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表皮生长因子受体19号外显子缺失突变的晚期肺腺癌在表皮生长因子受体酪氨酸激酶抑制剂治疗后转化为鳞状细胞癌:一例报告

Advanced Lung Adenocarcinoma with EGFR 19-del Mutation Transformed into SCC after EGFR-tyrosine Kinase inhibitors Treatment: A Case report.

作者信息

Ji Xing-Zu, Liu Zhong-Da, Ye Yi-Ping, Li Quan, Liu Xiao-Jing, Zhou Min-Hua, Jin Yi

机构信息

Department of Respiratory and Critical Care Medicine, Lishui Hospital of Traditional Chinese Medicine, Lishui 323000, Zhejiang Province, China.

Traditional Chinese Medicine Oncology, Lishui Hospital of Traditional Chinese Medicine, Lishui 323000, Zhejiang Province, China.

出版信息

World J Clin Cases. 2024 Jul 16;12(20):4405-4411. doi: 10.12998/wjcc.v12.i20.4405.

Abstract

BACKGROUND

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) significantly improve the survival of patients with Epidermal growth factor receptor (EGFR) sensitive mutations in non-small cell lung cancer (NSCLC).

CASE SUMMARY

A 67-year-old female patient in advanced lung adenocarcinoma suffered from drug resistance after EGFR-TKIs treatment. Secondary pathological tissue biopsy confirmed squamous cell carcinoma (SCC) transformation. Patients inevitably encountered drug resistance issues after receiving EGFR-TKIs treatment for a certain period of time, while EGFR-TKIs can significantly improve the survival of patients with EGFR-sensitive mutations in NSCLC. Notably, EGFR-TKIs resistance includes primary and acquired. Pathological transformation is one of the mechanisms of acquired resistance in EGFR-TKIs, with SCC transformation being relatively rare. Our results provide more detailed results of the patient's diagnosis and treatment process on SCC transformation after EGFR-TKIs treatment for lung adenocarcinoma.

CONCLUSION

Squamous cell carcinoma transformation is one of the acquired resistance mechanisms of EGFR-TKIs in advanced lung adenocarcinoma with EGFR mutations.

摘要

背景

表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKIs)显著提高了非小细胞肺癌(NSCLC)中表皮生长因子受体(EGFR)敏感突变患者的生存率。

病例摘要

一名67岁晚期肺腺癌女性患者在接受EGFR-TKIs治疗后出现耐药。二次病理组织活检证实为鳞状细胞癌(SCC)转化。患者在接受EGFR-TKIs治疗一段时间后不可避免地会遇到耐药问题,而EGFR-TKIs可显著提高NSCLC中EGFR敏感突变患者的生存率。值得注意的是,EGFR-TKIs耐药包括原发性和获得性。病理转化是EGFR-TKIs获得性耐药的机制之一,其中SCC转化相对少见。我们的结果提供了该患者肺腺癌EGFR-TKIs治疗后SCC转化的更详细诊断和治疗过程结果。

结论

鳞状细胞癌转化是EGFR-TKIs在伴有EGFR突变的晚期肺腺癌中获得性耐药机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00eb/11235554/382d7d16d259/WJCC-12-4405-g001.jpg

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