Beta-catenin and surviving expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions

Giuseppina Campisi, Giuseppe Pannone, Matthews, Pantaleo Bufo, Carla Loreto, Pastorino, Leonardi, Dos Santos, Musumeci, Lorenzo Lo Muzio

Risultato della ricerca: Article

7 Citazioni (Scopus)

Abstract

AIM: To determine the epithelial expression of β-catenin and survivin in sporadic (primary, and recurrent) and nevoid basal cell carcinoma syndrome (NBCCS) keratocystic odontogenic tumour (KCOT) in order to assess activation of the β-catenin pathway and evidence of apoptotic inhibition, processes that may contribute to the known differences in their biological behaviour. MATERIALS AND METHODS: Sections from 40 cases of KCOT (19 sporadic/primary; 9 sporadic/recurrent and 12 NBCCS-associated) were immunohistochemically stained for β-catenin and survivin. The extent and intensity of immunoreactivity within the lining epithelium was assessed, using semi-quantitative scales, independently by two pathologists who were blinded to the clinical-pathological data. Data were analysed using Kruskal-Wallis test and, for pair-wise comparisons, Mann-Whitney test with Bonferroni correction. RESULTS: All cystic epithelial linings stained for β-catenin and survivin but there were differences in the pattern and intensity of staining among KCOT types. Sporadic primary KCOT showed weaker staining for β-catenin (P=0.0003) and survivin (P<0.0048) that was restricted to the basal and para-basal layers only, compared to sporadic recurrent and NBCCS-associated KCOT, which showed expression throughout all epithelial layers. There were no differences in β-catenin expression among recurrent and NBCCS-associated KCOT, whereas the intensity of survivin staining was higher in NBCCS-KCOT (P=0.0003). Nuclear staining for β-catenin was found exclusively in recurrent (5/9 cases) and NBCCS-associated (4/12 cases) KCOT. CONCLUSION: The data demonstrate β-catenin delocalization and survivin over-expression in recurrent sporadic and NBCCS-associated KCOT suggesting that these pathways related to apoptotic inhibition have a role in KCOT growth and recurrence.
Lingua originaleEnglish
pagine (da-a)1175-1184
Numero di pagine10
RivistaHistology and Histopathology
Volume28
Stato di pubblicazionePublished - 2013

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Basal Cell Nevus Syndrome
Odontogenic Tumors
beta Catenin
Staining and Labeling
Epithelium

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Histology

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Beta-catenin and surviving expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions. / Campisi, Giuseppina; Pannone, Giuseppe; Matthews; Bufo, Pantaleo; Loreto, Carla; Pastorino; Leonardi; Dos Santos; Musumeci; Lo Muzio, Lorenzo.

In: Histology and Histopathology, Vol. 28, 2013, pag. 1175-1184.

Risultato della ricerca: Article

Campisi, Giuseppina ; Pannone, Giuseppe ; Matthews ; Bufo, Pantaleo ; Loreto, Carla ; Pastorino ; Leonardi ; Dos Santos ; Musumeci ; Lo Muzio, Lorenzo. / Beta-catenin and surviving expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions. In: Histology and Histopathology. 2013 ; Vol. 28. pagg. 1175-1184.
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title = "Beta-catenin and surviving expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions",
abstract = "AIM: To determine the epithelial expression of β-catenin and survivin in sporadic (primary, and recurrent) and nevoid basal cell carcinoma syndrome (NBCCS) keratocystic odontogenic tumour (KCOT) in order to assess activation of the β-catenin pathway and evidence of apoptotic inhibition, processes that may contribute to the known differences in their biological behaviour. MATERIALS AND METHODS: Sections from 40 cases of KCOT (19 sporadic/primary; 9 sporadic/recurrent and 12 NBCCS-associated) were immunohistochemically stained for β-catenin and survivin. The extent and intensity of immunoreactivity within the lining epithelium was assessed, using semi-quantitative scales, independently by two pathologists who were blinded to the clinical-pathological data. Data were analysed using Kruskal-Wallis test and, for pair-wise comparisons, Mann-Whitney test with Bonferroni correction. RESULTS: All cystic epithelial linings stained for β-catenin and survivin but there were differences in the pattern and intensity of staining among KCOT types. Sporadic primary KCOT showed weaker staining for β-catenin (P=0.0003) and survivin (P<0.0048) that was restricted to the basal and para-basal layers only, compared to sporadic recurrent and NBCCS-associated KCOT, which showed expression throughout all epithelial layers. There were no differences in β-catenin expression among recurrent and NBCCS-associated KCOT, whereas the intensity of survivin staining was higher in NBCCS-KCOT (P=0.0003). Nuclear staining for β-catenin was found exclusively in recurrent (5/9 cases) and NBCCS-associated (4/12 cases) KCOT. CONCLUSION: The data demonstrate β-catenin delocalization and survivin over-expression in recurrent sporadic and NBCCS-associated KCOT suggesting that these pathways related to apoptotic inhibition have a role in KCOT growth and recurrence.",
author = "Giuseppina Campisi and Giuseppe Pannone and Matthews and Pantaleo Bufo and Carla Loreto and Pastorino and Leonardi and {Dos Santos} and Musumeci and {Lo Muzio}, Lorenzo",
year = "2013",
language = "English",
volume = "28",
pages = "1175--1184",
journal = "Histology and Histopathology",
issn = "0213-3911",
publisher = "Histology and Histopathology",

}

TY - JOUR

T1 - Beta-catenin and surviving expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions

AU - Campisi, Giuseppina

AU - Pannone, Giuseppe

AU - Matthews, null

AU - Bufo, Pantaleo

AU - Loreto, Carla

AU - Pastorino, null

AU - Leonardi, null

AU - Dos Santos, null

AU - Musumeci, null

AU - Lo Muzio, Lorenzo

PY - 2013

Y1 - 2013

N2 - AIM: To determine the epithelial expression of β-catenin and survivin in sporadic (primary, and recurrent) and nevoid basal cell carcinoma syndrome (NBCCS) keratocystic odontogenic tumour (KCOT) in order to assess activation of the β-catenin pathway and evidence of apoptotic inhibition, processes that may contribute to the known differences in their biological behaviour. MATERIALS AND METHODS: Sections from 40 cases of KCOT (19 sporadic/primary; 9 sporadic/recurrent and 12 NBCCS-associated) were immunohistochemically stained for β-catenin and survivin. The extent and intensity of immunoreactivity within the lining epithelium was assessed, using semi-quantitative scales, independently by two pathologists who were blinded to the clinical-pathological data. Data were analysed using Kruskal-Wallis test and, for pair-wise comparisons, Mann-Whitney test with Bonferroni correction. RESULTS: All cystic epithelial linings stained for β-catenin and survivin but there were differences in the pattern and intensity of staining among KCOT types. Sporadic primary KCOT showed weaker staining for β-catenin (P=0.0003) and survivin (P<0.0048) that was restricted to the basal and para-basal layers only, compared to sporadic recurrent and NBCCS-associated KCOT, which showed expression throughout all epithelial layers. There were no differences in β-catenin expression among recurrent and NBCCS-associated KCOT, whereas the intensity of survivin staining was higher in NBCCS-KCOT (P=0.0003). Nuclear staining for β-catenin was found exclusively in recurrent (5/9 cases) and NBCCS-associated (4/12 cases) KCOT. CONCLUSION: The data demonstrate β-catenin delocalization and survivin over-expression in recurrent sporadic and NBCCS-associated KCOT suggesting that these pathways related to apoptotic inhibition have a role in KCOT growth and recurrence.

AB - AIM: To determine the epithelial expression of β-catenin and survivin in sporadic (primary, and recurrent) and nevoid basal cell carcinoma syndrome (NBCCS) keratocystic odontogenic tumour (KCOT) in order to assess activation of the β-catenin pathway and evidence of apoptotic inhibition, processes that may contribute to the known differences in their biological behaviour. MATERIALS AND METHODS: Sections from 40 cases of KCOT (19 sporadic/primary; 9 sporadic/recurrent and 12 NBCCS-associated) were immunohistochemically stained for β-catenin and survivin. The extent and intensity of immunoreactivity within the lining epithelium was assessed, using semi-quantitative scales, independently by two pathologists who were blinded to the clinical-pathological data. Data were analysed using Kruskal-Wallis test and, for pair-wise comparisons, Mann-Whitney test with Bonferroni correction. RESULTS: All cystic epithelial linings stained for β-catenin and survivin but there were differences in the pattern and intensity of staining among KCOT types. Sporadic primary KCOT showed weaker staining for β-catenin (P=0.0003) and survivin (P<0.0048) that was restricted to the basal and para-basal layers only, compared to sporadic recurrent and NBCCS-associated KCOT, which showed expression throughout all epithelial layers. There were no differences in β-catenin expression among recurrent and NBCCS-associated KCOT, whereas the intensity of survivin staining was higher in NBCCS-KCOT (P=0.0003). Nuclear staining for β-catenin was found exclusively in recurrent (5/9 cases) and NBCCS-associated (4/12 cases) KCOT. CONCLUSION: The data demonstrate β-catenin delocalization and survivin over-expression in recurrent sporadic and NBCCS-associated KCOT suggesting that these pathways related to apoptotic inhibition have a role in KCOT growth and recurrence.

UR - http://hdl.handle.net/10447/95623

UR - http://www.hh.um.es

M3 - Article

VL - 28

SP - 1175

EP - 1184

JO - Histology and Histopathology

JF - Histology and Histopathology

SN - 0213-3911

ER -