Glucocorticoid receptor in cervical cancer: an immunhistochemical analysis
- 20 Downloads
Cervical cancer is one of the most frequent cancers in women worldwide. In most of all cases, a persistent HPV infection is the leading cause. HPV-specific sequences are able to bind glucocorticoid receptor (GR). Dexamethasone can increase the activity of early promoters in HPV16 and HPV18 interfering in transcription control of viral oncogenes. The aim of our study was to evaluate glucocorticoid receptor as transcriptional factor in its active form in the nucleus of in cervical cancer cells and to correlate the results with clinical patient specific parameters.
A total of 250 paraffin-embedded cervical cancer samples obtained from patients having undergone surgery for cervical cancer were used for the study. The expression of GR was immunhistochemical examined and evaluated by a semi-quantitative scoring. SPSS software was used for the statistical evaluation of staining results and survival analysis of patients with cervical cancer.
GR is frequently expressed in cervical carcinoma tissue in favor of squamous cell carcinoma (SCC). An enhanced expression is correlated with rather small clinical stages. The expression of the GR is correlated with better overall survival and progression-free survival.
The glucocorticoid receptor is frequently expressed in cervical carcinoma tissue in favor of squamous cell carcinoma. An enhanced expression is correlated with rather small clinical stages. The expression of the analyzed receptor is correlated with better overall survival. Further studies are needed to determine useful treatment targets for glucocorticoid receptor manipulation.
KeywordsCervical cancer Glucocorticoid receptor Survival
BPK: project development, data collection. SB: experiments, manuscript writing. LS: data collection, manuscript editing. JZ: data analyses. DM: supervision, data analyses. CK: experiments, methodology. SS: experiments, methodology. SH: experiments, methodology. SM: data analyses, supervision, funding. UJ: supervision. HH: manuscript edition, data analyses
The study was supported by the “Heuer Stiftung” for Bernd P. Kost. The authors would like to thank Prof. Dr. med. Jutta Engel, M.P.H. and Max Wiedemann (The Munich Cancer Registry of the Tumorzentrum München [TZM—Munich Tumor Center]) for the follow-up data.
Compliance with ethical standards
Conflict of interest
All authors declare that they have no conflict of interest.
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. This article does not contain any studies with animals performed by any of the authors.
The study was approved by the ethics committee of the Ludwig-Maximilians University Munich (reference number 259-16). Patient data were anonymized.
- 6.Munoz N, Bosch FX, de Sanjose S, Herrero R, Castellsague X, Shah KV, Snijders PJ, Meijer CJ, International Agency for Research on Cancer Multicenter Cervical Cancer Study G (2003) Epidemiologic classification of human papillomavirus types associated with cervical cancer. N Engl J Med 348:518–527CrossRefPubMedCentralGoogle Scholar
- 33.Hunt H, Donaldson K, Strem M, Zann V, Leung P, Sweet S, Connor A, Combs D, Belanoff J (2017) Assessment of safety, tolerability, pharmacokinetics, and pharmacological effect of orally administered cort125134: An adaptive, double-blind, randomized, placebo-controlled phase 1 clinical study. Clin Pharmacol Drug Dev 7(4):408–421. https://doi.org/10.1002/cpdd.389 CrossRefPubMedPubMedCentralGoogle Scholar
- 34.Hunt HJ, Belanoff JK, Walters I, Gourdet B, Thomas J, Barton N, Unitt J, Phillips T, Swift D, Eaton E (2017) Identification of the clinical candidate (r)-(1-(4-fluorophenyl)-6-((1-methyl-1 h-pyrazol-4-yl)sulfonyl)-4,4a,5,6,7,8-hexah ydro-1 h-pyrazolo[3,4-g]isoquinolin-4a-yl)(4-(trifluoromethyl)pyridin-2-yl)methano ne (cort125134): a selective glucocorticoid receptor (gr) antagonist. J Med Chem 60:3405–3421CrossRefPubMedCentralGoogle Scholar