10.6084/m9.figshare.5230417.v1
Tajima Y.
Tajima
Y.
Murakami T.
Murakami
T.
Saito T.
Saito
T.
Hiromoto T.
Hiromoto
T.
Akazawa Y.
Akazawa
Y.
Sasahara N.
Sasahara
N.
Mitomi H.
Mitomi
H.
Yao T.
Yao
T.
Watanabe S.
Watanabe
S.
Supplementary Material for: Distinct Involvement of the Sonic Hedgehog Signaling Pathway in Gastric Adenocarcinoma of Fundic Gland Type and Conventional Gastric Adenocarcinoma
Karger Publishers
2017
Gastric adenocarcinoma of fundic gland type
Sonic hedgehog signaling pathway
β-Catenin
Guanine nucleotide binding protein, alpha stimulating complex
2017-07-21 08:34:10
Dataset
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Distinct_Involvement_of_the_Sonic_Hedgehog_Signaling_Pathway_in_Gastric_Adenocarcinoma_of_Fundic_Gland_Type_and_Conventional_Gastric_Adenocarcinoma/5230417
<p><b><i>Background/Aims:</i></b> Gastric adenocarcinoma of fundic gland
type (GAFG), which is a rare variant of gastric cancer, is reportedly
associated with both Wnt/β-catenin signaling activation and guanine
nucleotide binding protein, alpha stimulating complex (<i>GNAS</i>) mutations. This study aimed to elucidate potential roles of the Sonic hedgehog (Shh) signaling pathway in GAFG. <b><i>Methods:</i></b>
We performed immunostaining for β-catenin and Shh signal-associated
proteins, including Patched (Ptch), Smoothened (Smo), and
Glioma-associated oncogene-1 (Gli1), and the direct sequencing of <i>GNAS</i>/<i>BRAF</i>/<i>KRAS</i> in 27 GAFGs, and compared them with 30 conventional gastric adenocarcinomas (CGAs). <b><i>Results:</i></b>
GAFGs exhibited significantly lower immunoreactivity scores for Ptch,
Smo, and Gli1 than CGAs. Moreover, while the Ptch score was
significantly lower in the GAFG tumor areas than in the non-neoplastic
areas adjacent to GAFG, the score was significantly higher in the CGA
tumor areas than in the non-neoplastic areas. Similar trends were
observed in the scores for Smo and Gli1. β-Catenin expression and <i>GNAS</i>
mutations were found in 22 (81%) and 8 (30%) of the 27 GAFGs
respectively. Gli1 expression was significantly associated with
mutations in <i>GNAS</i>. <b><i>Conclusion:</i></b> GAFG and CGA
exhibited distinct Ptch, Smo, and Gli1 expression patterns.
Downregulation of the Shh signaling pathway, as well as activation of
the Wnt/β-catenin signaling pathway, may therefore be associated with
tumorigenesis in GAFG.</p>