甲状腺癌患者放射性碘治疗不良反应相关的遗传标记

Q2 Pharmacology, Toxicology and Pharmaceutics

Drug metabolism and personalized therapy Pub Date : 2023-06-30 DOI:10.1515/dmdi-2023-0007

Natalia P Denisenko, Anastasia A Kachanova, Ivan V Sychev, Gregory N Shuev, Oksana M Perfilieva, Reis H Mukhamadiev, Ruslan E Kazakov, Olga I Milyutina, Olga V Konenkova, Sergey A Ryzhkin, Elena M Zhmaeva, Sergey L Kirienko, Dmitriy V Ivashchenko, Irina V Bure, Alexander S Ametov, Irina V Poddubnaya, Karin B Mirzaev, Dmitry A Sychev

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TT genotype carriers of ATG10 rs1864183 had higher frequency of gastrointestinal symptoms (vs. CC+CT), the CC genotype carriers of ATG10 rs10514231 had significantly more frequent cerebral symptoms (vs. CT+TT), as well as AA genotype carriers of TGFB1 rs1800469 (vs. AG+GG). CC genotype of ATG10 rs10514231 increased the incidence of radioiodine-induced fatigue, whereas GA genotype of the ATM rs11212570 had a protective role against fatigue. 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引用次数: 3

摘要

目的:放射性碘治疗被考虑用于具有某些临床病理因素的患者，这些因素可预测甲状腺癌复发、远处转移或疾病特异性死亡率的显著风险。本研究旨在探讨甲状腺癌患者DNA损伤反应和自噬过程相关基因多态性与放射性碘治疗不良反应之间的关系。方法:纳入181例患者(男性37例，女性144例;中位年龄56 [41];66.3]年)，组织学证实甲状腺癌，有甲状腺切除术史，接受放射性碘治疗。通过等位基因特异性实时pcr检测NFKB1、ATM、ATG16L2、ATG10、TGFB1和TNF多态性。结果:不良反应发生率为胃肠道症状(57.9 %)、局部症状(65.8% %)、脑症状(46.8 %)、疲劳(54.4 %);放射碘治疗后6个月出现涎腺炎症状- 25.2 %。ATG10 rs1864183的TT基因型携带者出现胃肠道症状的频率高于CC+CT, ATG10 rs10514231的CC基因型携带者出现大脑症状的频率高于CT+TT, TGFB1 rs1800469的AA基因型携带者出现大脑症状的频率高于AG+GG。ATG10 rs10514231的CC基因型增加了放射性碘诱导的疲劳发生率，而ATG10 rs11212570的GA基因型对疲劳具有保护作用。TGFB1 rs1800469与放射碘治疗后6个月涎腺炎的体征相关。结论:遗传因素可能与甲状腺癌患者放射性碘治疗不良反应的发生有关。

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Genetic markers associated with adverse reactions of radioiodine therapy in thyroid cancer patients.

Objectives: Radioactive iodine therapy is considered for patients with certain clinicopathological factors that predict a significant risk of recurrence, distant metastases of thyroid cancer or disease-specific mortality. The aim of the study was to investigate the association between polymorphisms of genes, products of which are involved in the processes of DNA damage response and autophagy, and the adverse reactions of radioiodine therapy in thyroid cancer patients.

Methods: The study included 181 patients (37 men, 144 women; median age 56 [41; 66.3] years) with histologically confirmed thyroid cancer and a history of thyroidectomy who received radioiodine therapy. NFKB1, ATM, ATG16L2, ATG10, TGFB1, and TNF polymorphisms were determined by allele-specific realtime-PCR.

Results: The frequency of adverse reactions was the following: gastrointestinal symptoms - 57.9 %, local symptoms - 65.8 %, cerebral symptoms - 46.8 %, fatigue - 54.4 %; signs of sialoadenitis six months after radioiodine therapy - 25.2 %. TT genotype carriers of ATG10 rs1864183 had higher frequency of gastrointestinal symptoms (vs. CC+CT), the CC genotype carriers of ATG10 rs10514231 had significantly more frequent cerebral symptoms (vs. CT+TT), as well as AA genotype carriers of TGFB1 rs1800469 (vs. AG+GG). CC genotype of ATG10 rs10514231 increased the incidence of radioiodine-induced fatigue, whereas GA genotype of the ATM rs11212570 had a protective role against fatigue. TGFB1 rs1800469 was associated with signs of sialoadenitis six months after radioiodine therapy.

Conclusions: Genetic factors may contribute to the occurrence of adverse reactions of radioiodine therapy in thyroid cancer patients.

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来源期刊

Drug metabolism and personalized therapy Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)

CiteScore

2.30

自引率

0.00%

发文量

期刊介绍： Drug Metabolism and Personalized Therapy (DMPT) is a peer-reviewed journal, and is abstracted/indexed in relevant major Abstracting Services. It provides up-to-date research articles, reviews and opinion papers in the wide field of drug metabolism research, covering established, new and potential drugs, environmentally toxic chemicals, the mechanisms by which drugs may interact with each other and with biological systems, and the pharmacological and toxicological consequences of these interactions and drug metabolism and excretion. Topics: drug metabolizing enzymes, pharmacogenetics and pharmacogenomics, biochemical pharmacology, molecular pathology, clinical pharmacology, pharmacokinetics and drug-drug interactions, immunopharmacology, neuropsychopharmacology.