ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Monoamine Oxidase B in Renal Cell Carcinoma.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting monoamine oxidases in cancer: advances and opportunities.Trends in molecular medicine · 2025Review
- A multi-cohort validated OXPHOS signature predicts survival and immune profiles in grade II/III glioma patients.Frontiers in immunology · 2025Article
- Targeting MAO-B with Small-Molecule Inhibitors: A Decade of Advances in Anticancer Research (2012-2024).Molecules (Basel, Switzerland) · 2024Review
- Identification and validation of a risk model and molecular subtypes based on tryptophan metabolism-related genes to predict the clinical prognosis and tumor immune microenvironment in lower-grade glioma.Frontiers in cellular neuroscience · 2023Article
- The clinical value and potential molecular mechanism of the downregulation of MAOA in hepatocellular carcinoma tissues.Cancer medicine · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Studies on monoamine oxidase B (MAO-B) expression in renal cell carcinoma (RCC) are lacking. This study focused on the immunohistochemical evaluation of MAO-B in RCC. MATERIAL AND METHODS Sixty-three RCC samples were compared on basic clinical and histopathological parameters, including histopathological type and tumor grade. RCC samples were divided according to the histopathological type into 2 groups: conventional type (51 samples) and other types (12 samples). For MAO-B detection, a standard immunohistochemical procedure was employed. RESULTS In healthy kidney samples, MAO-B was detected predominantly in tubules. Fifty-two cancer tissue samples were MAO-B negative and 11 tissue samples were MAO-B low positive. Enzymes were detected only in the cytoplasm. We did not find any significant correlation between the percentage of positive MAO-B specimens and nuclear grade. Additionally, Fisher's test did not reveal any difference in numbers of positive and negative MAO-B samples between the 2 RCC types (P>0.05). CONCLUSIONS From our results, it was clear that MAO-B expression played no significant role in stimulation of renal cancer development. We found that MAO-B occurred only in 19% of kidney tumors and that the positivity of protein expression was low. Moreover, it seems that the disappearance of this enzyme in RCC is a consequence of replacement of healthy tissue by cancer cells. On the other hand, one can assume that the loss of MAO-B expression could be associated with severe pathological processes in the kidney.
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Registered trials
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