Re: World Health Organization results: Passive Smoking in Childhood Prevents Lung Cancer

DZ <18260@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx> wrote in news:8691@
275867185.698323651.1876.31431.14145:

David Winsemius <doe_snot@xxxxxxxxxxx> wrote:
DZ wrote:
David Winsemius <doe_snot@xxxxxxxxxxx> wrote:
Ray Johnstone <ray@xxxxxxxxxxxx> wrote:
World Health Organization results: Passive Smoking in Childhood
Prevents Lung Cancer

However, quoting Vogelstein & Kinzler (Nat Genet 2004),
(http://cmpd.umd.edu/chordoma/vogelstein.pdf)

"The revolution in cancer research can be summed up in a single
sentence: cancer is, in essence, a genetic disease".

One should remember that biochemists generally think at the level of
cell division rather than at the organismal level. I have no real
argument with the notion that the mechanisms for development of
cancer are mediated through cellular DNA events. That is quite a
different statement however, than saying tumorigenesis is entirely
inherited.

That cancer mechanisms are related to molecular events having to do
with DNA is too long known and trivial, so I don't think that's what
they mean, especially considering that much of the paper talks about
cancer promoting and supressing VARIATION, even though a lot of it has
to do with somatic cells.

They are using "genetic" to refer to acquisition of new somatic DNA
features in stem cell chromosomes that then alter cellular behavior. The
first sentence is: "The cast. Alterations in three types of genes are
responsible for tumorigenesis: oncogenes, tumor-suppressor genes and
stability genes". The only time germline mutations enter into their
discussion is when an inherited predisposition allows the random mistakes
and influences by carcinogens on the sequence leading toward
tumorigenesis to be more easily observed.

Imagine an experiment where fully consenting pairs of identical twins
are assigned in a randomized fashion to smoke or not to smoke for many
years. Would the rates of lung cancer be more similar between
genetically similar individuals compared to individuals that smoked?

That's the kind of a question that I'm fairly certain nobody knows the
answer to.

The twin and sibling studies I have seen put the proportion of the
variability in cancer incidence due to inherited factors at around 30%. I
am not sure why you think randomizing monozygotic twins needs to be done
for this question. They do have identical genetic "substrate". Why
wouldn't studying cohorts of the identical twins in which only one had
adopted a smoking habit be analyzable? What I see implicates tobacco
smoke as a stronger influence than genetics in lung cancer and
cardivascular mortality.

National Academy of Sciences/National Research Council Twin Registry.
<http://pmid.us/7914565>
"No genetic effect on lung cancer mortality was observed. The ratio of
observed to expected concordance among monozygotic twins did not exceed
that among dizygotic twins (overall rate ratio 0.75 [95% CI 0.35-1.6]),
even though monozygotic twin pairs are more likely to be concordant for
smoking than dizygotic twin pairs in this population."

From the Swedish Twin Registry:
<http://pmid.us/3403128>
"The comparison of deaths in cigarette-smoking twins and their non-
smoking co-twins gave the following risk estimates for monozygotic (MZ)
men: death all causes 1.6 (35 versus 22 first deaths), CHD death 2.8 (11
versus 4)."

And from a Finnish twin study:
<http://pmid.us/2814591>
"Analyzing on first deaths from concordant pairs, there were 13 deaths in
the smokers of male CS MZ pairs and 1 death in the nonsmoking cotwins
(relative risk = 13.0, P less than 0.01). Excess mortality was also found
for male CS DZ smokers (RR = 2.43, P less than 0.01)."

--
David Winsemius
.

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