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. 2007 Dec 27;99(3):524–530. doi: 10.1111/j.1349-7006.2007.00707.x

Figure 1.

Figure 1

Disruption of the ataxia telangiectasia mutated (ATM)–Chk2 pathway in human oral epithelial lesions. (a) Representative illustrations of immunohistochemistry on the expression of phosphorylated (p) Chk2, Chk2, fragile histidine triad (Fhit), p53, and Ki‐67 in human squamous epithelial lesions (normal epithelia, dysplasia, oral squamous cell carcinoma [OSCC]in situ, and invasive OSCC) Original magnification, ×100. (b) Summary of immunohistochemical analyses. (c) Microsatellite analysis at D3S1234 of the FHIT locus. Loss of heterozygosity (white arrow) and allelic imbalance (black arrow) are shown.