-
Abstract: Thyroid carcinoma is the most common endocrine maligancy,and the worldwide incidence has been rising in recent years.Differentiated thyroid carcinoma is the most common thyroid malignancy,which include thyroid papillary carcinoma and follicular thyroid carcinoma,accounting for about 90 percent of thyroid carcinoma incidence.Currently,surgical treatment,iodine radiotherapy and TSH suppressive therapy are the commonly accepted effective treatments for differentiated thyroid carcinoma,and most patients can be cured.But there are still some patients not sensitive to the general treatments,who have lost the treatment of opportunity.Molecular targeted therapy is an agonistic or suppressive treatment for molecular biology targets of malignant tumor,and currently is a frontier research in the field of malignancy treatment.By retrieving and analyzing the related literature of molecular targeted therapy of thyroid carcinoma through PUBMED in the past 5 years,the article introduced the current status of molecular targeted therapy of thyroid carcinoma.
-
Key words:
- thyroid neoplasms /
- molecular therapy /
- targeted therapy
-
[1] PACINI F,CASTAGNA M G,BRILLI L,et al.Thyroid cancer:ESMO Clinical Practice Guidelines for diagnosis,treatment and follow-up[J].Ann Oncol,2012,23 Suppl 7:vii110-119.
[2] GUERRA A,DI CRESCENZO V,GARZI A,et al.Genetic mutations in the treatment of anaplastic thyroid cancer:a systematic review[J].BMC Surg,2013,13 Suppl 2:S44-44.
[3] SCHNEIDER T C,KAPITEIJN E,CORSSMIT E P,et al.To treat or not to treat:developments in the field of advanced differentiated thyroid cancer[J].Neth J Med,2014,72:401-406.
[4] JASIM S,OZSARI L,HABRA M A.Multikinase inhibitors use in differentiated thyroid carcinoma[J].Biologics,2014,8:281-291.
[5] XING M,HAUGEN B R,SCHLUMBERGER M.Progress in molecular-based management of differentiated thyroid cancer[J].Lancet,2013,381:1058-1069.
[6] KIM J G.Molecular pathogenesis and targeted therapies in well-differentiated thyroid carcinoma[J].Endocrinol Metab(Seoul),2014,29:211-216.
[7] HALL R D,KUDCHADKAR R R.BRAF mutations:signaling,epidemiology,and clinical experience in multiple malignancies[J].Cancer Control,2014,21:221-230.
[8] WONG K P,LANG B H.New molecular targeted therapy and redifferentiation therapy for radioiodinerefractory advanced papillary thyroid carcinoma:literature review[J].J Thyroid Res,2012,2012:818204-818204.
[9] OWONIKOKO T K,CHOWDRY R P,CHEN Z,et al.Clinical efficacy of targeted biologic agents as second-line therapy of advanced thyroid cancer[J].Oncologist,2013,18:1262-1269.
[10] KIM T Y,KIM W G,KIM W B,et al.Current status and future perspectives indifferentiated thyroid cancer[J].Endocrinol Metab(Seoul),2014,29:217-225.
[11] SANTARPIA L,LIPPMAN S M,EL-NAGGAR A K.Targeting the MAPK-RAS-RAF signaling pathway in cancer therapy[J].Expert Opin Ther Targets,2012,16:103-119.
[12] KAMIYAMA M,NAGURO I,ICHIJO H.In vivo gene manipulation reveals the impact of stress-responsive MAPK pathways on tumor progression[J].Cancer Sci,2015,106:785-796.
[13] KOUL H K,PAL M,KOUL S.Role of p38 MAP Kinase Signal Transduction in Solid Tumors[J].Genes Cancer,2013,4(9-10):342-359.
[14] XING M.Molecular pathogenesis and mechanisms of thyroid cancer[J].Nat Rev Cancer,2013,13:184-199.
[15] WARD L S.Immune response in thyroid cancer:widening the boundaries[J].Scientifica(Cairo),2014,2014:125450-125450.
[16] XING M.Genetic alterations in the phosphatidylinositol-3kinase/Akt pathway in thyroid cancer[J].Thyroid,2010,20:697-706.
[17] FALLAHI P,MAZZI V,VITA R,et al.New therapies for dedifferentiated papillary thyroid cancer[J].Int J Mol Sci,2015,16:6153-6182.
[18] FALLAHI P,FERRARI S M,MAZZI V,et al.Personalization of targeted therapy in advanced thyroid cancer[J].Curr Genomics,2014,15:190-202.
[19] TYAGI S,GUPTA P,SAINI A S,et al.The peroxisome proliferator-activated receptor:A family of nuclear receptors role in various diseases[J].J Adv Pharm Technol Res,2011,2:236-240.
[20] BOITIER E,GAUTIER J C,ROBERTS R.Advances in understanding the regulation of apoptosis and mitosis by peroxisome-proliferator activated receptors in pre-clinical models:relevance for human health and disease[J].Comp Hepatol,2003,2:3-3.
[21] VU-PHAN D,KOENIG R J.Genetics and epigenetics of sporadic thyroid cancer[J].Mol Cell Endocrinol,2014,386(1-2):55-66.
[22] TUTTLE R M,LUKES Y,ONSTAD L,et al.ret/PTC activation is not associated with individual radiation dose estimates in a pilot study of neoplastic thyroid nodules arising in Russian children and adults exposed to Chernobyl fallout[J].Thyroid,2008,18:839-846.
[23] HANLY E K,RAJORIA S,DARZYNKIEWICZ Z,et al.Disruption of mutated BRAF signaling modulates thyroid cancer phenotype[J].BMC Res Notes,2014,7:187-187.
[24] SONG Y S,LIM J A,PARK Y J.Mutation Profile of Well-Differentiated Thyroid Cancer in Asians[J].Endocrinol Metab(Seoul),2015,30:252-262.
[25] SHI C L,SUN Y,DING C,et al.Correlation between the BRAF V600E mutation status and the clinicopathologic features of papillary thyroid carcinoma[J].Genet Mol Res,2015,14:7377-7385.
[26] HOWELL G M,HODAK S P,YIP L.RAS mutations in thyroid cancer[J].Oncologist,2013,18:926-932.
[27] RAMAN P,KOENIG R J.Pax-8-PPAR-γ fusion protein in thyroid carcinoma[J].Nat Rev Endocrinol,2014,10:616-623.
[28] THOMAS L,LAI S Y,DONG W,et al.Sorafenib in metastatic thyroid cancer:a systematic review[J].Oncologist,2014,19:251-258.
[29] JI B,LIU Y,ZHANG P,et al.COX-2expression and tumor angiogenesis in thyroid carcinoma patients among northeast Chinese population-result of a singlecenter study[J].Int J Med Sci,2012,9:237-242.
[30] KRAWCZYK-RUSIECKA K,LEWIHSKI A.Cyclooxygenase-2 expression and its association with thyroid lesions[J].Arch Med Sci,2010,6:653-657.
计量
- 文章访问数: 51
- PDF下载数: 29
- 施引文献: 0