[ RadSafe ] Two interesting papers on DNA repair mechanisms

[Howard Long]

To further complicate it, what quantity of DNA breaks and the (Pollycove) reported 10 orders of magnitude greater repair occur with the various types of cancers?

The numbers are beyond my comprehension, so as with the many factors in an individual patient's healing, I am guided by apparent end results, as much art as science and not manageable with limited information like codes.

Howard Long 

On Jul 2, 2010, at 12:31 PM, Clayton J Bradt <CJB01 at health.state.ny.us> wrote:

> 
> Barbara,
>  
> I still have the same job essentially, I've just been moved to where they
> think I will cause less trouble.
> 
> Not being a biologist I have difficulty even formulating the questions I
> have about the whole cancer-radiation process.  Let me try again:
> 
> Every somatic cell regardless of tissue type has identical DNA - all the
> same genes.  Cancers are all characterized by the loss of differentiation
> and uncontrolled proliferation of cells.  What causes a cell to go bad, so
> to speak?  It is presumed to be the result of some change or changes in the
> cell's genetic make-up.   Since all cell's start off with the same DNA it
> is reasonable to assume that the same specific change(s) must occur in any
> cell before it undifferentiates and begins proliferating uncontrollably.
> The HPV/cervical cancer example supports this.  The mutations are not
> random but consist of very specific genetic sequences that are spliced into
> the somatic cell's DNA.  Would different genes spliced into the DNA have
> the same effect? That seems unlikely.
> 
> Does each type of cancer result from specific sets of genes being either
> spliced into or deleted from cell DNA? The similarity of all cancers (loss
> of differentiation and uncontrolled proliferation) suggests that very
> similar if not identical genes are involved. But if so, how does random DNA
> damage, such as results from ionizing radiation (and presumably from
> chemical agents), result in specific genetic mutations?
> 
> 
> Clayton J. Bradt
> Principal Radiophysicist
> Laboratory for Inorganic & Nuclear Chemistry
> NYS Dept. of Health
> 518-474-1993
> 
> blreider at aol.com wrote on 07/02/2010 02:28:08 PM:
> 
>> blreider at aol.com
>> 07/02/2010 02:28 PM
>> 
>> To
>> 
>> CJB01 at health.state.ny.us, radsafe at health.phys.iit.edu
>> 
>> cc
>> 
>> Subject
>> 
>> Re: [ RadSafe ] Two interesting papers on DNA repair mechanisms
>> 
>> Clayton,
>> 
>> Hope you are well.  I see from your signature that you either have
>> changed jobs or you have new stationary yet again.
>> 
>> I don't understand why the two statements are a contradiction.
>> Cancer is a general name for numerous diseases with numerous causes.
>> Not all non-radiation initiated cancers have to also be initiated by
>> radiation.  Are you saying that all radiation initiated cancers
>> also don't have another cause?  I guess that could be true if there
>> are no non-radiation causes for random DNA strand breaks.*
>> 
>> I don't know enough about the different cervical cancers to add
>> anything about the molecular structure, however for other cancers
>> there can be many different initial cell types all lumped together
>> under the name of the organ involved.  Is all cervical cancer
>> initiated in the same type of cell?  Lung cancer has numerous
>> initial lung cell types, and some of the same types of lung cancers
>> that are attributed to smoking are also attributed to radiation
>> (Adenocarcenoma).  Smoking also is linked to other types of lung
>> cancers that are not thought to be radiation induced (small cell).
>> 
>> The research to find mechanisms for cancer production is interesting
>> as applied to the statistics used in our field, hence previous
>> comments about LET and QF.
>> 
>> Regards
>> 
>> Barbara Reider, CHP
>> 
>> *And to make this more difficult, perhaps indirect radiation induced
>> strand breaks are not all random.  I though the early cell data
>> showed random breaks though (anyone with newer info?).
>> 
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