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垂体细胞瘤的行为学分析

时间:2023-03-12 理论教育 版权反馈
【摘要】:许多证据已证实垂体肿瘤是单克隆起源的,有多种因素共同参与垂体肿瘤的形成,早期DNA 改变形成突变的垂体干细胞,这些“起始”细胞随后在多种内分泌信号的不规则调节和刺激下导致肿瘤细胞克隆扩增。由于参与因素众多,各种调控机制复杂多变,故尽管对垂体瘤发病机制进行了大量研究,并取得了不少新的进展,但其确切的机制仍需进一步阐述。

许多证据已证实垂体肿瘤是单克隆起源的,有多种因素共同参与垂体肿瘤的形成,早期DNA 改变(gsp突变,11q13抑癌基因失活)形成突变的垂体干细胞,这些“起始”细胞随后在多种内分泌信号的不规则调节和刺激下(下丘脑激素及受体,旁分泌生长因子)导致肿瘤细胞克隆扩增。分泌各种激素的腺瘤生物学行为和其生长特征都同其原癌基因变化和所受生长因子的作用相关,而很少情况下发生恶性转化可能与第二次癌基因转化相关(包括ras突变,13号染色体等位基因丢失)。由于参与因素众多,各种调控机制复杂多变,故尽管对垂体瘤发病机制进行了大量研究,并取得了不少新的进展,但其确切的机制仍需进一步阐述。

(王 清 惠国桢)

参考文献

[1] 王 清,惠国桢.人脑垂体腺瘤遗传学研究的进展.国外医学神经病学神经外科学分册,2002, 29(5):398-401.

[2] 王 清,惠国桢,蔺玉昌,等.垂体瘤遗传变异的初步研究.癌症,2002,21(10):1120-1123.

[3] 俞文华,惠国桢,施达仁,等.PCNA、P53、nm-23H1蛋白表达与垂体腺瘤生物学行为的关系.中华神经外科杂志,1999,15(6):371-374.

[4] 凌伟华,惠国桢,马文雄,等. Hst基因在垂体腺瘤中的表达及其与肿瘤侵袭性的关系.中华神经外科杂志,2000,16(4):263.

[5] Dworakowska D, Grossman AB. The pathophysiology of pituitary adenomas. Best Practice & Research Clinical Endocrinology & Metabolism, 2009,23:525-541.

[6] Scheithauer BW, Gaffey TA, Lloyd RV, et al. Pathobiology of pituitary adenomas and carcinomas. Neurosurgery, 2006,59:341-353.

[7] Ezzat S, Asa SL, Couldwell WT, et al. The prevalence of pituitary adenomas: a systematic review. Cancer, 2004,101:613-619.

[8] Daly AF, Burlacu MC, Livadariu E, et al. The epidemiology and management of pituitary incidentalomas. Hormone Research, 2007,68(Suppl. 5):195-198.

[9] Levy A. Molecular and trophic mechanisms of tumorigenesis. Endocrinology and Metabolism Clinics of North America, 2008,37:23-50.

[10] Gueorguiev M & Grossman AB. Pituitary gland and beta-catenin signaling: from ontogeny to oncogenesis. Pituitary, 2008.

[11] Boikos SA & Stratakis CA. Molecular genetics of the cAMP-dependent protein kinase pathway and of sporadic pituitary tumorigenesis. Human Molecular Genetics, 2007,16(Spec No 1): R80-R87.

[12] Beckers A & Daly AF. The clinical, pathological, and genetic features of familial isolated pituitary adenomas. European Journal of Endocrinology, 2007,157:371-382.

[13] Karhu A & Aaltonen LA. Susceptibility to pituitary neoplasia related to MEN-1, CDKN1B and AIP mutations: an update. Human Molecular Genetics, 2007,16(Spec No 1): R73-R79.

[14] Horvath A & Stratakis CA. Clinical andmolecular genetics of acromegaly: MEN1, Carney complex, McCune-Albright syndrome, familial acromegaly and genetic defects in sporadic tumors. Reviews in Endocrine & Metabolic Disorders, 2008,9:1-11.

[15] Vierimaa O, Georgitsi M, Lehtonen R et al. Pituitary adenoma predisposition caused by germline mutations in the AIPgene. Science, 2006,312:1228-1230.

[16] Igreja S, Chahal HS, Akker SA et al. Assessment of p27 (cyclin-dependent kinase inhibitor 1B) and AIP (aryl hydrocarbon receptor-interacting protein) genes in MEN1 syndrome patients without any detectable MEN1 gene mutations. Clinical Endocrinology, 2008.

[17] Daly AF, Jaffrain-Rea ML, Ciccarelli A, et al. Clinical characterization of familial isolated pituitary adenomas. The Journal of Clinical Endocrinology and Metabolism, 2006,91:3316-3323.

[18] Georgitsi M, Raitila A, Karhu A, et al. Germline CDKN1B/p27Kip1 mutation in multiple endocrine neoplasia. The Journal of Clinical Endocrinology and Metabolism, 2007,92:3321-3325.

[19] Bossis I, Voutetakis A, Matyakhina L, et al. A pleiomorphic GH pituitary adenoma from a Carney complex patient displays universal allelic loss at the protein kinase A regulatory subunit 1A (PRKARIA) locus. Journal of Medical Genetics, 2004,41: 596-600.

[20] Daly AF, Vanbellinghen JF, Khoo SK, et al. Aryl hydrocarbon receptor-interacting protein gene mutations in familial isolated pituitary adenomas: analysis in 73 families. The Journal of Clinical Endocrinology and Metabolism, 2007,92:1891-1896.

[21] Tanizaki Y, Jin L, Scheithauer BWet al. P53 gene mutations in pituitary carcinomas. Endocrine Pathology, 2007,18:217-222.

[22] Salehi F, Kovacs K, Scheithauer BWet al. Pituitary tumor-transforming gene in endocrine and other neoplasms: a review and update. Endocrine-related Cancer, 2008, 15:721-743.

[23] Chamaon K, Kirches E, Kanakis D, et al. Regulation of the pituitary tumor transforming gene by insulin-like-growth factor-I and insulin differs between malignant and non-neoplastic astrocytes. Biochemical and Biophysical Research Communications, 2005,331:86-92.

[24] Tong Y, Tan Y, Zhou C, et al. Pituitary tumor transforming gene interacts with Sp1 to modulate G1/S cell phase transition. Oncogene, 2007,26:5596-5605.

[25] Chesnokova V, Zonis S, Rubinek T, et al. Senescence mediates pituitary hypoplasia and restrains pituitary tumor growth. Cancer Research, 2007,67:10564-10572.

[26] Chesnokova V, Kovacs K, Castro AV, et al. Pituitary hypoplasia in Pttg_/_ mice is protective for Rbt/_ pituitary tumorigenesis. Molecular Endocrinology, 2005,19: 2371-2379.

[27] Filippella M, Galland F, Kujas M, et al. Pituitary tumour transforming gene (PTTG) expression correlates with the proliferative activity and recurrence status of pituitary adenomas: a clinical and immunohistochemical study. Clinical Endocrinology, 2006,65: 536-543.

[28] Minematsu T, Suzuki M, Sanno N, et al. PTTG overexpression is correlated with angiogenesis in human pituitary adenomas. Endocrine Pathology, 2006,17:143-153.

[29] Minematsu T, Egashira N, Kajiya H, et al. PTTG is a secretory protein in human pituitary adenomas and in mouse pituitary tumor cell lines. Endocrine Pathology, 2007,18:8-15.

[30] Yoshino A, Katayama Y, Ogino A, et al. Promoter hypermethylation profile of cell cycle regulator genes in pituitary adenomas. Journal of Neuro-oncology, 2007,83: 153-162.

[31] Ruebel KH, Leontovich AA, Jin L, et al. Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression. Endocrine, 2006,29:435-444.

[32] Evans CO, Moreno CS, Zhan X, et al. Molecular pathogenesis of human prolactinomas identified by gene expression profiling, RT-qPCR, and proteomic analyses. Pituitary, 2008,11:231-245.

[33] Moreno CS, Evans CO, Zhan X, et al. Novel molecular signaling and classification of human clinically nonfunctional pituitary adenomas identified by gene expression profiling and proteomic analyses. Cancer Research, 2005,65:10214-10222.

[34] Elston MS, Gill AJ, Conaglen JV, et al. Wnt pathway inhibitors are strongly downregulated in pituitary tumors. Endocrinology, 2008,149:1235-1242.

[35] Morris DG, Musat M, Czirjak S, et al. Differential gene expression in pituitary adenomas by oligonucleotide array analysis. European Journal of Endocrinology, 2005,153:143-151.

[36] Ribeiro-Oliveira A, Franchi G, Kola B, et al. Protein western array analysis in human pituitary tumours: insights and limitations. Endocrine-related Cancer, 2008.

[37] Bilodeau S, Vallette-Kasic S, Gauthier Y, et al. Role of Brg1 and HDAC2 in GR trans-repression of the pituitary POMC gene and misexpression in Cushing disease. Genes & Development 2006,20:2871-2886.

[38] Drouin J, Bilodeau S & Vallette S. Of old and new diseases: genetics of pituitary ACTH excess (Cushing) and deficiency. Clinical Genetics, 2007,72:175-182.

[39] Asa SL, Digiovanni R, Jiang J, et al. A growth hormone receptor mutation impairs growth hormone autofeedback signaling in pituitary tumors. Cancer Research, 2007, 67:7505-7511.

[40] Giacomini D, Acuna M, Gerez J, et al. Pituitary action of cytokines: focus on BMP-4 and gp130 family. Neuroendocrinology, 2007,85:94-100.

[41] Dworakowska D & Grossman A. Are neuroendocrine tumours a feature of tuberous sclerosis? Endocrine-related Cancer, 2009,16:45-58.

[42] Ewing I, Pedder-Smith S, Franchi G, et al. A mutation and expression analysis of the oncogene BRAF in pituitary adenomas. Clinical Endocrinology, 2007,66:348-352.

[43] Vlotides G, Siegel E, Donangelo I, et al. Rat prolactinoma cell growth regulation by epidermal growth factor receptor ligands. Cancer Research, 2008,68:6377-6386.

[44] Carbia-Nagashima A, Gerez J, Perez-Castro C, et al. RSUME, a small RWD-containing protein, enhances SUMO conjugation and stabilizes HIF-1alpha during hypoxia. Cell, 2007,131:309-323.

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