Leukemia
Lung
: Development.
2006 Feb 15; [Epub ahead of print] AIM: To examine the
expression of Egr-1, c-fos and cyclin D1 at both transcript and protein levels in
esophageal carcinoma and to correlate the level of their expressions with
precancerous and paracancerous esophageal lesions
and esophageal carcinoma. METHODS: In situ hybridization and immunohistochemistry were used respectively to detect
the expression of mRNA and proteins of Egr-1, c-fos
and cyclin D1 in 70 cases of esophageal squamous cell carcinoma and their corresponding para-cancerous mucosa and upper cut edge mucosa.
RESULTS: In situ hybridization and immunohistochemistry
showed positive staining of all three mRNAs in the cytoplasm and those of
the proteins in nuclei. Overexpression of Egr-1,
c-fos and cyclin D1
mRNAs and their proteins was found in dysplasia
and squamous carcinomas. The expression level of
Egr-1 and c-fos was high, and cyclin
D1 was low in dysplasia mucosa, whereas the
expression of Egr-1 was decreased, c-fos was
maintained and cyclin D1 was increased in the
cancers. The expression of both c-fos and
cyclinD1 was consistent between the mRNA and protein in their corresponding
high expression lesions. CONCLUSION: The expression of Egr-1, c-fos and cyclin D1 varies in
esophageal precancerous lesions and cancer tissues, suggesting an
involvement of these genes in the development of esophageal carcinoma.
(2006)
Schmidt-Ullrich R, Tobin DJ, Lenhard
D, Schneider P,
Paus
R, Scheidereit
C.
A novel function of NF-kappaB in the development
of most ectodermal appendages, including two
types of murine pelage hair follicles, was
detected in a mouse model with suppressed NF-kappaB
activity (c(IkappaBalphaDeltaN)).
However, the developmental processes regulated by NF-kappaB in hair follicles has remained unknown.
Furthermore, the similarity between the phenotypes of c(IkappaBADeltaN)
mice and mice deficient in Eda A1 (tabby) or its
receptor EdaR (downless)
raised the issue of whether in vivo NF-kappaB
regulates or is regulated by these novel TNF family members. We now
demonstrate that epidermal NF-kappaB activity is
first observed in placodes of primary guard hair
follicles at day E14.5, and that in vivo NF-kappaB
signalling is activated downstream of Eda A1 and EdaR. Importantly,
ectopic signals which activate NF-kappaB can also stimulate guard hair placode formation, suggesting a crucial role for NF-kappaB in placode
development. In downless and c(IkappaBalphaDeltaN) mice, placodes
start to develop, but rapidly abort in the absence of EdaR/NF-kappaB
signalling. We show that NF-kappaB
activation is essential for induction of Shh and cyclin D1 expression and subsequent placode
down growth. However, cyclin D1 induction appears
to be indirectly regulated by NF-kappaB, probably
via Shh and Wnt. The
strongly decreased number of hair follicles observed in c(IkappaBalphaDeltaN) mice compared with tabby mice,
indicates that additional signals, such as
PMID: 16481354 [PubMed - as supplied by
publisher]
PMID: 14966901 [PubMed - in process]