Talk:Myc

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Hello, isn't it a logical mistake to say that "A mutated version of Myc is found in many cancers, which causes Myc to be constitutively (persistently) expressed" ? It should be the opposite, shouldn't it? — Preceding unsigned comment added by Alblab91 (talk • contribs) 15:37, 20 September 2017 (UTC)


 * I agree - myc itself isn't mutated Harveyjamesm (talk) 13:18, 10 May 2018 (UTC)

distinction between n-Myc, c-Myc, l-Myc, and v-Myc
There should be more distinction between n-Myc, c-Myc, l-Myc, and v-Myc throughout this article. Although they fall under the same Myc family, these proteins are expressed and function differently amongst cell types. It's very misleading to make such sweeping generalizations about all Myc family member when many of the cited studies clearly focus on one Myc family member. Stateboi69 (talk) 18:55, 3 September 2010 (UTC)

(2008) rewording the first line of intro
I edited it because the actual first line is wrong. It is not incorrect binding of the transcription factor to the DNA which results in the formation of cancer. It is increased expression of genes by myc. That cannot be the result of a decreased level of binding! It is normally caused by increased expression of myc, this in turn will bind DNA more frequently and transcribe the target genes. I agree that it could be too indepth. Please rephrase was I have explained above. —Preceding unsigned comment added by 82.10.78.130 (talk) 17:16, 5 May 2008 (UTC)


 * OK, I've been wrong before. Let's look at it.


 * Just remember, though, that Wikipedia is written for the general, nonspecialist reader. I'm willing to ignore that rule in the body of an entry, but not in the lead. That means we can't put too much detail in the lead.


 * I also like to keep the vocabulary simple, because (according to a recent article in the New Scientist) most people who use English are not native speakers.


 * One of the reasons we're having problems with this entry is that it doesn't have a good, simple, verifiable source to check the definition against. I tried to simlify the original language of the entry. It really should have a WP:RS with a simple definition of myc. (And I couldn't find one myself, neither on the Internet nor on my bookshelf.)


 * You wrote:


 * Myc (cMyc) is a gene which encodes for a protein (transcription factor) that regulates the transcription of other genes. A mutated version of Myc is found in many cancers which causes Myc to be persistently expressed. This leads to the unregulated expression of many genes some of which are involved in cell proliferation and results in the formation of cancer.


 * If I were explaining this to a high school class, I wouldn't expect them to know what "encodes" or "transcription" means. I think "overexpression" is easier to understand than "unregulated expression."


 * I wrote:


 * Myc (cMyc) is a gene that regulates other genes. It codes for a protein that binds to the DNA of other genes. When Myc is mutated, or overexpressed, the protein doesn't bind correctly, and often causes cancer.


 * You say:


 * It is not incorrect binding of the transcription factor to the DNA which results in the formation of cancer. It is increased expression of genes by myc. That cannot be the result of a decreased level of binding!


 * The entry says:


 * Myc protein is a transcription factor that activates expression of a great number of genes through binding on consensus sequences (Enhancer Box sequences (E-boxes)) and recruiting histone acetyltransferases (HATs). It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the p300 co-activator, it inhibits expression of Miz-1 target genes.


 * I was trying to summarize that.


 * My understanding of that (and the illustration) is that it works like this: Myc expresses a protein. The protein binds on enhancer and repressor sequences. So yes, it sometimes inhibits expression.


 * When I say, "the protein doesn't bind correctly," I meant that the protein was supposed to bind to an enhancer or repressor sequence, but something went wrong, and it didn't bind right -- there was too much Myc protein, or it was truncated or didn't bind right, like the mutations in genes for heart muscle proteins or AML.


 * But maybe they're not. If you know for certain that the myc oncogene is always a problem of overexpression, and never a problem of truncation or binding -- then we'll have to change it. But you need a source.


 * The closest I could get to it was the following. Apparently myc sometimes upregulates some genes, and downregulates others. I'm not surprised. In those molecular flow charts, one protein is always inhibiting a second protein, which normally inhibits a third protein ...


 * http://www.sciencemag.org/cgi/content/full/sci;289/5485/1670
 * Science 8 September 2000:
 * Vol. 289. no. 5485, pp. 1670 - 1672
 * DOI: 10.1126/science.289.5485.1670
 * News Focus: MEDICINE: DNA Arrays Reveal Cancer in Its Many Forms
 * Jean Marx


 * "The MIT group, in collaboration with Robert Eisenman's team at the Fred Hutchinson Cancer Research Center in Seattle, has also looked at the changes elicited in cells by activation of the MYC oncogene. In results reported in the 28 March issue of the Proceedings of the National Academy of Sciences, they found that MYC activity turned up the expression of 27 genes, including some that promote cell division, and turned down the activity of another nine. "We're discovering the malignant pathways of these tumors," Staudt says. "Now we can ask whether interfering with these pathways can help."


 * Do you want to write another introduction? Just make sure (1) It's accurate (2) It's simple to understand and (3) It has a reliable source. Nbauman (talk) 20:24, 5 May 2008 (UTC)

Ok well I was not able to read that article my institution does not have access. But from the paragraph I understand your point and I agree that the article should be easy to understand. I don't have a problem with the article at the moment. But I have yet to find an example of mutations in myc's E-box sequence which is what your comment is suggesting "doesn't bind correctly" I have however found other mutations in myc's conserved sequences that lead to either decreased or increased expression of certain genes (comparative to wild type). I think you are correct in saying that myc encodes for a protein that may decrease the expression of another gene. But I cannot see how a transcription factor can act as an inhibitor. Anyway here is the article I have found.

http://www.nature.com/onc/journal/v20/n42/full/1204827a.html 20 September 2001, Volume 20, Number 42, Pages 6084-6094

c-myc box II mutations in Burkitt's lymphoma-derived alleles reduce cell-transformation activity and lower response to broad apoptotic stimuli

Nature: Oncogene Fabien Kuttler1, Patricia Amé1, Helen Clark2, 82.10.78.130 (talk) 11:05, 7 May 2008 (UTC)


 * I have no emotional investment in this entry; I just want it to be accurate, and if somebody who knows more than me comes along and corrects it, that's fine with me (as long as it meets the WP standard of being comprehensible to the non-specialist).


 * As for a transcription factor acting as an inhibitor -- I can understand that. A transcription factor binds to an enhancer, or it binds to a silencer. What's the difference? I imagine they're sending signals to RNA polymerase somehow.


 * I wish someone would find a link to a page that would explain it better. Nbauman (talk) 14:42, 7 May 2008 (UTC)


 * Found one. Gerard Evan explains in simple language how myc causes both proliferation and cell death. Nbauman (talk) 14:57, 7 May 2008 (UTC)

Image
Oh well, and people can't make sections. The included image description is wrong and I would delete the image itself too. Reason: the image depicts actually only a small part of the protein. The whole protein is still not crystallized, as of this writing. --Ayacop (talk) 08:40, 20 May 2009 (UTC)

The interactions section is kind of a cluster****
Any ideas on how to de-clutter it and make it more readable? — Preceding unsigned comment added by 129.81.92.57 (talk) 12:07, 4 October 2011 (UTC)
 * Similar to the Interactions section of many protein articles. Possibly they are automatically generated from a literature search. Probably best to discuss it at either of the interested projects ? - Rod57 (talk) 16:07, 16 March 2016 (UTC)

MYC Helps Cancer Hide
[http://www.the-scientist.com//?articles.view/articleNo/45545/title/MYC-Helps-Cancer-Hide/ MYC Helps Cancer Hide. March 2016] says " The researchers then demonstrated that decreasing the expression of CD47 and PD-L1 is likely to be necessary for tumor regression. They found that if Myc is inhibited but CD47 and PD-L1 are continually overexpressed, tumors in mice with MYC-driven T-ALL cells persisted. This confirmed the role of these Myc targets in regulating immune system evasion, said Gajewski. While inhibiting Myc overexpression normally prevents angiogenesis, continued expression of the two immune proteins despite Myc inhibition allowed angiogenesis to continue.

MYC directly bound to the promoters of these two immune genes in both mouse and human transformed cells, the researchers showed. Using a human bone cancer cell line, the team found that MYC bound the promoters of the two genes only when present at the high levels found in cancer cells.

To Felsher’s mind, the findings validate Myc as a promising anticancer target." - Rod57 (talk) 15:58, 16 March 2016 (UTC)

Clinical significance section has wrong content
It should say what diseases relate to aberrations (mutations or misregulation) of Myc ? Most of the material seems to belong in the Function section ? Then it can have a subsection about Myc as a potential drug target ? - Rod57 (talk) 16:17, 16 March 2016 (UTC)