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Androgen Receptor and PIM1 Expression in Tumor Tissue of Patients With Triple-negative Breast Cancer
- Source :
- Cancer Genomics Proteomics
- Publication Year :
- 2021
- Publisher :
- International Institute of Anticancer Research, 2021.
-
Abstract
- Background/aim Effective targeted therapies for triple-negative breast cancer (TNBC) are limited. In a subset of TNBC, androgen receptor (AR) plays an important role, while the human proviral integration site for Moloney murine leukemia virus-1 (PIM1) overexpression is also implicated. PIM1 kinases phosphorylate AR, thus regulating its transcriptional activity, regardless of the presence or not of androgens. We evaluated the expression of AR and PIM1 and their prognostic significance in TNBC. Materials and methods AR and PIM1 transcripts were quantified by quantitative reverse transcription polymerase chain reaction in formalin-fixed paraffin-embedded tumor from 141 patients with TNBC. Results AR was expressed in 38.3%, PIM1 in 10.6%, while co-expression of AR and PIM1 was detected in 7/141 cases (5.0%). No prognostic significance of AR or PIM1 was reached for overall or disease-free survival. Conclusion Co-expression of AR and PIM1 exists in only in a small percentage of patients with TNBC. The implications of this finding in the therapeutic management of patients with TNBC should be investigated in larger patient cohorts.
- Subjects :
- Adult
Cancer Research
PIM1
Triple Negative Breast Neoplasms
Biochemistry
03 medical and health sciences
Mice
Young Adult
0302 clinical medicine
Breast cancer
Proto-Oncogene Proteins c-pim-1
Genetics
medicine
Animals
Humans
Molecular Biology
Triple-negative breast cancer
Aged
Aged, 80 and over
Kinase
business.industry
Middle Aged
medicine.disease
Androgen receptor
Reverse transcription polymerase chain reaction
Leukemia
Receptors, Androgen
030220 oncology & carcinogenesis
Cancer research
Phosphorylation
Female
business
Research Article
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Journal :
- Cancer Genomics Proteomics
- Accession number :
- edsair.doi.dedup.....748dce7e0494cf16a87021994f7eb10d