Persistent High-Risk HPV Infection and Molecular Changes Related to the Development of Cervical Cancer

Author:

Moreno-Acosta Pablo12,Romero-Rojas Alfredo3,Vial Nicolas4,Huertas Antonio5,Acosta Jinneth6,Mayorga Diana1,Carrillo Schyrly2,Molano Monica7,Gamboa Oscar8,Cotes Martha9,Casadiego Camila9,Vallard Alexis4,Magne Nicolas4ORCID

Affiliation:

1. Research Group in Radiobiology Clinical, Molecular and Cellular, National Cancer Institute, Bogota, Colombia

2. Research Group in Cancer Biology, National Cancer Institute, Bogota, Colombia

3. Group of Pathology Oncology, National Cancer Institute, Bogota, Colombia

4. Department of Radiation Oncology, Institut de cancérologie de la Loire-Lucien Neuwirth, 108 bis, Avenue Albert Raimond, BP 60008, 42271 Saint-Priest en Jarez, France

5. Biobank, Group of Pathology Oncology, National Cancer Institute, Bogota, Colombia

6. Pathology Group, National University of Colombia, Bogota, Colombia

7. Microbiology and Infection Diseases, The Royal Women’s Hospital, Melbourne, Australia

8. Unit of Analysis, National Cancer Institute, Bogota, Colombia

9. Group Area Radiotherapy Oncology, National Cancer Institute, Bogota, Colombia

Abstract

This article is a preliminary investigational study that is aimed at giving hints about the interesting biomarkers involved in the transition process from low-grade cervix lesion to invasive cervical cancer. Our study focuses on the risk factors and tumour molecular changes in one patient. First in 1986, she was diagnosed a preinvasive cervix lesion. Then, 16 years later, she was diagnosed an invasive cervical cancer. The 2002 diagnosis was a squamous cell carcinoma of the cervix, stage IIIB (FIGO), whereas in 1986, she had been diagnosed a high-grade squamous intraepithelial cervical lesion. Retrospectively, the analysis of samples of preneoplastic lesions and invasive cervical cancer confirmed the histopathological diagnoses and detected the presence of HPV type and HPV-16 variants, as well as the overexpression of proteins such as hTERT, IGF1Rα, IGF1Rβ, CAIX, and GLUT1. Finally, the Arg72Pro polymorphism was detected in TP53. The role of high-risk HPV and HPV-16 variants and of hTERT, IGF1Rα, IGF1Rβ, CAIX, and GLUT1 variations seemed confirmed in the development and progression of cervical cancer. As a result, analyzing the molecular changes in one and same tumour that progresses from a low-grade cervix lesion to invasive cervical cancer could provide valuable information in order to improve detection, diagnosis, and treatment in the future.

Publisher

Hindawi Limited

Subject

Obstetrics and Gynecology

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