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Bad Manners and Good Gossip

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October 22, 2006


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George L. Gabor Miklos

What can one say...?

The "landmark" Science paper is an almost complete waste of time, and money.

Recall that a very large number of the mutations are changes from CG doublets to TG doublets, which simply indicates deamination of unmethylated Cs to uracil that are then recognized as T in the next replication. cancer cells the methylation system has gone awry...surprise..surprise.

This sequencing madness won't stop because there are all those machines around...and they need to be fed.

Peter Duesberg

At the risk of redundancy, may I say again what I answered when first being asked what I thought of tumor genome sequencing as a way forward.

"Why don't they start with the diploid ones?"


At the risk of my own redundant addition, permit me to recall the thoughts of the one and only Max Delbruck on the subject of "Homo scientificus", and which served as my introduction to what is now YBYL.

They may be read here.

Darin C. Brown

And at the certainty of my own redundancy, and in the spirit with which this essay by MOTYR was obviously written, and in which it has been received by the three "good, *'ole* docs" leaving comments here before me, let me point to some remarks of the mathematician, logician, philosopher, G. Spencer Brown, which serve as the Epilogue to the Serge Lang Archive at the AIDS wiki.

Roberto Stock

"But in the last twenty-five years... biochemistry has been made into the handmaiden of the new and ill-defined science of molecular biology of which it is not easy to say in what, if anything, its practitioners are trained thoroughly (...) Those would still accept the jocular definition that I proposed many years ago: Molecular Biology is the practice of biochemistry without a license. (...) This shift has had the consequence that a great number of valid biochemical problems are no longer pursued, since, considered as unfashionable, they are not funded. (...) Twenty morons at the right places can kill a science."

In retrospect: a commentary by Erwin Chargaff on 'Studies on the structure of ribonucleic acids', Bioch. Biophy. Acta 1000: 15-16, 1989.


"There can, however, be little doubt that the whole complex of the natural sciences has become a substitute religion, fulfilling the double roles of mysterious incomprehensibility to the lay public and a means of livelihood for its practitioners. The first function could easily be taken over by another creed or pseudo creed, but not the second. The institutionalization of science as a mass occupation, which began during my lifetime, has brought with it the necessity of its continual growth --- similar in that respect to such mythical entities as the 'gross national product' --- not because there is so much more to discover, but because there are so many who want to be paid to do it. Any attempt at reform is, therefore, met by insincere cries about the 'freedom of scientific inquiry'; and this will be followed by the immediate constitution of all sorts of pressure groups, marching under the banner of Galilei. Entrepreneurs disguised as freedom-fighters may look ludicrous, but they are usually effective, for there is little as irresistible as the momentum of the pocketbook."

Heraclitean Fire by Erwin Chargaff, p.117, 1978.



Regarding your diploid comment, and not trying to sound too lazy but I don't want to read all of "Oncogenes and Aneuploidy" right now, are you referring to the fact that there are indeed no diploid cancer genes? (Diploid being the normal state of human genes, if I recall my biology correctly.) Or am I missing something else here?



Allow me to answer you on behalf of Prof. Duesberg (although since you apparently know him well enough to call him by his first name, I wonder why you do not ask him personally via telephone or email?) who I do not think has any time to spare to address your "lazy" question.

Be that as it might. Yes. There is no completely clean example of a diploid tumor in the vast medcial literature relating to cancer cytogentics for a very long time.

But you seem to be so consumed by oncogenetics that you even write "diploid cancer genes" instead of diploid cancer cells.


Thanks, Otis. I suppose I should have made a more general comment rather than addressing Prof. Duesberg directly (with whom I am not actually on a first-name basis, but since he signed himself "Peter Duesberg" instead of "Professor Duesberg", I felt that it would be friendlier to refer to him as "Peter").

In any case, I had a feeling that he was trying to be funny and was just double-checking that. I am not in fact "consumed by oncogenetics", just a curious bystander.


Hi Steve,

You are welcome and I hope you forgive my slight over-sensitivity on the point of the salutation to the "near universally despised professor" Duesberg.

And yes, he was being funny, but as is typical, he was also making a very serious point, which I trust you have now gotten.

May I ask you to say either publicly or via email why you read YBYL?



Hey, don't know who you are but I did appreciate your very amusing analysis. You really hit the nail on the head on several issues. I must say that being the anti-cancer genome poster boy has taken a bit of a toll on me, especially since the Vogelstein paper. So few people are willing to say what they think it is disheartening and how completely some of them have been bought off is a sight to see. I am especially disappointed in Harold Varmus. Stillman I can understand because he knows nothing about cancer, but Varmus, I thought he had more to him. Anyway, I wish more people would speak up and try to put some rationality in this. I think I am the voice of reason but I am being painted as an old stick in the mud who can't see into the future by people like F. Collins. Such is life, but I really did enjoy your essay. And, of course, I am a big fan of Alice.....



George L. Gabor Miklos

I have been in correspondence.

I wanted to ensure that I had absolutely and correctly understood the tissue samples used in the Science paper I wrote directly to the authors, and they confirmed my fears.....Oi vey indeed.

People should look very carefully at the samples that were used for sequencing and then compared ....their jaws will drop.

The discovery phase consisted not of DNA from *real primary tissues*...oh no...we couldn't do that! consisted of 11 samples of cells that had *metastazied from the colon to the liver*; consisting of *3 cell lines* and *8 xenografts*....human cells grown in that's an interesting mutational environment. The cell lines were **years old.

For the breast cancer discovery samples there was *no* xenograft derived material; *only* cell line material originally from primary breast in this case it was not metastatic material.
For validation, microdissected primary tumor tissue from the breast was used.

Thus the two types of tissue source being compared, liver mets and breast primary differ; one was from metastatic material, the other was from primary tumors! There were also differences as regards cell lines and xenografts were used in the breast samples.

So what we have are metastatic cells being compared to primary tissue.....apples to oranges.

It is also obvious to Blind they say here generically...(and that I wrote before) -- the high frequency of "mutation" CG to TG doublets is likely due to deamination of unmethylated Cs to uracil and their subsequent recognition during replication as Ts. All this tells me is that the cellular methylation controls are whacked around in cancer cells...hello?

Finally the differences in mutation frequencies are meaningless...because of the type of comparisons being made. Different cell types will have different levels of initial methylation...and as those cell types struggle to find their identity in the new unstable aneuploid lineages of the cancer...their methylation characteristics ...and hence their deamination probabilities will differ...hello?

I rest my case Your Honour!

As for Varmus...his nickname is ...

One thing is for sure...deep down I'm not shallow.

your pal on the hill.

People should indeed be encouraged to think outside the box, but only when there is evidence of some thinking going on inside the box.


And one more thing..... it is quite possible that many of the repeating mutant genes in cancer, the CAN genes, are mutant not because of a role in cancer, but because they are simply more prone to mutagenesis due to some other common property such as their transcriptional or chromatin state or even the position within the nucleus. A property that would differ between different tissues. I have considered that caveat but until I read your article I did not know how to test that. But you pointed out the solution, to analyze the frequency of synonymous mutations in the same genes. If they are also above average, then the increased frequency of the nonsynonymous mutations would not be significant. Unfortunately the numbers are so small that statistical significance might be a problem. But your essay gave me that idea.

Thanks Mr. Mouth of the Yellow River.

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