Investigation of Succession Model for Goiter in Iodine Deficiency Area_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

LIU Xiaoli , ZOU Xiaowei , SUN Hui , ZHANG Deheng

Department of Thyroid Surgery, ChinaJapan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China;

Corresponding?author：

Keywords：

Nodular goiter; Thyroid carcinoma; Hyperthyroidism; Proliferating cell nuclear antigen; Immunohistochemistry; Angiogenesis

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ObjectiveTo investigate the succession model for hyperthyroidism and thyroid carcinoma secondary to nodular goiter in iodine deficiency area. MethodsA total of 216 specimens of goiter patients from iodine deficiency area were collected in the former 3rd hospital of Norman Bethune Medical College from January 1980 to December 1994. Twentyfour heteroploid samples were selected by the method of Hedley with Flow cytometry (FCM) analysis. Paraffin-embedded tissues from the same position were used to perform immunohistochemical staining for proliferating cell nuclear antigen (PCNA), laminin (LN), factor Ⅷ related antigen (FⅧ-RAg), and p53. The proliferative activity, stroma change, and angiogenesis were observed. ResultsPCNA label index (PCNA-LI) and proliferation index (PI) consistent in 24 heteroploid samples with PCNA staining were significantly higher value. PCNA positive cells were mainly distributed over nonfollicular parenchymatous structures, small follicles, and multilayered structures with large bubbly follicles. Destroyed basement membrane and necrosis were found by LN staining in PCNA positive position with vigorous reproductive capacity. Combining FⅧ-RAg staining with LN staining, interstitial proliferation and angiogenesis were obvious in follicular epithelial cells with vigorous reproductive capacity, providing nutrition and superior environment for them. ConclusionsThe reproduction of thyroid follicular epithelial cells, interstitial proliferation, and angiogenesis are all involved in tuberosis and hyperthyroidism, forming precancerous lesion, which suggest the succession model of goiter in iodine deficiency area.

Citation： LIU Xiaoli,ZOU Xiaowei,SUN Hui,ZHANG Deheng,.. Investigation of Succession Model for Goiter in Iodine Deficiency Area. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2011, 18(8): 809-814. doi: Copy

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1. 張德恒，孫輝，崔俊生，等. 長期補碘后甲狀腺疾病的變遷 [J]. 中國實用外科雜志， 1998， 18（5）： 277278.
2. Ronald A.D, Ricardo VL, Philipp UH, et al. Pathology and Genetics of Tumors of Endocrine Organs： WHO Classification of Tumors [M]. IARC Press， Lyon： 2004: 5191.
3. Kreicbergs A, Brostrm LA, Cewrien G, et al. Cellular DNA content in human osteosarcoma: aspects on diagnosis and prognosis [J]. Cancer, 1982, 50(11): 24762481.
4. De BB, Mclean E, Andersson M, et al. Iodine deficiency in 2007: global progress since 2003 [J]. Food Nutr Bull, 2008, 29(3): 195202.
5. 孫團起，邊建超，朱曉麗，等. 甲狀腺乳頭狀癌組織中線粒體DNA含量的變化 [J]. 復旦學報(醫學版)， 2008， 35（5）： 635640.
6. LaytragoonLewin N, Chen F, Castro J, et al. DNA content and methylation of p16, DAPK and rassf1a gene in tumour and distant, normal mucosal tissue of head and neck squamous cell carcinoma patients [J]. Anticancer Res, 2010, 30(11): 46434648.
7. Nguyen HG, Ravid K. Polyploidy: mechanisms and cancer promotion in hematopoietic and other cells [J]. Adv Exp Med Biol, 2010, 676: 105122.
8. 辛波，肖光，張德恒，等. 長期補碘后地方性甲狀腺腫246例流式細胞分析 [J]. 中國實用外科雜志， 2003， 23（3）： 148150.
9. Lu C, Mishra A, Zhu YJ, et al. Genomic profiling of genes contributing to metastasis in a mouse model of thyroid follicular carcinoma [J]. Am J Cancer Res, 2011, 1(1): 113.
10. Kim HY, Park WY, KE LE, et al. Comparative analysis of gene expression profiles of papillary thyroid microcarcinoma and papillary thyroid carcinoma [J]. J Cancer Res Ther, 2010, 6(4): 452457.
11. Salehian B, Liu Z. Genetic alterations in differentiated thyroid cancers [J]. Endocr Metab Immune Disord Drug Targets, 2009, 9(3): 257268.
12. Liang HS, Zhong YH, Luo ZJ, et al. Comparative analysis of protein expression in differentiated thyroid tumours: a multicentre study [J]. J Int Med Res, 2009, 37(3): 927938.
13. Naryzhny SN, Lee H. Proliferating cell nuclear antigen in the cytoplasm interacts with components of glycolysis and cancer [J]. FEBS Lett, 2010, 584(20): 42924298.
14. Strzalka W, Ziemienowicz A. Proliferating cell nuclear antigen (PCNA): a key factor in DNA replication and cell cycle regulation [J]. Ann Bot, 2011, 107(7): 11271140.
15. 宋楠萌，桑建利，徐恒. 增殖細胞核抗原(PCNA)的分子結構及其生物學功能研究進展 [J]. 自然科學進展， 2006， 16（10）： 12011209.
16. Kohlberger P, Beneder C, Horvat R, et al. Immunohistochemical expression of laminin5 in cervical intraepithelial neoplasia [J]. Gynecol Oncol, 2003, 89(3): 391394.
17. Nordstrm B, Einhorn N, Silfverswrd C, et al. Laminin5 gamma 2 chain as an invasivity marker for uniand multifocal lesions in the lower anogenital tract [J]. Int J Gynecol Cancer, 2002, 12(1): 105109.
18. Fiorentino M, Fu L, Shi YB. Mutational analysis of the cleavage of the cancerassociated laminin receptor by stromelysin3 reveals the contribution of flanking sequences to site recognition and cleavage efficiency [J]. Int J Mol Med, 2009, 23(3): 389397.
19. Kim TH, Lee SY, Rho JH, et al. Mutant p53 (G199V)gains antiapoptotic function through signal transducer and activator of transcription 3 in anaplastic thyroid cancer cells [J]. Mol Cancer Res, 2009, 7(10): 16451654.
20. Gauchotte G, Philippe C, Lacomme S, et al. BRAF, p53 and SOX2 in anaplastic thyroid carcinoma: evidence for multistep carcinogenesis [J]. Pathology, 2011, 43(5): 447452.
21. Lavra L, Rinaldo C, Ulivieri A, et al. The loss of the p53 activator HIPK2 is responsible for galectin3 overexpression in well differentiated thyroid carcinomas [J]. PLoS One, 2011, 6(6): e20665.
22. Linda MR, Sanfilippo M, Vella V, et al. Reactivation of p53 mutants by prima1 in thyroid cancer cells [J]. Int J Cancer, 2011, doi: 10.1002/ijc.26228.
23. Tan A, Etit D, Bayol U, et al. Comparison of proliferating cell nuclear antigen,thyroid transcription factor1, Ki67, p63, p53 and highmolecular weight cytokeratin expressions in papillary thyroid carcinoma,follicular carcinoma, and follicular adenoma [J]. Ann Diagn Pathol, 2011, 15(2): 108116.
24. 田興松，朱見，叢明華，等. 甲狀腺癌組織EG1和VEGFC及p53表達及臨床意義的探討 [J]. 中華腫瘤防治雜志， 2010， 17（18）： 14371440.
25. Bhowmick NA, Moses HL. Tumorstroma interactions [J]. Curr Opin Genet Dev, 2005, 15(1): 97101.
26. Giatromanolaki A, Lyberakidis G, Lyratzopoulos N, et al. Angiogenesis and angiogenic factor expression in thyroid cancer [J]. J BUON, 2010, 15(2): 357361.
27. Stabenow E, Tavares MR, Ab’saber AM, et al. Angiogenesis as an indicator of metastatic potential in papillary thyroid carcinoma [J]. Clinics (Sao Paulo, Brazil), 2005, 60(3): 233240.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Investigation of Succession Model for Goiter in Iodine Deficiency Area

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