Epidermal Growth Factor Receptor and Ki-67 Expression in Canine Gliomas

Fraser, A.R.; Bacci, Barbara; Chevoir, Matthias Le; Long, Sam

doi:10.1177/0300985816644301

Cited by 15 publications

(18 citation statements)

References 39 publications

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“…These data may be explained by the high proliferative rate of this tumour . This is also confirmed by the elevated expression of Ki‐67 protein, a widely used proliferation marker, in our COM cases as compared to other canine tumours such as mast cell tumours, indolent lymphoma, gastrointestinal stromal tumours, mammary tumours, peripheral nerve sheath tumours and gliomas …”

Section: Discussionsupporting

confidence: 83%

Cyclin D1 immunohistochemical expression and somatic mutations in canine oral melanoma

Zamboni

Brocca

Ferraresso

et al. 2019

Vet Comparative Oncology

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Canine oral melanoma (COM) is the most frequent tumour with oral localization in dogs. Copy number gains and amplifications of CCND1, a gene coding for Cyclin D1, are the most frequent chromosomal aberrations described in human non-UV induced melanomas. Twenty-eight cases of COM were retrieved from paraffin-blocks archives. A total of 4 μm thick sections were immunostained with an antibody against human Cyclin D1 and Ki-67. Cyclin D1 and Ki-67 expressions were scored through two counting methods. DNA was extracted from 20 μm thick sections of formalin-fixed paraffin-embedded blocks. Pathological and surrounding healthy tissue was extracted independently. Cyclin D1 immunolabelling was detected in 69% (18/26) while Ki-67 was present in 88.5% (23/26) of cases. Statistical analysis revealed correlation between two counting methods for Cyclin D1 (r = 0.54; P = .004) and Ki-67 (r = 0.56; P = .003). The correlation found between Ki-67 and Cyclin D1 indexes in 16/26 cases labelled by both antibodies (r = 0.7947; P = .0002) suggests a possible use of Cyclin D1 index as prognostic marker. Polymerase chain reaction analysis on CCND1 coding sequence revealed the presence of nine somatic mutations in seven samples producing synonymous, missense and stop codons. Since none of the single-nucleotide polymorphisms was found to be recurrent, it is suggested that overexpression of Cyclin D1 may be the consequence of alterations of CCND1 upstream regions or other genetic aberrations not detectable with the methodology used in this study. Future studies are needed to verify the potential use of Cyclin D1 index as prognostic indicator and to highlight the molecular events responsible for Cyclin D1 overexpression in COMs. K E Y W O R D S CCND1, Cyclin D1, dog, immunohistochemistry, melanoma

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Section: Discussionsupporting

confidence: 83%

Cyclin D1 immunohistochemical expression and somatic mutations in canine oral melanoma

Zamboni

Brocca

Ferraresso

et al. 2019

Vet Comparative Oncology

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“…However, studies investigating the relationship between ki-67 and EGFR in glioma patients are scarce. Fraser et al reported a moderate correlation between the expression of EGFR and ki-67 LI in the tumor tissues in canine gliomas ( r = 0.47, P = 0.007) 58. We compared ki-67 LI between high-grade and low-grade patients.…”

Section: Resultsmentioning

confidence: 97%

Evaluation of serum extracellular vesicles as noninvasive diagnostic markers of glioma

Wang¹,

Jiang

et al. 2019

Theranostics

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Rationale : Glioma is the most common malignant primary brain tumor in the central nervous system (CNS). The lack of reliable noninvasive diagnostic and prognostic methods is one of the main reasons for the high mortality of glioma. Serum has become a useful biomarker for the diagnosis and prognosis prediction of glioma because extracellular vesicles (EVs) carry molecular components from their parental cells. Methods : To detect EVs and perform molecular analysis of serum EVs, we established and optimized a microbead-assisted method based on flow cytometry and estimated the efficacy of EGFR protein expression and NLGN3 and PTTG1 mRNA in serum EVs from glioma patients (n=23) and healthy individuals (n=12). We evaluated the ability of EGFR + EVs to differentiate high-grade and low-grade glioma patients and checked the correlation between EGFR in EVs and the ki-67 labeling index (LI) in the tumor tissue. Results : We demonstrated that EGFR + EVs are effective diagnostic and prognostic markers of glioma. The expression of EGFR in serum EVs can accurately differentiate high-grade and low-grade glioma patients, and EGFR in EVs positively correlates with ki-67 LI in the tumor tissue. We also showed the potential of NLGN3 and PTTG1 mRNA in EVs for detecting glioma patients. Conclusions : We demonstrate that the protein expression of EGFR in serum EVs is an effective diagnostic marker of glioma. EGFR in EVs highly correlates with the malignancy of glioma. We also show the potential of NLGN3 and PTTG1 in EVs for detecting glioma. The optimized flow cytometry with the aid of microbead-based EV enrichment show its potential as a noninvasive method for the detection of glioma and will be beneficial to the management of glioma.

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“…Meanwhile, in vivo studies, as showed that infected with AHNAK vectors glioma cells could decrease tumor of xenograft model growth and weight. Considered Ki-67 is a marker of proliferation and a prognostic indicator 30 , we examined the expression of Ki-67-positive cells in the tumors, and Ki-67 low expression was found in overexpression AHNAK group which possibly prompted the ability of proliferation and aggressiveness was decreased in AHNAK overexpression group. In a meta-analysis of human gliomas, Ki-67 overexpression predicted poor progression-free survival and poor overall survival 31 .…”

Section: Discussionmentioning

confidence: 99%

AHNAK as a Prognosis Factor Suppresses the Tumor Progression in Glioma

Zhao¹,

Xiao²,

Yuan

et al. 2017

J. Cancer

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Purpose: AHNAK is originally identified as a giant protein based on the estimated size of approximately 700 kDa. The aim of this study is to identify the role of AHNAK in the pathogenesis of glioma.Methods: We tested AHNAK mRNA level in a panel of six human glioma cell lines, and in 30 cases of normal brain tissues and 73 cases of glioma tissue samples using a qRT-PCR method. Further, we analyzed the relationship of AHNAK expression with clinicopathological characteristics in glioma patients. Meanwhile, we analyzed the relationship of expression of AHNAK and survival of glioma patients in survival analyses. Then, in vitro, we analyzed the biological effects of AHNAK in glioma cell lines (U87 and U251) including proliferation assay, cell transwell assay, and apoptosis. And in vivo, we examined the effects of AHNAK on tumor growth using xenograft model of human glioma cells in nude mice. Then we examined the expression of Ki-67-positive cells in these tumors.Results: We found that the mRNA levels of AHNAK were down-regulated in 4 of 6 human glioma cell lines, especially in U87 and U251 cell lines. Meanwhile, in glioma patients, a negative correlation was found between the expression of AHNAK and the glioma histopathology. And a low expression of AHNAK was a significant and independent prognostic factor for poor survival of glioma patients. Through over expression of AHNAK in both of U87 and U251, we demonstrated that overexpression of AHNAK could inhibit glioma cell proliferation and invasion, induce apoptosis, and inhibit in vivo glioma tumor growth and ki-67 expression.Conclusions: The AHNAK acts as a potential tumor suppressor. Our study provides a preclinical basis for developing AHNAK as a reliable clinical prognostic indicator for glioma patients, and a new biomarker for treatment response, and a potentially therapeutic target in glioma management options.

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Epidermal Growth Factor Receptor and Ki-67 Expression in Canine Gliomas

Cited by 15 publications

References 39 publications

Cyclin D1 immunohistochemical expression and somatic mutations in canine oral melanoma

Cyclin D1 immunohistochemical expression and somatic mutations in canine oral melanoma

Evaluation of serum extracellular vesicles as noninvasive diagnostic markers of glioma

AHNAK as a Prognosis Factor Suppresses the Tumor Progression in Glioma

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