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. 2016 Jun 10;7(3):293–301. doi: 10.5306/wjco.v7.i3.293

Figure 4.

Figure 4

Histological and molecular analyses of HCT116 tumor samples. A-D: Histological examination of representative HCT116 tumor samples. Xenografts were harvested, paraffin embedded and processed for hematoxylin/eosin/safran. A and B are representative histological examinations from the uninfected xenograft group. C and D are representative histological examinations from the pks-positive-E. coli infected xenograft group. We noted that HCT116 tumor cells (arrowheads) infected with pathogenic E. coli strains are characterized by megalocytosis and progressive enlargement of the cell body and nucleus. Tumor cells in the pks-positive E. coli-infected xenograft group were surrounded by a remarkable infiltration of inflammatory cells (red arrow) compared to the uninfected xenograft group. Tumor necrosis was observed, especially in the infected xenograft group (black arrow). (Scale bars: 50 μm = × 20); E: MPO levels by enzyme-linked immunosorbent assay (ELISA) on HCT116 tumor specimens. An ELISA test was performed on tumor specimens after mouse sacrifice (day 34 post-xenograft). MPO standardized levels were significantly higher (1556 ± 313.6 vs 234.6 ± 121.6, aP = 0.001) in xenografts infected with pathogenic pks-positive E. coli strains. E. coli: Escherichia coli; MPO: Myeloperoxidase.