AW: [ RadSafe ] cancer is the result of defective tissue/immunecontrol
Rainer.Facius at dlr.de
Rainer.Facius at dlr.de
Fri Jun 30 05:47:35 CDT 2006
This very Thursday I was discussing with the head of our Institute - a medical Professor holding also the chair of Aerospace Medicine of our very prestigious University RWTH Aachen - the curriculum for a new Course on Space Medicine in our institute.
Among the topics in physiology, the altered immunocompetence in microgravity was assigned to an extra lecture. Without thinking about my post I drew his attention to the fact that - according to recently emerging empirical evidence - such alterations might well affect seriously our space radiation cancer risk estimates, e.g. for planned missions to Mars if indeed - as I surmised - tumourigenesis were significantly controlled (also) by the immune system. In response he looked at me with an expression of astonishment and (in essence) said:
"Well, this is really an old hat!"
In other words, for him - the Professor of Medicine - these exciting observations by Kim et al. provide just an animal-experimental corroboration of matters of fact which for man are already established.
I in turn was surprised seeing him consider this as a matter of course and was not prepared to argue against it. I certainly will pick up this topic on the next occasion with him and you as well might wish to reconsider it.
Kind regards, Rainer
Dr. Rainer Facius
German Aerospace Center
Institute of Aerospace Medicine
Voice: +49 2203 601 3147 or 3150
FAX: +49 2203 61970
Von: radsafe-bounces at radlab.nl [mailto:radsafe-bounces at radlab.nl] Im Auftrag von John Jacobus
Gesendet: Donnerstag, 29. Juni 2006 23:20
An: Facius, Rainer; radsafe at radlab.nl
Betreff: Re: [ RadSafe ] cancer is the result of defective tissue/immunecontrol
As you note, at least in murine gastrointestinal cancer (sic) this is true. However, I do not think you can say this about other cancers. I guess you could, but do you think all cancers are due to defective tissue/immune control? It is a question of recognition of "self," e.g., cancers are recognized as normal tissues, which they are to the immune system.
--- Rainer.Facius at dlr.de wrote:
> For those who always knew that (at least murine
> gastrointestinal) cancer is the result of defective tissue/immune
> "The results support the concept that cancer, as an outcome, reflects
> the loss of the normal communication between the cellular constituents
> of a given organ8, and indicate that Smad4-deficient T cells
> ultimately send the wrong message to their stromal and epithelial
> Regards, Rainer
> Dr. Rainer Facius
> German Aerospace Center
> Institute of Aerospace Medicine
> Linder Hoehe
> 51147 Koeln
> Voice: +49 2203 601 3147 or 3150
> FAX: +49 2203 61970
> Nature 441, 1015-1019 (22 June 2006) | doi:10.1038/nature04846;
> Received 9 February 2006; Accepted 28 April 2006
> Byung-Gyu Kim1, Cuiling Li2, Wenhui Qiao2, Mizuko Mamura1, Barbara
> Kasperczak3, Miriam Anver3, Lawrence Wolfraim1, Suntaek Hong1,
> Elizabeth Mushinski4, Michael Potter4, Seong-Jin Kim1, Xin-Yuan Fu5,
> Chuxia Deng2 and John J. Letterio1
> Smad4 signalling in T cells is required for suppression of
> gastrointestinal cancer
> SMAD4 (MAD homologue 4 (Drosophila)), also known as
> DPC4 (deleted in pancreatic cancer), is a tumour suppressor gene that
> encodes a central mediator of transforming growth factor- signalling1,
> 2, 3, 4.
> Germline mutations in SMAD4 are found in over 50% of patients with
> familial juvenile polyposis, an autosomal dominant disorder
> characterized by predisposition to hamartomatous polyps and
> gastrointestinal cancer5, 6. Dense inflammatory cell infiltrates
> underlay grossly normal appearing, non-polypoid colonic and gastric
> mucosa of patients with familial juvenile polyposis7. This prominent
> stromal component suggests that loss of SMAD4-dependent signalling in
> cells within the epithelial microenvironment has an important role in
> the evolution of intestinal tumorigenesis in this syndrome. Here we
> show that selective loss of Smad4-dependent signalling in T cells
> leads to spontaneous epithelial cancers throughout the
> gastrointestinal tract in mice, whereas epithelial-specific deletion
> of the Smad4 gene does not. Tumours arising within the colon, rectum,
> duodenum, stomach and oral cavity are stroma-rich with dense plasma
> cell infiltrates. Smad4-/- T cells produce abundant TH2-type cytokines
> including interleukin (IL)-5, IL-6 and IL-13, known mediators of
> plasma cell and stromal expansion. The results support the concept
> that cancer, as an outcome, reflects the loss of the normal
> communication between the cellular constituents of a given organ8, and
> indicate that Smad4-deficient T cells ultimately send the wrong
> message to their stromal and epithelial neighbours.
> . . .
"You get a lot more authority when the workforce doesn't think it's amateur hour on the top floor."
GEN. MICHAEL V. HAYDEN, President Bush's nominee for C.I.A. director.
John Jacobus, MS
Certified Health Physicist
e-mail: crispy_bird at yahoo.com
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