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ORIGINAL ARTICLE |
1 International Society for the Study of Comparative Oncology (ISSCO), Silver Spring, MD 209 06, USA
2 Department of Biochemistry and Biophysics "F. Cedrangolo", Section of Anatomic Pathology, Second University of Naples, Naples 80138, Italy
3 Department of Medicine and Public Health, Section of Clinical Anatomy, Second University of Naples
4 Section of Oncology, Campus BioMedico University, Rome 00100, Italy
5 Section of Plastic and Reconstructive Surgery, Campus BioMedico University
6 Department of Cardiological, Respiratory and Thoracic Medical Sciences, Second University of Naples
7 SAFU Department, Regina Elena Cancer Institute, Rome 00100, Italy
Correspondence to:
Dr A Baldi
Via G. Orsi 25, 80128 Naples, Italy; alfonsobaldi{at}tiscali.it
Background: Experimental evidence suggests that lung cancer development and progression can be linked to an increased proliferation rate.
Aims/Methods: To evaluate the immunohistochemical expression of seven components of the cell cycle machinery in a series of well characterised non-small cell lung cancer (NSCLC) specimens (n = 105).
Results: Multivariate analysis revealed that simultaneous loss of expression of three of these factorscyclin D1, the cyclin dependent kinase inhibitor p16, and the tumour suppressor retinoblastoma protein Rb2/p130correlated with survival, confirming the hypothesis that the cyclin D1p16retinoblastoma tumour suppressor pathway is inactivated in most lung cancer samples.
Conclusions: These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancer and support the idea that functional cooperation between different cell cycle regulatory proteins constitutes another level of regulation in cell growth control and tumour suppression.
Abbreviations: CI, confidence interval; NSCLC, non-small cell lung cancer; PCNA, proliferating nuclear cell antigen; pRb, retinoblastoma protein
Keywords: non-small cell lung cancer; p53; pRb2/p130; p16; cyclin D1; immunohistochemistry; prognosis
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