p53 expression in repair/reactive renal tubular cells: A potential pitfall leading to a false-positive diagnosis of urine cytology.


Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
12 2021
Historique:
revised: 07 09 2021
received: 17 07 2021
accepted: 13 09 2021
pubmed: 17 11 2021
medline: 18 3 2022
entrez: 16 11 2021
Statut: ppublish

Résumé

p53 immunostaining is routinely used as a surrogate marker for TP53 mutational status. In urine cytology, p53 immunocytochemistry is reportedly useful in detecting urothelial carcinoma cells as well as in improving the detection sensitivity and specificity. However, to the best of our knowledge, p53 expression in repair/reactive renal tubular cells (RRTCs) from urine cytologic specimens has not been assessed to date. We evaluated the immunoexpression of p53 and homogentisate 1,2-dioxygenase (HGD) antibody, a renal tubular cells marker, in RRTCs using voided urine and renal biopsy samples from 80 patients who were histologically diagnosed with glomerular disease. Repair/reactive renal tubular cells were detected in 68 (68/80, 85%) samples at a mean count of 141.1 cells per sample (range, 5-4220). Immunocytochemical analysis found p53-positive RRTCs in all the samples (68/68, 100%) with an average p53 positivity rate of RRTCs per sample at 47.7% (range, 3.8%-96.5%). Of the 68 p53-positive RRTC samples, 38 (55.9%) included cells that were HGD positive for cytoplasm. Similarly, renal biopsy analysis revealed p53-positive RRTCs in all the specimens (68/68, 100%). All 68 (100%) cases showed RRTCs that were positive for both p53 and HGD. To avoid false positives of p53 immunocytochemistry, cytologists must consider the fact that RRTCs from patients with glomerular disease are positive for p53.

Sections du résumé

BACKGROUND
p53 immunostaining is routinely used as a surrogate marker for TP53 mutational status. In urine cytology, p53 immunocytochemistry is reportedly useful in detecting urothelial carcinoma cells as well as in improving the detection sensitivity and specificity. However, to the best of our knowledge, p53 expression in repair/reactive renal tubular cells (RRTCs) from urine cytologic specimens has not been assessed to date.
METHODS
We evaluated the immunoexpression of p53 and homogentisate 1,2-dioxygenase (HGD) antibody, a renal tubular cells marker, in RRTCs using voided urine and renal biopsy samples from 80 patients who were histologically diagnosed with glomerular disease.
RESULTS
Repair/reactive renal tubular cells were detected in 68 (68/80, 85%) samples at a mean count of 141.1 cells per sample (range, 5-4220). Immunocytochemical analysis found p53-positive RRTCs in all the samples (68/68, 100%) with an average p53 positivity rate of RRTCs per sample at 47.7% (range, 3.8%-96.5%). Of the 68 p53-positive RRTC samples, 38 (55.9%) included cells that were HGD positive for cytoplasm. Similarly, renal biopsy analysis revealed p53-positive RRTCs in all the specimens (68/68, 100%). All 68 (100%) cases showed RRTCs that were positive for both p53 and HGD.
CONCLUSION
To avoid false positives of p53 immunocytochemistry, cytologists must consider the fact that RRTCs from patients with glomerular disease are positive for p53.

Identifiants

pubmed: 34783171
doi: 10.1002/cam4.4389
pmc: PMC8683536
doi:

Substances chimiques

Biomarkers, Tumor 0
Tumor Suppressor Protein p53 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

8846-8853

Informations de copyright

© 2021 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

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Auteurs

Kaori Enomoto (K)

Department of Medical Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.

Toru Matsunaga (T)

Department of Diagnostic Pathology, University Hospital, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Tadashi Sofue (T)

Department of Cardiorenal and Cerebrovascular Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Akihiro Nakamura (A)

Department of Clinical Laboratory Science, Faculty of Health Care, Tenri Health Care University, Tenri, Japan.

Eiichiro Hirakawa (E)

Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Kagawa, Japan.

Emi Ibuki (E)

Department of Diagnostic Pathology, University Hospital, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Reiji Haba (R)

Department of Diagnostic Pathology, University Hospital, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Shingo Kamoshida (S)

Department of Medical Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.

Hiroyuki Ohsaki (H)

Department of Medical Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.

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