IMP3, a new biomarker to predict progression of cervical intraepithelial neoplasia into invasive cancer
Department of Cancer Biology; Department of Medicine, Division of Preventive and Behavioral Medicine; Department of Pathology
Adult; Carcinoma, Squamous Cell; Cell Movement; Cell Proliferation; Cervical Intraepithelial Neoplasia; Disease Progression; Disease-Free Survival; Female; HeLa Cells; Humans; Kaplan-Meier Estimate; Massachusetts; Middle Aged; Neoplasm Invasiveness; Neoplasm Staging; Prognosis; RNA Interference; RNA-Binding Proteins; Time Factors; Tumor Markers, Biological; Uterine Cervical Neoplasms; Young Adult
The expression of IMP3, an oncofetal protein, has been strongly associated with aggressive cancers. In this study, we investigated whether IMP3 can serve as a biomarker to predict invasive squamous cell carcinoma (SCC) in patients with cervical intraepithelial neoplasia (CIN) II and III. A total of 1249 patients with no dysplasia, CINs, or invasive SCC were studied for IMP3 expression. The 710 patients with CIN II and III in their cervical biopsies were further evaluated for invasive cancer-free survival analysis. The role of IMP3 in the regulation of cell proliferation and migration of HeLa cervical cancer cells was examined by modification of IMP3 expression with small interference RNA. Compared with CIN I or cervical tissues without dysplasia, IMP3 expression was significantly increased not only in invasive SCC but also most importantly in a subset of CIN III cases with concurrent invasive SCC. Importantly, invasive cancer was found only in patients with IMP3-positive CIN II and III, whereas no invasive cancer was detected in patients with IMP3-negative CIN II and III in their follow-up resections (P
Lu, Di; Yang, Xiaofang; Jiang, Naomi Y.; Woda, Bruce A.; Liu, Qin; Dresser, Karen A.; Mercurio, Arthur M.; Rock, Kenneth L.; and Jiang, Zhong, "IMP3, a new biomarker to predict progression of cervical intraepithelial neoplasia into invasive cancer" (2011). Cancer Biology Publications and Presentations. Paper 213.