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犬肾上腺肿瘤中 C-kit、flt-3、PDGFR-β 和 VEGFR2 的表达及其与肾上腺切除术后预后的相关性。

C-kit, flt-3, PDGFR-β, and VEGFR2 expression in canine adrenal tumors and correlation with outcome following adrenalectomy.

机构信息

University of Florida College of Veterinary Medicine, 2015 SW 16th Ave, PO Box 100116, Gainesville, Florida 32610, USA.

出版信息

Can J Vet Res. 2021 Oct;85(4):279-284.

PMID:34602732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8451711/
Abstract

The objective of this retrospective study was to evaluate the expression of receptor tyrosine kinases (RTKs) in canine adrenal tumors and correlate this expression with features of tumor aggressiveness and survival in dogs undergoing adrenalectomy. Forty-three canine adrenal tumors were evaluated for expression of c-kit, fms-like tyrosine kinase 3 (flt-3), platelet-derived growth factor receptor-β (PDGFR-β), and vascular endothelial growth factor receptor 2 (VEGFR2) using immunohistochemistry. Tumor RTK staining characteristics were compared to normal adrenals. Medical records were reviewed for data regarding patient outcome and tumor characteristics. Expression of c-kit, flt-3, PDGFR-β, and VEGFR2 was detected in 26.9%, 92.3%, 96.2%, and 61.5% of cortical tumors and 0%, 63.2%, 47.4%, and 15.8% of pheochromocytomas, respectively. Expression of RTKs was not significantly increased when compared to normal adrenals and did not correlate with survival after adrenalectomy. Receptor tyrosine kinases are not overexpressed in canine adrenal tumors compared to normal adrenal tissue. Therapeutic inhibition of these receptors may still represent an effective approach in cases where receptor activation is present.

摘要

本回顾性研究的目的是评估犬肾上腺肿瘤中受体酪氨酸激酶(RTKs)的表达,并将其与接受肾上腺切除术的犬的肿瘤侵袭性和生存特征相关联。使用免疫组织化学方法评估了 43 例犬肾上腺肿瘤中 c-kit、fms 样酪氨酸激酶 3(flt-3)、血小板衍生生长因子受体-β(PDGFR-β)和血管内皮生长因子受体 2(VEGFR2)的表达。比较了肿瘤 RTK 染色特征与正常肾上腺。回顾了病历,以获取有关患者预后和肿瘤特征的数据。皮质肿瘤中 c-kit、flt-3、PDGFR-β 和 VEGFR2 的表达分别为 26.9%、92.3%、96.2%和 61.5%,嗜铬细胞瘤中分别为 0%、63.2%、47.4%和 15.8%。与正常肾上腺相比,RTKs 的表达并未显著增加,与肾上腺切除术后的生存也没有相关性。与正常肾上腺组织相比,犬肾上腺肿瘤中 RTKs 的表达并未过度表达。在存在受体激活的情况下,这些受体的治疗性抑制仍可能是一种有效的方法。

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