[ RadSafe ] cancer is the result of defective tissue/immune control

[John Jacobus]

Rainer,
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 control.
> 
> "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."
> 
>
http://www.nature.com/nature/journal/v441/n7096/full/nature04846.html
> 
> 
> 
> Regards, Rainer
> 
> Dr. Rainer Facius
> German Aerospace Center
> Institute of Aerospace Medicine
> Linder Hoehe
> 51147 Koeln
> GERMANY
> 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
> 
> Abstract
> 
> 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
John Jacobus, MS
Certified Health Physicist
e-mail:  crispy_bird at yahoo.com

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