
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
1 Biological Repository Centre at Research Centre; 2 Research Centre at King Fahad National Center for Children's Cancer and Research, and 3 Department of Pathology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia; 4 Pathology Services Division, Dhahran Health Centre, Saudi Aramco Medical Services Organization, Dhahran, Saudi Arabia; 5 Departments of Medical and Clinical Operations, and 6 Pediatric Oncology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
Requests for reprints: Khawla Al-Kuraya, Research Centre at KFNCCC&R, King Faisal Specialist Hospital and Research Centre, MBC 98-16, P.O. Box 3354, Riyadh 11211, Saudi Arabia. Phone: 966-1-229-4444, ext. 51813; Fax: 966-1-205-5170. E-mail: kkuraya{at}kfshrc.edu.sa
Aim: The fragile histidine triad (FHIT) gene was discovered and proposed as a tumor suppressor gene for most human cancers. It encodes the most active common human chromosomal fragile region, FRA3B. We studied the prevalence of loss of FHIT expression in various tumors and correlated its loss with various clinicopathologic features.
Methods: To determine whether the absence of FHIT expression correlates with clinical variables such as grade, stage, and survival time, we assessed FHIT expression using immunohistochemistry. More than 1,800 tumors from more than 75 tumor categories were analyzed by immunohistochemistry in a tissue microarray format.
Results: Loss of FHIT expression ranged from 19% in ovarian tumors to 67% in lung cancers. Clinical and pathologic features like grade, stage, tumor size, and lymph node metastasis showed correlation with loss of FHIT expression in some tumors. No difference was seen in the survival patterns and loss of FHIT expression in any of the tumor groups studied.
Conclusions: Loss of FHIT expression is an ubiquitous event in the multistep, multifactorial carcinogenesis process. FHIT may be altered at different stages in different types of cancers. Most of the tumors with a wider prevalence of loss of FHIT expression as an early event show a correlation with clinicopathologic features. However, in some of the tumors, FHIT expression is lost as a late event and is only seen in a fraction of the tumors. (Cancer Epidemiol Biomarkers Prev 2006;15(9):170818)
This article has been cited by other articles:
![]() |
S. Uddin, M. Ahmed, P. Bavi, R. El-Sayed, N. Al-Sanea, A. AbdulJabbar, L. H. Ashari, S. Alhomoud, F. Al-Dayel, A. R. Hussain, et al. Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer Cancer Res., May 1, 2008; 68(9): 3379 - 3388. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Abubaker, Z. Jehan, P. Bavi, M. Sultana, S. Al-Harbi, M. Ibrahim, A. Al-Nuaim, M. Ahmed, T. Amin, M. Al-Fehaily, et al. Clinicopathological Analysis of Papillary Thyroid Cancer with PIK3CA Alterations in a Middle Eastern Population J. Clin. Endocrinol. Metab., February 1, 2008; 93(2): 611 - 618. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |