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具有表皮生长因子受体突变和间变性淋巴瘤激酶基因重排的肺腺癌的细胞形态学和组织形态学特征

Cytomorphological and histomorphological features of lung adenocarcinoma with epidermal growth factor receptor mutation and anaplastic lymphoma kinase gene rearrangement.

作者信息

Gardić Nikola, Lovrenski Aleksandra, Sekeruš Vanesa, Kašiković Lečić Svetlana, Bijelović Milorad, Lakić Tanja, Ilić Aleksandra, Zarić Bojan, Glumac Sofija

机构信息

Department of Pathology, Faculty of Medicine, University of Novi Sad, Novi Sad 21000, Serbia.

Institute for Pulmonary Diseases of Vojvodina, Sremska Kamenica 21204, Serbia.

出版信息

Oncol Lett. 2024 Nov 4;29(1):40. doi: 10.3892/ol.2024.14786. eCollection 2025 Jan.

DOI:10.3892/ol.2024.14786
PMID:39530007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11552093/
Abstract

Lung cancer is among the lethal and most prevalent oncological diseases globally. It is known that two types of mutations, namely anaplastic lymphoma kinase (ALK) gene rearrangement and epidermal growth factor receptor (EGFR) gene mutation, are responsible for the development of lung adenocarcinoma. The present study aimed to investigate the differences in the frequency of clinical, cytomorphological and histomorphological features of ALK and EGFR-positive lung adenocarcinomas. The present retrospective study comprised 101 patients diagnosed with lung adenocarcinoma. Based on the molecular findings, the patients were categorized into three groups as follows: The ALK-rearranged group (n=28), the EGFR group (n=42) and the negative group (n=31). The clinical features analyzed included sex, age, smoking status and disease stage. The cytomorphological and histomorphological features examined encompassed the following: Cell cluster size, the arrangement of tumor cells, the size of nuclei, nuclear atypia, the visibility of nucleoli, the presence of necrosis, intracytoplasmic vacuoles, signet ring cells, stromal characteristics and the presence of inflammatory infiltrate presence. The results indicated that the female sex was more prevalent in the EGFR group, but statistically significant differences (P<0.05) were observed between the EGFR and negative group. A significantly greater percentage of non-smokers was identified in the EGFR group compared with the ALK group (P<0.01). The majority of patients with confirmed ALK or EGFR mutations received onco-specific treatment. Focal and abundant necrosis was significantly less common in cytological samples in the EGFR group than in the other groups (21.43 vs. 57.14 and 51.61%, combined, P<0.01). No significant differences were observed in other cytomorphological features between the groups. Intracytoplasmic vacuoles, signet ring cells and cells with visible nucleoli were significantly more frequent in histological specimens of the ALK group (P<0.01). The predictive model composed of these features or combined with sex and smoking habits exhibited statistically significant differences for mutation status as a criterion (P<0.01). Collectively, the findings of the present study confirmed that, in addition to clinical characteristics, certain cytological and histological features of lung adenocarcinoma are associated with the mutational status of the tumor.

摘要

肺癌是全球致死率最高且最为常见的肿瘤疾病之一。已知两种类型的突变,即间变性淋巴瘤激酶(ALK)基因重排和表皮生长因子受体(EGFR)基因突变,是肺腺癌发生发展的原因。本研究旨在探讨ALK和EGFR阳性肺腺癌在临床、细胞形态学和组织形态学特征频率上的差异。本回顾性研究纳入了101例被诊断为肺腺癌的患者。根据分子检测结果,将患者分为以下三组:ALK重排组(n = 28)、EGFR组(n = 42)和阴性组(n = 31)。分析的临床特征包括性别、年龄、吸烟状况和疾病分期。所检查的细胞形态学和组织形态学特征包括:细胞团大小、肿瘤细胞排列、细胞核大小、核异型性、核仁可见性、坏死情况、胞浆内空泡、印戒细胞、间质特征以及炎症浸润情况。结果表明,EGFR组中女性更为常见,但EGFR组与阴性组之间存在统计学显著差异(P < 0.05)。与ALK组相比,EGFR组中不吸烟者的比例显著更高(P < 0.01)。大多数确诊为ALK或EGFR突变的患者接受了针对性的肿瘤治疗。EGFR组细胞学样本中局灶性和大量坏死明显少于其他组(21.43% 对 57.14% 和51.61%,合并后,P < 0.01)。各组之间在其他细胞形态学特征上未观察到显著差异。ALK组组织学标本中胞浆内空泡、印戒细胞和核仁可见的细胞明显更为常见(P < 0.01)。由这些特征组成或与性别和吸烟习惯相结合的预测模型,以突变状态作为标准显示出统计学显著差异(P < 0.01)。总体而言,本研究结果证实,除了临床特征外,肺腺癌的某些细胞学和组织学特征与肿瘤的突变状态相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/a3e20dfb6cc0/ol-29-01-14786-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/e7b24e8f92f8/ol-29-01-14786-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/e7b24e8f92f8/ol-29-01-14786-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/859c6e8cde08/ol-29-01-14786-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/838332c25856/ol-29-01-14786-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/1ca478625452/ol-29-01-14786-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7775/11552093/a3e20dfb6cc0/ol-29-01-14786-g04.jpg

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