Journal of Otolaryngology and Ophthalmology of Shandong University ›› 2020, Vol. 34 ›› Issue (3): 26-31.doi: 10.6040/j.issn.1673-3770.1.2020.029

Previous Articles     Next Articles

Advances in molecular mechanisms of anaplastic thyroid cancer

QING Xiaoyan1,XU Yiquan2Overview,LI Chao3Guidance   

  1. 1. Department of Oncology, Chengdu Seventh People's Hospital, Chengdu 610041, Sichuan, China;
    2. Department of Anesthesiology Medical Center, Sichuan Cancer Hospital & Institute, the Affiliated Cancer Hospital School of Medicine, University of Electronic Science and Technology, Chengdu 610041, Sichuan, China;
    3. Department of Head and Neck Surgery, Sichuan Cancer Hospital & Institute, the Affiliated Cancer Hospital School of Medicine, University of Electronic Science and Technology, Chengdu 610041, Sichuan, China
  • Published:2020-06-29

PDF (PC)

405

Abstract: Anaplastic thyroid cancer(ATC)is a rare invasive thyroid tumor associated with rapid progression and poor prognosis. Currently, there is no effective treatment or early diagnosis. Some scholars have shown that the poor prognosis of ATC is due to the early mutation and invasive growth of the tumor; consequently, new directions in research involve the driving mutation of the pathogenesis of ATC and targeted drug therapies. Different molecular pathways related to tumor progression are involved in ATC. Some scholars have explored the implementation of new therapies that act on these molecular pathways to improve patients' quality of life. The research results on the molecular structural characteristics of ATC bring hope for new targeted therapies. The new molecular mechanisms will help us discover more potential therapeutic targets. We have reviewed the recent research on the molecular mechanisms of ATC.

Key words: Anaplastic thyroid carcinoma, Invasive malignancy, Molecular mechanism, Genes, Targeted therapy

CLC Number: 

  • R739.91
[1] 宋晓宇, 宋西成. 缺氧诱导因子-1α在甲状腺癌中的调节机制[J]. 山东大学耳鼻喉眼学报, 2019, 33(2): 136-138, 148. doi:10.6040/j.issn.1673-3770.0.2018.317. SONG Xiaoyu, SONG Xicheng. Research progress on the regulation of HIF-1α expression in thyroid carcinoma[J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2019, 33(2): 136-138, 148. doi:10.6040/j.issn.1673-3770.0.2018.317.
[2] 中华人民共和国国家卫生健康委员会. 甲状腺癌诊疗规范(2018年版)[J]. 中华普通外科学文献(电子版), 2019, 13(1): 1-15. doi:10.3877/cma.j.issn.1674-0793.2019.01.001.
[3] Zheng JX, Cheng X, Xu SC, et al. Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells[J]. Food Funct, 2019, 10(11): 7253-7261. doi:10.1039/c9fo00646j.
[4] Araque KA, Gubbi S, Klubo-Gwiezdzinska J. Updates on the management of thyroid cancer[J]. Horm EtMetab, 2020,10. doi:10.1055/a-1089-7870.
[5] Hugen N, Sloot YJE, Netea-Maier RT, et al. Divergent metastatic patterns between subtypes of thyroid carcinoma results from the nationwide Dutch pathology registry[J]. J Clin Endocrinol Metab, 2020, 105(3): dgz078. doi:10.1210/clinem/dgz078.
[6] Jiao C, Li L, Zhang P, et al. REGγ ablation impedes dedifferentiation of anaplastic thyroid carcinoma and accentuates radio-therapeutic response by regulating the Smad7-TGF-β pathway[J]. Cell Death Differ, 2020, 27(2): 497-508. doi:10.1038/s41418-019-0367-9.
[7] Ma YH, Cang SD, Li GQ, et al. Integrated analysis of transcriptome data revealed MMP3 and MMP13 as critical genes in anaplastic thyroid cancer progression[J]. J Cell Physiol, 2019, 234(12): 22260-22271. doi:10.1002/jcp.28793.
[8] Kohler H, Latteyer S, HönesGS, et al. Increased anaplastic lymphoma kinase activity induces a poorly differentiated thyroid carcinoma in mice[J]. Thyroid, 2019, 29(10): 1438-1446. doi:10.1089/thy.2018.0526.
[9] Wang Q, Sui GQ, Wu XL, et al. A sequential targeting nanoplatform for anaplastic thyroid carcinoma theranostics[J]. Acta Biomater, 2020, 102: 367-383. doi:10.1016/j.actbio.2019.11.043.
[10] Weber F, Junger H, Werner JM, et al. Increased cytoplasmatic expression of cancer immune surveillance receptor CD1d in anaplastic thyroid carcinomas[J]. Cancer Med, 2019, 8(16): 7065-7073. doi:10.1002/cam4.2573.
[11] Schürch CM, Roelli MA, Forster S, et al. Targeting CD47 in anaplastic thyroid carcinoma enhances tumor phagocytosis by macrophages and is a promising therapeutic strategy[J]. Thyroid, 2019, 29(7): 979-992. doi:10.1089/thy.2018.0555.
[12] Ferrari SM, Elia G, Ragusa F, et al. Novel treatments for anaplastic thyroid carcinoma[J]. Gland Surg, 2020, 9(Suppl 1): S28-S42. doi:10.21037/gs.2019.10.18.
[13] Hao Z, Wang P. Lenvatinib in Management of Solid Tumors[J]. Oncologist,2020,25(2):e302-e310. doi: 10.1634/theoncologist.2019-0407.
[14] Stenman A, Hellgren LS, Jatta K, et al. Metastatic anaplastic thyroid carcinoma in complete remission: morphological, molecular, and clinical work-up of a rare case[J]. Endocr Pathol, 2020, 31(1): 77-83. doi:10.1007/s12022-020-09606-5.
[15] Paulsson JO, Backman S, Wang N, et al. Whole-genome sequencing of synchronous thyroid carcinomas identifies aberrant DNA repair in thyroid cancer dedifferentiation[J]. J Pathol, 2020, 250(2): 183-194. doi:10.1002/path.5359.
[16] Calabrese G, Dolcimascolo A, Caruso G, et al. MiR-19a is involved in progression and malignancy of anaplastic thyroid cancer cells[J]. Onco Targets Ther, 2019, 12: 9571-9583. doi:10.2147/OTT.S221733.
[17] Pellecchia S, Sepe R, Decaussin-Petrucci M, et al. The long non-coding RNA Prader willi/angelman region RNA5(PAR5)is downregulated in anaplastic thyroid carcinomas where it Acts as a tumor suppressor by reducing EZH2 activity[J]. Cancers(Basel), 2020, 12(1): E235. doi:10.3390/cancers12010235.
[18] Credendino SC, Bellone ML, Lewin N, et al. A Cernacircuitry involving the long noncoding RNA Klhl14-AS, Pax8, and Bcl2 drives thyroid carcinogenesis[J]. Cancer Res, 2019, 79(22): 5746-5757. doi:10.1158/0008-5472.CAN-19-0039.
[19] Wächter S, Vorländer C, Schabram J, et al. Anaplastic thyroid carcinoma: changing trends of treatment strategies and associated overall survival[J]. Eur Arch Otorhinolaryngol, 2020, 277(5): 1507-1514. doi:10.1007/s00405-020-05853-8.
[20] Nikitski AV, Rominski SL, Condello V, et al. Mouse model of thyroid cancer progression and dedifferentiation driven by STRN-ALK expression and loss of p53: evidence for the existence of two types of poorly differentiated carcinoma[J]. Thyroid, 2019, 29(10): 1425-1437. doi:10.1089/thy.2019.0284.
[21] Lin B, Ma HQ, Ma MG, et al. The incidence and survival analysis for anaplastic thyroid cancer: a SEER database analysis[J]. Am J Transl Res, 2019, 11(9): 5888-5896.
[22] Yan P, Su ZJ, Zhang ZH, et al. LncRNA NEAT1 enhances the resistance of anaplastic thyroid carcinoma cells to cisplatin by sponging miR?9?5p and regulating SPAG9 expression[J]. Int J Oncol, 2019, 55(5): 988-1002. doi:10.3892/ijo.2019.4868.
[23] Revilla G, Pons MP, Baila-Rueda L, et al. Cholesterol and 27-hydroxycholesterol promote thyroid carcinoma aggressiveness[J]. Sci Rep, 2019, 9(1): 10260. doi:10.1038/s41598-019-46727-2.
[24] Zhong ZM, Chen X, Qi X, et al. Adaptor protein LNK promotes anaplastic thyroid carcinoma cell growth via 14-3-3 ε/γ binding[J]. Cancer Cell Int, 2020, 20: 11. doi:10.1186/s12935-019-1090-9.
[25] Pereira M, Williams VL, Hallanger Johnson J, et al. Thyroid cancer incidence trends in the United States: association with changes in professional guideline recommendations[J]. Thyroid, 2020,3. doi:10.1089/thy.2019.0415.
[26] Minna E, Brich S, Todoerti K, et al. Cancer associated fibroblasts and senescent thyroid cells in the invasive front of thyroid carcinoma[J]. Cancers(Basel), 2020, 12(1): E112. doi:10.3390/cancers12010112.
[27] Haddad RI, Nasr C, Bischoff L, et al. NCCN guidelines insights: thyroid carcinoma, version 2.2018[J]. J Natl Compr Canc Netw, 2018, 16(12): 1429-1440. doi:10.6004/jnccn.2018.0089.
[28] Saini S, Tulla K, Maker AV, et al. Therapeutic advances in anaplastic thyroid cancer: a current perspective[J]. Mol Cancer, 2018, 17(1): 154. doi:10.1186/s12943-018-0903-0.
[29] Mirian C, Grnhj C, Jensen DH, et al. Trends in thyroid cancer: Retrospective analysis of incidence and survival in Denmark 1980-2014[J]. Cancer Epidemiol, 2018, 55: 81-87. doi:10.1016/j.canep.2018.05.009.
[30] Gunda V, Gigliotti B, Ndishabandi D, et al. Combinations of BRAF inhibitor and anti-PD-1/PD-L1 antibody improve survival and tumour immunity in an immunocompetent model of orthotopic murine anaplastic thyroid cancer[J]. Br J Cancer, 2018, 119(10): 1223-1232. doi:10.1038/s41416-018-0296-2.
[31] Ljubas J, Ovesen T, Rusan M. A systematic review of phase II targeted therapy clinical trials in anaplastic thyroid cancer[J]. Cancers(Basel), 2019, 11(7): E943. doi:10.3390/cancers11070943.
[1] SONG QingOverview,SONG XichengGuidance. Research progress of anlotinib combination therapy in cancer treatment [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(5): 106-112.
[2] WANG Xingxin, YANG Xinyu, ZHENG Xiaojun, DING Lin, SHENG Yawen, BI Xiaoyun, YANG Jiguo. Acupoint application therapy for adenoid hypertrophy in children: a case report [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(5): 122-124.
[3] WANG MeiOverview,LI ZhihaiGuidance. Laryngeal cancer stem cells: potential therapeutic targets for overcoming multidrug resistance [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(4): 120-128.
[4] LIN Hai, ZHU Ying,ZHANG Weitian. The roles of ion channels in the pathogenesis of chronic rhinosinusitis [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(3): 64-70.
[5] LI Jiani, ZHU Dongdong,MENG Cuida. The role of epigenetics in the pathogenesis of chronic rhinosinusitis with nasal polyps [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(3): 84-91.
[6] HAN Yingying,LI Yanzhong. Obstructive sleep apnea hypopnea syndrome and subclinical arteriosclerosis [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2022, 36(2): 126-132.
[7] QI Wenwen, CHEN Luqiu, JIA Tao, CHEN Xuemei, ZHANG Jie, ZHANG Hao, JIN Peng, ZHANG Hu. Potential biomarkers and bioinformatics analysis of differentially expressed genes in recurrent laryngeal papilloma [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2021, 35(5): 75-84.
[8] WANG Yuting，,WANG Jiaxi. Research developments on microRNA in the pathogenesis of allergic rhinitis [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2021, 35(5): 98-104.
[9] WEI Ya'nan,CHEN Xi. Progress in chemotherapy and targeted drug therapy for locally advanced head and neck squamous cell carcinoma [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2021, 35(3): 118-124.
[10] XIANG Liulan, YE YuanhangOverview,JIANG Luyun, LIU YangGuidance. Elucidating the role and mechanism of Tim-3 in allergic rhinitis [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(6): 118-122.
[11] ZHU ZhengruOveriew,ZHANG XiaobingGuidance. Correlation between high-mobility group box-1 and allergic rhinitis [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(6): 123-128.
[12] ObjectiveThe aim of this study was to provide new perspectives and targets for the treatment of HNSCC by screening differentially expressed genes during cetuximab treatment of head and neck squamous cell carcinoma(HNSCC)using bioinformatics. MethodsThe chip dataset, GSE109756, was downloaded from the GEO database, and the online analysis tool, GEO2R, was used to screen differentially expressed genes in head and neck squamous cell carcinoma tissues treated with and without cetuximab. The DAVID 6.8 and STRING online software were used to analyze the function of the differentially expressed genes, their pathway enrichment, and their protein interactions. Cytoscape was used to visualize and analyze the protein interactions. The online analysis tool, X2K, was used to find the transcription factors, the kinases of differentially expressed genes, and their mutual regulatory relationship with the targeted genes. ResultsNinety-one differentially expressed genes, including 50 up-regulated and 41 down-regulated genes(P<0.05; | logFC | > 1), were found in head and neck squamous cell carcinoma tissues treated with and without cetuximab. The GO and KEGG pathway analyses suggested that these differentially expressed genes were mainly enriched with immunomodulation, extracellular matrix, and other processes. Through the construction of a protein-protein interaction network, we screened CD163, VSIG4, and 3 other core differentially expressed genes(P<0.05), which were up-regulated after cetuximab treatment. In addition, our analysis shows that transcription factors, including SUZ12, TP63, and ESR1, played a key role in cetuximab treatment(P<0.05)and MAPK14, CDK1, and MAPK1 were the most important kinases during the process(P<0.05). ConclusionCD163, VSIG4, and the aforementioned transcription factors and protein kinases may be involved in the biological processes that underlie cetuximab treatment of HNSCC. This study provides new perspectives to facilitate further understanding of the biological mechanism that underlies cetuximab treatment of HNSCC and the exploration of the effectiveness of HNSCC treatment.. Analysis of differentially expressed genes during cetuximab treatment of head and neck squamous cell carcinoma using bioinformaticsYU Kena1, SUN Kaiyue2, ZHANG Jie1, JIN Peng1 1. Department of Otorhinolaryngology & Head and Neck Surgery, The Second Hospital of Shandong University, Jinan 250033, Shandong, China; 2. Shandong Provincial Otorhinolaryngology Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250022, Shandong, ChinaAbstract: [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(4): 117-124.
[13] The occurrence and development of allergic rhinitis involves a variety of signal transduction pathways. Studying signal transduction pathways can promote the progress of pathogenesis research, suggesting that we can block the conduction of pathways in a pathway to achieve therapeutic effects. Open up new prospects for designing and developing more effective new drug treatments.The common signaling pathways in allergic rhinitis are reviewed in this article to provide a reference for the treatment of allergic rhinitis.. Advances in research on related signaling pathways in allergic rhinitisHUANG Jiali1 Review YANG Shurong2〓Guidance 1.Department of Clinical Medicine, Jiangxi University of Traditional Chinese Medicine,Nanchang 330000, Jiangxi, China 2.Department of Otolaryngology, Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang 330000, Jiangxi, ChinaAbstract: [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(4): 125-129.
[14] LIN XiaoqinOverview,WU MiaoqinGuidance. Pathogenesis and treatment of idiopathic epiretinal membranes [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(2): 121-128.
[15] Yupeng SHEN,Qi SONG,Xiaoming LI. Etiology, molecular mechanisms, and treatment strategies of precancerous laryngeal lesions [J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2019, 33(4): 25-30.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] . [J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2006, 20(2): 116 -118 .
[2] ZHOU Zi-ning,JIN Guo-wei . [J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2006, 20(5): 462 -465 .
[3] ZHOU Bin,LI Bin . Endoscopic sinus surgery for 75 patients with chronic sinusitis and nasal polyps[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2006, 20(1): 24 -26 .
[4] XU Sainan,YANG Lei . Apoptosis of epithelial cells in nasal polyps promoted by erythromycin[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2006, 20(1): 27 -29 .
[5] . [J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2006, 20(1): 94 -95 .
[6] LIU Lian-he . Treatment of deep neck abscess in 37 cases[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2008, 22(2): 180 -181 .
[7] . [J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2008, 22(3): 200 -203 .
[8] QIAO Yi,NI Guan-sen,CHEN Wen-wen . Effect of H-UPPP and nasal operations on obstructive sleep apnea syndrome in 38 cases
[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2008, 22(3): 206 -208 .
[9] WANG Xiao-feng,LIN Chang,CHENG Jin-mei . Expression of ABAD in inner ears and its clinical significance in different age mice[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2008, 22(3): 207 -211 .
[10] FAN Qi-jun,HUANG Zhi-wu,MEI Ling,XIAO Bo-kui . Expression of the heat shock protein 27 in rat cochlea induced by sodium salicylate injection by the FQ-PCR technique[J]. JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY), 2008, 22(3): 212 -214 .
Website Copyright: Editorial Office of Journal of Otolaryngology and Ophthalmology of Shandong University
Address: No.27 Shanda South Road, Jinan, Shandong, China. Post code: 250100 Tel: +86-0531-88366912 Email: ebhxb@sdu.edu.cn Supported by Beijing Magtech Co.Ltd