The abnormal expression of c-kit is implicated in the pathogenesis of a variety
of solid tumors. The Rb pathway and p53 act as cell cycle regulators. The purpose of this study
was to assess the expression of c-kit, Rb, p53, p16 and cyclin D1 and their relationship to clinical
and pathological parameters in patients with non-small cell lung carcinomas (NSCLCs).
Methods : Tissue microarrays consisting of 2 mm cores from the corresponding blocks were
constructed from 54 NSCLCs. Immunohistochemical staining for c-kit, Rb, p53, p16 and cyclin
D1 was performed. C-kit immunostaining was considered positive if ≥≥10% of tumor cells were
immunoreactive along the membrane and/or in cytoplasm. For Rb, p53, p16 and cyclin D1,
tumor cells showing a nuclear staining pattern were interpreted as positive. Results : We found
that c-kit was expressed in 13 (24%) cases, Rb was lost in 39 (72%) cases, p53 was expressed
in 28 (52%) cases, p16 was lost in 42 (78%) cases and cyclin D1 was expressed in 33 (61%)
cases. The c-kit expression was significantly higher in adenocarcinoma (39%) than in squamous
cell carcinoma (8%). We did not find any correlation between c-kit, Rb, p53, p16 and
cyclin D1 expression and clinicopathological parameters such as: age, tumor size, lymph node
involvement, disease stage and distant metastasis. There was a direct correlation between
p53 expression and Rb loss. Conclusions : These results suggest that c-kit may be a useful
therapeutic target for patients with c-kit positive tumors, and that the disruption of Rb and p53
pathways may play an important role in the development and progression of NSCLCs.
The abnormal expression of c-kit is implicated in the pathogenesis of a variety
of solid tumors. The Rb pathway and p53 act as cell cycle regulators. The purpose of this study
was to assess the expression of c-kit, Rb, p53, p16 and cyclin D1 and their relationship to clinical
and pathological parameters in patients with non-small cell lung carcinomas (NSCLCs).
Methods : Tissue microarrays consisting of 2 mm cores from the corresponding blocks were
constructed from 54 NSCLCs. Immunohistochemical staining for c-kit, Rb, p53, p16 and cyclin
D1 was performed. C-kit immunostaining was considered positive if ≥≥10% of tumor cells were
immunoreactive along the membrane and/or in cytoplasm. For Rb, p53, p16 and cyclin D1,
tumor cells showing a nuclear staining pattern were interpreted as positive. Results : We found
that c-kit was expressed in 13 (24%) cases, Rb was lost in 39 (72%) cases, p53 was expressed
in 28 (52%) cases, p16 was lost in 42 (78%) cases and cyclin D1 was expressed in 33 (61%)
cases. The c-kit expression was significantly higher in adenocarcinoma (39%) than in squamous
cell carcinoma (8%). We did not find any correlation between c-kit, Rb, p53, p16 and
cyclin D1 expression and clinicopathological parameters such as: age, tumor size, lymph node
involvement, disease stage and distant metastasis. There was a direct correlation between
p53 expression and Rb loss. Conclusions : These results suggest that c-kit may be a useful
therapeutic target for patients with c-kit positive tumors, and that the disruption of Rb and p53
pathways may play an important role in the development and progression of NSCLCs.