Guidelines For Clinical Practice
Copyright ©2010 Baishideng Publishing Group Co.
World J Gastrointest Pathophysiol. Oct 15, 2010; 1(4): 129-136
Published online Oct 15, 2010. doi: 10.4291/wjgp.v1.i4.129
Figure 1
Figure 1 Contrast-enhanced computed tomography image of liver metastasis of protein induced by vitamin K absence or antagonist II-producing gastric cancer. Multiple low density nodules, which are poorly enhanced, are observed in the liver.
Figure 2
Figure 2 Gross appearance of a case of protein induced by vitamin K absence or antagonist II-producing gastric cancer. A large Borrmann type 3 tumor occupies the gastric body.
Figure 3
Figure 3 Gross appearance of liver metastasis of protein induced by vitamin K absence or antagonist II-producing gastric cancer. Multiple nodular tumors and portal vein tumor thrombi (arrows) are observed.
Figure 4
Figure 4 Microscopic appearance of protein induced by vitamin K absence or antagonist II-producing gastric cancer. A: Gastric tumor with the appearance of a moderately to poorly differentiated adenocarcinoma (HE stain; the scale bar indicates 50 μm); B: Intravenous tumor with a hepatoid pattern (HE stain; the scale bar indicates 100 μm); C: Metastatic liver tumor with a hepatoid pattern (HE stain; the scale bar indicates 50 μm).
Figure 5
Figure 5 The results of immunohistochemical staining. A: The tumor cells forming glandular structure are positive for protein induced by vitamin K absence or antagonist II; B: The tumor cells are also positive for alpha-fetoprotein. All scale bars indicate 25 μm.