention it when describing how you would identify potential TF inhibitors.
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    (Original post by T-Toe)
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    Of course none of them are feasible. Do you really think that hundreds of scientists with PhDs and lives worth of experience haven't already tried all these ideas and found that they don't work?
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    (Original post by gateshipone)
    Oh dear, actually I know quite a lot about what you're talking about, and it just so happens I don't agree with the "evidence" in favour of it. It's actually VERY important and wise to be critical of things, especially things that don't have a lot of data to back them up.
    i highly doubt you know the depths. yeah no data apart from a couple of thousand people cured who actually attempted it. anyways as i said not trying to convince you.
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    Just smoke a joint, shrinks cancer tumors.
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    (Original post by T-Toe)
    Decomcracy I need your help.

    In my experiment E.coli was transformed by the implementation of a plasmid which contained lac operon, some antibiotic resistant genes as well as the gene which encodes AP-1.

    I'm trying to relate the the lac operon gene with a lac gene repressor which if added, would prevent the production of AP-1. I'm now trying to relate that with human biology. I know AP-1 can cause cancer. So if a repressor that stops the formation of a oncogenic transcription factor is added to the human genome it may help prevent the formation of cancers formed by transcription factors.

    Are there known repressors already in the body which stop the formation of oncogenic transcription factors?
    Have you done a literature search yet?

    Plugging the string "ap-1 transcription factor inhibitor cancer" into PubMed yields some interesting (and possibly relevant results):

    http://www.ncbi.nlm.nih.gov/pubmed/20531301

    e.g. the above is discussing the role of the SARI (Suppressor of activator protein-1, regulated by interferon) gene in blocking the actions of AP1 via adenovirus induced expression. More on SARI here:

    http://www.ncbi.nlm.nih.gov/pubmed/19074269

    Another paper reveals that SARI may have potential therapeutic benefits for CML:

    http://www.ncbi.nlm.nih.gov/pubmed/21892628

    Hope this helps somewhat (if it's all irrelevant to you please accept my apologies!).
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    Well, on the one hand, you could be wrong... and on the other hand, your idea has now been stolen.

    Congratz
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    Most drugs act by being inhibitors. It's nothing new.

    Problem: there are a ridiculous amount of different typed of cancers and there is also a large amount of drugs that can inhibit their growth and/or destruct them (chemotherapy). Using trial and error to find drugs with less side effects would take a lot of time and effort and would likely prove to be fruitless.
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    (Original post by T-Toe)

    Like how prokaryotes have repressors ingrained in their genome e.g lacI which prevents the encoding of lac genes. Ingrain a human repressor into the human genome preventing the production of oncogenic transcription factors?
    We have these. In fact, we have multiple different ones to the extent that there's redundancy.

    When a cell becomes cancerous, it will usually involve the failure of multiple repressors in the first place... Implanting a new one into our genome would be ineffective in the face of mutations and other mediated ways in which repressive influences are knocked out. Additional to the lack of efficacy, throwing a new inhibitory gene into our genome isn't really feasible - it could interrupt other genes to catastrophic effect (maybe even making cancer more likely), and since the cell cycle is normally a non-pathological process, could interfere with the life cycle of non-cancerous cells.
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    (Original post by susuthemusu)
    ...china has the second highest life expectancy despite it being classified as a developing country a few years ago. the highest cancer rates are all mainly in the west, and the surgical equipment being used today was used in china and india 150 years ago roughly...
    (Original post by HCubed)
    China actually has very high rates of some cancers (stomach, head, neck, lung) and low rates of others (breast, prostate, ovarian). This is nothing to do with the medical treatment being superior in China, and everything to do with diet and lifestyle factors. I suggest you know very little about western medicine - did they have Cyberknife 150 years ago in China?
    Also China does not have anywhere near the 2nd highest life expectancy. Macau and Hong Kong are in the top 10, but the rest of China (99% of the population) is around 80th.
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    (Original post by T-Toe)
    How do I mention all this and relate it back to transcription factors?
    You can look at the proteins involved in each process and suggest treatments that either increase or decrease the rate at which the processes occur, via altering the rate of transcription of the relevant proteins.

    E.G.

    Immortality-look at inhibiting TFs for telomerase
    Restriction of apoptosis - look at activating TFs for p53, and inhibiting TFs for p21, p27, etc
    Angiogenesis - look at inhibiting TFs for VEGF (I think)
    Incorrect response to growth factors - look at protein cascades like RAS, suggesting ideal times to attack the pathway and inhibit it
    Metastatic potential - I don't know anything about this.

    I would definitely focus on p53 - preventing apoptosis is one of the traits present in almost ALL tumors, and p53 is the primary protein involved in initiating apoptosis. Focus on its domains, it has three: a tetramerising domain, a DNA binding domain and a TF domain. You could attempt to increase the efficiency of tetramerization, the affinity of DNA binding, or the rate at which the p53 is synthesized. This could be done through altering the amino acid sequence of synthetic p53: for example, adding a hydrophobic group in the tetramerizing domain could encourage more efficient formation of the tetramer, and so increase the rate of apoptosis.

    Also... you could look at a protein called mdm2 which is involved in controlling levels of p53. It does this by binding to p53 and marking it for destruction in a proteolysing complex, proteosome. This process can be disturbed to encourage apoptosis by either inhibiting a TF for mdm2, preventing binding between mdm2 and p53, or some like method.

    Hope this isn't stuff you already know, I'm just putting down some stuff to get you started!
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    (Original post by susuthemusu)
    i highly doubt you know the depths. yeah no data apart from a couple of thousand people cured who actually attempted it. anyways as i said not trying to convince you.
    People saying they are cured isn't evidence. Gimme a paper that's been published in a peer reviewed journal and then I'll believe you.
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    (Original post by susuthemusu)
    although i strongly disagree with most western medicine, and believe cancer can be fairly easily cured/treated.
    to your question, i appreciate it can theoretically work but there are way to many variables not taken into account

    bring on the negs people!!!
    You actually just said you think it can be easily cured?!?! Have you ever read a book or studied science? Stick to your photography or whatever... Fool!!!!!
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    (Original post by T-Toe)
    I'm doing a research project and I'm coming up with ways of how cancer cell grow could be reduced.

    Monitoring the activity of transcription factors and decipher which ones are oncogenic. Then via a series of trial and errors use various compounds which could be possible inhibitors. These inhibitors may have side effects so proper research is required.

    Like how prokaryotes have repressors ingrained in their genome e.g lacI which prevents the encoding of lac genes. Ingrain a human repressor into the human genome preventing the production of oncogenic transcription factors?

    Well?
    I'm not sure from this what your project brief is, but I think what I would probably do is focus on one particular transcription factor, discuss which types and sub-types of cancers it aberrantly functions in, any transcriptional co-factors it binds, how it is regulated and how it is dysregulated in transformed cells. This will enable your introduction to spend a lot of time talking about how different cancers are caused by aberrant function of different proteins with particular reference to TFs. Depending on how much detail you want to go into, you can identify the active site, protein-protein interacting interfaces, etc. and talk about disrupting interactions. Then in your discussion you can talk about current TF inhibiting therapies (a lot have been mentioned in this thread).

    (Original post by Hypocrism)
    I would definitely focus on p53 - preventing apoptosis is one of the traits present in almost ALL tumors, and p53 is the primary protein involved in initiating apoptosis. Focus on its domains, it has three: a tetramerising domain, a DNA binding domain and a TF domain. You could attempt to increase the efficiency of tetramerization, the affinity of DNA binding, or the rate at which the p53 is synthesized. This could be done through altering the amino acid sequence of synthetic p53: for example, adding a hydrophobic group in the tetramerizing domain could encourage more efficient formation of the tetramer, and so increase the rate of apoptosis.

    Also... you could look at a protein called mdm2 which is involved in controlling levels of p53. It does this by binding to p53 and marking it for destruction in a proteolysing complex, proteosome. This process can be disturbed to encourage apoptosis by either inhibiting a TF for mdm2, preventing binding between mdm2 and p53, or some like method.
    p53 seems like an odd choice to be targeted by "rational treatments" simply because it's much harder to upregulate a protein's function with small molecules than it is to inhibit it. Yes, adding groups (by what mechanism) may increase tetramerisation slightly, but p53 function is not disrupted by a constitutive inability to tetramerise, rather by specific point mutations. Nor is it a problem of excessive regulation by Mdm2

    Incidentally increasing p53's specific binding to its consensus site seems to decrease apoptotic function, not increase it. High specific binding would lead to senescence, while binding highly dependent on cooperativity leads more to apoptosis. This balance between functions is another reason it's not such a great idea to try and alter p53's constitutive function.

    Perhaps one way to target p53 would be to build an inhibitor that binds to mutated p53 and prevents tetramerisation. This would solve the problem of when one copy of the gene is mutated and mutant proteins bind in tetramers with wild type copies, causing the whole tetramer to lose function (this being the reason p53 doesn't necessarily conform to the two-hit hypothesis). But this would be a very difficult way of targeting a small proportion of the malfunctioning p53 in the world. Oncogenes are definitely the way forward when looking at rational treatments.

    I'm not saying you're giving bad advice - I'm not sure if anyone knows the right advice to give given OP's vagueness regarding her project brief. I find it hard to believe it's just "In 8000 words or fewer, cure cancer." If it's a general cancer related project, obviously p53 needs to be a significant part of it.
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    (Original post by susuthemusu)
    if theres something you cannot comprehend, it doesnt make it illogical. china has the second highest life expectancy despite it being classified as a developing country a few years ago. the highest cancer rates are all mainly in the west, and the surgical equipment being used today was used in china and india 150 years ago roughly.
    you hardly know anything about the practise apart from "herbs" which is the least significant method, so you are no position to judge. if every person had your attitude its no wonder why modern medicine has only managed to get so far.
    Second highest of what? China has a below average life expectancy. Sure, its not terrible, but at 73.3 years, thats only just above the world average of 69.6 years. And please enlighten me as to what surgical equipment was being used 150 years ago in china/india.

    And no, my mum believes in more than herbs. She also thinks massage and acupuncture works, and she believes that highly skilled practitioners can tell what is wrong with you by simply feeling your pulse. I'm not saying none of it works - I reckon massage and acupuncture can probably help in physiotherapy and muscular problems, just not all the things she thinks it can cure. However, my attitude is one of skepticism - yours is one of faith. Modern medicine is so great because of skepticism - everything that it prescribes has been proven to work.
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    (Original post by T-Toe)
    What if you cannot find anything. What then? Could you not just mention how the experiment could be done?
    Sure you could but you do need some form of evidence or experimental data to back your thoughts up. Surely some tests have been done on mice or something that can back your ideas?
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    (Original post by T-Toe)
    Decomcracy I need your help.

    In my experiment E.coli was transformed by the implementation of a plasmid which contained lac operon, some antibiotic resistant genes as well as the gene which encodes AP-1.

    I'm trying to relate the the lac operon gene with a lac gene repressor which if added, would prevent the production of AP-1. I'm now trying to relate that with human biology. I know AP-1 can cause cancer. So if a repressor that stops the formation of a oncogenic transcription factor is added to the human genome it may help prevent the formation of cancers formed by transcription factors.

    Are there known repressors already in the body which stop the formation of oncogenic transcription factors?
    Just a couple of points:

    -Bacterial gene regulation is a fair bit simpler than in eukaryotes.

    -In cancer, it's virtually never down to a single failure or over-expression of a gene.

    -Gene therapy is a tricky beast. Certain vectors can stably integrate at a given locus (for example, the AAV2/5 vector will insert at a known locus on chromosome 19), but many lead to random insertions which can be catastrophic. It's also virtually impossible to find a vector that can lead to global transfection throughout the body (not that that would necessarily be necessary).

    -Modulation of gene regulation is much more easily achieved with chemical inhibitors of regulatory elements, or with RNA interference etc.
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    (Original post by susuthemusu)
    although i strongly disagree with most western medicine, and believe cancer can be fairly easily cured/treated.
    to your question, i appreciate it can theoretically work but there are way to many variables not taken into account

    bring on the negs people!!!
    Here, watch this funny cartoon:

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