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来那度胺治疗成人T细胞白血病/淋巴瘤后肿瘤细胞中CC趋化因子受体4表达降低：一例报告

Reduced CC Chemokine Receptor 4 Expression in Tumor Cells after Lenalidomide Treatment for Adult T-Cell Leukemia/Lymphoma: A Case Report.

作者信息

Shimizu Masatomo, Yokote Taiji, Hatooka Jun, Kinoshita Yuuki, Imagawa Akihisa, Yasuda Emi

机构信息

Department of Internal Medicine, Osaka Medical and Pharmaceutical University, Takatsuki, Japan.

Department of Pathology, Osaka Medical and Pharmaceutical University, Takatsuki, Japan.

出版信息

Case Rep Oncol. 2024 May 30;17(1):602-607. doi: 10.1159/000539122. eCollection 2024 Jan-Dec.

DOI:10.1159/000539122
PMID:39015631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11250255/
Abstract

INTRODUCTION

CC chemokine receptor 4 (CCR4), which is involved in leukocyte migration, is expressed in most tumor cells in patients with adult T-cell leukemia/lymphoma (ATLL).

CASE PRESENTATION

Here we report the case of a 78-year-old man diagnosed with lymphoma-type ATLL expressing CCR4. The patient was administered two cycles of lenalidomide but died because of sepsis 5 months after the initial diagnosis. Autopsy revealed ATLL cells at several sites. Immunohistochemical analysis revealed that these ATLL cells had reduced CCR4 expression.

CONCLUSION

The present case suggests that treatment should be carefully determined in ATLL with reference to a history of lenalidomide use and CCR4 expression.

摘要

引言

CC趋化因子受体4（CCR4）参与白细胞迁移，在成人T细胞白血病/淋巴瘤（ATLL）患者的大多数肿瘤细胞中表达。

病例报告

在此，我们报告一例78岁男性淋巴瘤型ATLL患者，其肿瘤细胞表达CCR4。该患者接受了两个周期的来那度胺治疗，但在初诊5个月后因败血症死亡。尸检发现多个部位存在ATLL细胞。免疫组化分析显示，这些ATLL细胞的CCR4表达降低。

结论

本病例提示，对于ATLL患者，应参考来那度胺使用史和CCR4表达情况谨慎确定治疗方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/93bc8b08b215/cro-2024-0017-0001-539122_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/5a23a4038f35/cro-2024-0017-0001-539122_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/853f80d4474b/cro-2024-0017-0001-539122_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/8a790a9d0d2d/cro-2024-0017-0001-539122_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/9ad541a0e4ca/cro-2024-0017-0001-539122_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/93bc8b08b215/cro-2024-0017-0001-539122_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/5a23a4038f35/cro-2024-0017-0001-539122_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/853f80d4474b/cro-2024-0017-0001-539122_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/8a790a9d0d2d/cro-2024-0017-0001-539122_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/9ad541a0e4ca/cro-2024-0017-0001-539122_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7638/11250255/93bc8b08b215/cro-2024-0017-0001-539122_F05.jpg

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本文引用的文献

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Hijacking of the AP-1 Signaling Pathway during Development of ATL.成人T细胞白血病（ATL）发展过程中AP-1信号通路的劫持
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Immunomodulatory agents lenalidomide and pomalidomide co-stimulate T cells by inducing degradation of T cell repressors Ikaros and Aiolos via modulation of the E3 ubiquitin ligase complex CRL4(CRBN.).
免疫调节剂来那度胺和泊马度胺通过调节 E3 泛素连接酶复合物 CRL4(CRBN)，诱导 T 细胞抑制因子 Ikaros 和 Aiolos 的降解，从而共同刺激 T 细胞。
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Treatment of adult T-cell leukemia/lymphoma: past, present, and future.成人T细胞白血病/淋巴瘤的治疗：过去、现在与未来。
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