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Oncogenes in Thyroid Cancer

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Thyroid Cancer

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Abstract

At the time of conception, the human organism is a single cell zygote. During the course of development into an adult, this cell expands into a complex mass of approximately 100 trillion cells, with an enormous variety of shapes, sizes, and functions. Normal tissue growth and development require prolific cell division, exquisitely regulated cell differentiation, and appropriately timed cell death or apoptosis. Neoplastic transformation of tissue generally occurs when abnormal regulatory mechanisms promote excessive cell division, impaired cell differentiation, and/or failure of apoptosis. In most tumor types, this aberrant control originates at the genetic level.

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References

  1. Jorde LB, Carey JC, White RL. Basic cell biology: structure and function of genes and chromosomes. In Medical Genetics. St. Louis: Mosby-Yearbook, 1995:7–29.

    Google Scholar 

  2. Weinberg RA. How cancer arises. Scientific American 1996; 275:62–70.

    PubMed  CAS  Google Scholar 

  3. Cline MJ, Slamom DJ, Lipsick JS. Oncogenes: implications for the diagnosis and treatment of cancer. Ann Intern Med 1984; 101:223–233.

    PubMed  CAS  Google Scholar 

  4. Gordon H. Oncogenes. Mayo Clin Proc 1985; 60:697–713.

    PubMed  CAS  Google Scholar 

  5. Druker BJ, Mamon HJ, Roberts TM. Oncogenes, growth factors, and signal transduction. N Engl J Med 1989; 321:1383–1391.

    Article  PubMed  CAS  Google Scholar 

  6. Krontiris TG. Molecular medicine: oncogenes. N Engl J Med 1995; 333:303–306.

    Article  PubMed  CAS  Google Scholar 

  7. Latchman DS. Transcription-factor mutations and disease. N Engl J Med 1995; 334:28–33.

    Article  Google Scholar 

  8. Friend SH, Dryja TP, Weinberg RA. Oncogenes and tumor-suppressing genes. N Engl J Med 1988; 318:618–622.

    Article  PubMed  CAS  Google Scholar 

  9. Weinberg RA. Tumor suppressor genes. Science 1991; 254:1138–1145.

    Article  PubMed  CAS  Google Scholar 

  10. Marshall CF. Tumor suppressor genes. Cell 1991; 64:313–326.

    Article  PubMed  CAS  Google Scholar 

  11. Knudson AG. Antioncogenes and human cancer. Proc Natl Acad Sci USA 1993; 90:10914–10921.

    Article  PubMed  CAS  Google Scholar 

  12. Hartwell LH, Kastan MB. Cell cycle control and cancer. Science 1994; 266:1821–1828.

    Article  PubMed  CAS  Google Scholar 

  13. Vogelstein B, Kinzler KW. The multistep nature of cancer. Trends Genet 1993; 9:138–141.

    Article  PubMed  CAS  Google Scholar 

  14. Bishop JM. Cancer: the rise of the genetic paradigm. Genes Dev 1995; 9:1309–1315.

    Article  PubMed  CAS  Google Scholar 

  15. Vassart G, Dumont JE. The thyrotropin receptor and the regulation of thyrocyte function and growth. Endocrine Rev 1992; 13:596–611.

    Article  CAS  Google Scholar 

  16. Paschke R, Tonacchera M, Van Sande J, et al. Identification and functional characterization of two new somatic mutations causing constitutive activation of the thyrotropin receptor in hyperfunctioning autonomous adenomas of the thyroid. J Clin Endocrinol Metab 1994; 79:1785–1789.

    Article  PubMed  CAS  Google Scholar 

  17. Porcellini A, Ciullo I, Laviola L, et al. Novel mutations of thyrotropin receptor gene in thyroid hyperfunctioning adenomas. Rapid identification by fine needle aspiration biopsy. J Clin Endocrinol Metab 1994; 79:657–661.

    Article  PubMed  CAS  Google Scholar 

  18. Russo D, Arturi F, Wicker R, et al. Genetic alterations in thyroid hyperfunctioning adenomas. J Clin Endocrinol Metab 1995; 80:1347–1351.

    Article  PubMed  CAS  Google Scholar 

  19. Ohno M, Endo T, Ohta K, et al. Point mutations in the thyrotropin receptor in human thyroid tumors. Thyroid 1995; 5:97–100.

    PubMed  CAS  Google Scholar 

  20. Parma J, Duprez L, Van Sande J, et al. Constitutively active receptors as a disease-causing mechanism. Mol Cell Endocrinology 1994; 100:159–162.

    Article  CAS  Google Scholar 

  21. Van Sande J, Parma J, Tonacchera M, et al. Somatic and germline mutations of the TSH receptor gene in thyroid diseases. J Clin Endocrinol Metab 1995; 80:2577–2585.

    Article  PubMed  Google Scholar 

  22. Takeshita A, Nagayama Y, Yokoyama N, et al. Rarity of oncogenic mutations in the thyrotropin receptor of autonomously functioning thyroid nodules in Japan. J Clin Endocrinol Metab 1995; 80:2607–2611.

    Article  PubMed  CAS  Google Scholar 

  23. Matsuo K, Friedan E, Gejman PV, Fagin JA: The thyrotropin receptor (TSH-R) is not an oncogene for thyroid tumors: structural studies of the TSH-R and the alpha subunit of Gs in human thyroid neoplasms. J Clin Endocrinol Metab 1993; 76:1446–1451.

    Article  PubMed  CAS  Google Scholar 

  24. Esapa C, Foster S, Johnson S, et al: G protein and thyrotropin receptor mutations in thyroid neoplasia. J Clin Endocrinol Metab 1997; 82:493–496.

    Article  PubMed  CAS  Google Scholar 

  25. Lyons J, Landis CA, Harsh G, et al. Two G protein oncogenes in human endocrine tumors. Science 1990; 249:655–658.

    Article  PubMed  CAS  Google Scholar 

  26. Dumont JE. Thyroid adenoma, Gsa expression and the cyclic adenosine monophosphate mitogenic cascade: A complex relationship. J Clin Endocrinol Metab 1995; 80:1518–1520.

    Article  PubMed  Google Scholar 

  27. Spalmberg D, Sharifi N, Elisei R, et al: Structural studies of the thyrotropin receptor and Gsa in human thyroid cancers: low prevalence of mutations predicts infrequent involvement in malignant transformation. J Clin Endocrinol Metab 1996; 81:3898–3901.

    Article  Google Scholar 

  28. Moretti F, Nanni S, Pontecorvi A. Molecular pathogenesis of thyroid nodules and cancer. Ballieres Best Prac Res Clin Endocrinol Metab 2000; 14:517–539.

    Article  CAS  Google Scholar 

  29. Bos JL. Ras oncogenes in human cancer: a review. Cancer Res 1989; 49:4682–4689.

    PubMed  CAS  Google Scholar 

  30. Karga H, Lee JK, Vickery AL, et al: Ras oncogene mutations in benign and malignant thyroid neoplasms. J Endocrinol Metab 1991; 73:832–836.

    Article  CAS  Google Scholar 

  31. Nikiforova MN, Lynch RA, Biddinger PW, et al. Ras point mutations and PAX8-PPARγ rearrangement in thyroid tumors: evidence for distinct molecular pathways in thyroid follicular carcinoma. J Clin Endocrinol Metab 2003; 88:2318–2326.

    Article  PubMed  CAS  Google Scholar 

  32. Lemoine NR, Mayall ES, Wyllie FS, et al. High frequency of ras oncogene activation in all stages of human thyroid tumorigenesis. Oncogene 1989; 4:159–164.

    PubMed  CAS  Google Scholar 

  33. Esapa CT, Johnson SJ, Kendall-Taylor P, et al. Prevalence of Ras mutations in thyroid neoplasia. Clin Endocrinol 1999; 50:529–535.

    Article  CAS  Google Scholar 

  34. Lemoine NR, Mayall ES, Wyllie FS, et al. Activated ras oncogenes in human thyroid cancers. Cancer Res 1988; 48:4459–4463.

    PubMed  CAS  Google Scholar 

  35. Zhu Z, Gandhi M, Nikiforova MN, et al. Molecular profile and clinical-pathologic features of the follicular variant of papillary thyroid carcinoma: an unusually high prevalence of ras mutations. Am J Clin Pathol 2003; 120:71–77.

    Article  PubMed  CAS  Google Scholar 

  36. Manenti G, Pilotti S, Re FC, et al. Selective activation of Ras oncogenes in follicular and undifferentiated thyroid carcinomas. Eur J Cancer 1994; 30A:987–993.

    Article  PubMed  CAS  Google Scholar 

  37. Kroll TG, Sarraf P, Pecciarini L, et al. PAX8/PPAR? fusion oncogene in human thyroid carcinoma. Science 2000; 289:1357–1360.

    Article  PubMed  CAS  Google Scholar 

  38. Schlumberger M, Pacini F. Oncogenes and tumor suppressor genes. In Thyroid Tumors. Paris: Editions Nucleon, 2003:63–83.

    Google Scholar 

  39. Nikiforova MN, Biddinger PW, Caudill CM, et al. PAX8-PPARgamma rearrangement in thyroid tumors: RT-PCR and immunohistochemical analyses. Am J Surg Path 2002; 26:1016–1023.

    Article  PubMed  Google Scholar 

  40. Marques AR, Espadinha C, Catarino AL, et al. Expression of PAX8-PPARγ1 rearrangements in both follicular thyroid carcinomas and adenomas. J Clin Endocrinol Metab 2002; 87:3947–3952.

    Article  PubMed  CAS  Google Scholar 

  41. Dwight T, Thoppe SR, Foukakis T, et al. Involvement of the PAX/Peroxisome proliferator-activated receptor γ rearrangement in follicular thyroid tumors. J Clin Endocrinol Metab 2003; 88:4440–4445.

    Article  PubMed  CAS  Google Scholar 

  42. Jhiang SM. The RET proto-oncogene in human cancers. Oncogene 2000; 19:5590–5597.

    Article  PubMed  CAS  Google Scholar 

  43. Alberti L, Carniti C, Miranda C, et al. RET and NTRK1 protooncogenes in human diseases. J Cell Phys 2003; 195:168–186.

    Article  CAS  Google Scholar 

  44. Ichihara M, Murakumo Y, Takahashi M. RET and neuroendocrine tumors. Cancer Lett 2004; 204:197–211.

    Article  PubMed  CAS  Google Scholar 

  45. Hofstra RMW, Landsvater RM, Ceccherini I, et al. A mutation in the RET protooncogene associated with multiple endocrine neoplasia type 2B and sporadic medullary thyroid carcinoma. Nature 1994; 367:375–376.

    Article  PubMed  CAS  Google Scholar 

  46. Smith DP, Eng C, Ponder BAJ. Mutations of the RET proto-oncogene in the multiple endocrine neoplasia type 2 syndromes and Hirschsprung disease. J Cell Science 1994; Suppl18:43–49.

    Google Scholar 

  47. Lips CJM, Landsvater RM, Hoppener JWM, et al. Clinical screening as compared with DNA analysis in families with multiple endocrine neoplasia type 2A. N Engl J Med 1994; 31:828–835.

    Article  Google Scholar 

  48. Zedenius J, Larsson C, Bergholm U, et al. Mutations of codon 918 in the RET proto-oncogene correlate to poor prognosis in sporadic medullary thyroid carcinomas. J Clin Endo Metabol 1995; 80:3088–3090.

    Article  CAS  Google Scholar 

  49. Romei C, Elisei R, Pinchera A, et al. Somatic mutations of the ret protooncogene in sporadic medullary thyroid carcinoma are not restricted to exon 16 and are associated with tumor recurrence. J Clin Endocrinol Metab 1996; 81:1619–1622.

    Article  PubMed  CAS  Google Scholar 

  50. Jhiang SM, Fithian L, Weghorst CM, et al. RET mutation screening in MEN2 patients and discovery of a novel mutation in a sporadic medullary thyroid carcinoma. Thyroid 1996; 6:115–121.

    Article  PubMed  CAS  Google Scholar 

  51. Wohllk N, Cote G, Bugalho MMJ, et al. Relevance of ret protooncogene mutations in sporadic medullary thyroid carcinoma. J Clin Endocrinol Metab 1996; 81:3740–3745.

    Article  PubMed  CAS  Google Scholar 

  52. Frank-Raue K, Hoppner W, Frilling A, et al. and the German Medullary Thyroid Cancer Study Group. Mutations of the ret protooncogene in German multiple endocrine neoplasia families: relation between genotype and phenotype. J Clin Endocrinol Metab 1996; 81:1780–1783.

    Article  PubMed  CAS  Google Scholar 

  53. Quadro L, Panariello L, Salvatore D, et al. Frequent RET protooncogene mutations in multiple endocrine neoplasia type 2A. J Clin Endocrinol Metab 1994; 79:590–594.

    Article  PubMed  CAS  Google Scholar 

  54. Mulligan LM, Ponder BAJ. Genetic basis of endocrine disease: multiple endocrine neoplasia type 2. J Clin Endocrinol Metab 1995; 80:1989–1995.

    Article  PubMed  CAS  Google Scholar 

  55. Eng C. The ret proto-oncogene in multiple endocrine neoplasia type 2 and Hirschsprung’s disease. N Engl J Med 1996; 335:943–951.

    Article  PubMed  CAS  Google Scholar 

  56. Asai N, Iwashita T, Matsuyama M, Takahashi M. Mechanism of activation of the ret proto-oncogene by multiple endocrine neoplasia 2A mutations. Mol Cell Biol 1995; 15:1613–1619.

    PubMed  CAS  Google Scholar 

  57. Borrello MG, Smith DP, Pasini B, et al. RET activation by germline MEN2A and MEN2B mutations. Oncogene 1995; 11:2419–2427.

    PubMed  CAS  Google Scholar 

  58. Santoro M, Carlomagno F, Romano A, et al. Activation of RET as a dominant transforming gene by germline mutations of MEN2A and MEN2B. Science 1995; 267:381–383.

    Article  PubMed  CAS  Google Scholar 

  59. Bongarzone I, Vigano E, Alberti L, et al. Full activation of MEN2B mutant RET by an additional MEN2A mutation or by ligand (GDNF) stimulation. Oncogene 1998; 16:2295–2301.

    Article  PubMed  CAS  Google Scholar 

  60. Nikiforov YE. RET/PTC rearrangement in thyroid tumors. Endocr Pathol 2002; 13:3–16.

    Article  PubMed  CAS  Google Scholar 

  61. Basolo F, Giannini R, Monaco C, et al. Potent mitogenicity of the RET/PTC3 oncogene correlates with its prevalence in tall-cell variant of papillary thyroid carcinoma. Am J Pathol 2002; 160:247–254.

    PubMed  CAS  Google Scholar 

  62. Thomas GA, Bunnell H, Cook HA, et al. High prevalence of RET/PTC rearrangements in Ukrainian and Belarussian post-Chernobyl thyroid papillary carcinomas: A strong correlation between RET/PTC3 and the solid-follicular variant. J Clin Endocrinol Metab 1999; 84:4232–4238.

    Article  PubMed  CAS  Google Scholar 

  63. Santoro M, Carlomagno F, Hay ID, et al. Ret oncogene activation in human thyroid neoplasms is restricted to the papillary cancer subtype. J Clin Invest 1992; 89:1517–1522.

    PubMed  CAS  Google Scholar 

  64. Jhiang SM, Mazzaferri EL. The ret/PTC oncogene in papillary thyroid carcinoma. J Lab Clin Med 1994; 123:331–337.

    PubMed  CAS  Google Scholar 

  65. Grieco M, Santoro M, Berlingieri MT, et al. PTC is a novel rearranged form of the ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. Cell 1990; 60:557–563.

    Article  PubMed  CAS  Google Scholar 

  66. Bongarzone I, Fugazzola L, Vigneri P, et al. Age-related activation of the tyrosine kinase receptor protooncogenes ret and ntrk1 in papillary thyroid carcinoma. J Clin Endocrinol Metab 1996; 81:2006–2009.

    Article  PubMed  CAS  Google Scholar 

  67. Sugg S, Zheng L, Rosen IB, et al. ret/PTC-1,-2, and-3 oncogene rearrangements in human thyroid carcinomas: implications for metastatic potential? J Clin Endocrinol Metab 1996; 81:3360–3365.

    Article  PubMed  CAS  Google Scholar 

  68. Lam KY, Lo CY, Leung PS. High prevalence of RET proto-oncogene activation (RET/PTC) in papillary thyroid carcinoma. Eur J Endocrinol 2002; 147:741–745.

    Article  PubMed  CAS  Google Scholar 

  69. Bounacer A, Wicker R, Caillou B, et al. High prevalence of activationg ret proto-oncogene rearrangements in thyroid tumors from patients who had received external radiation. Oncogene 1997; 15:1263–1273.

    Article  PubMed  CAS  Google Scholar 

  70. Elisei R, Romei C, Vorontsova T, et al. RET/PTC rearrangements in thyroid nodules: studies in irradiated and not irradiated, malignant and benign thyroid lesions in children and adults. J Clin Endocrinol Metab 2001; 86:3211–3216.

    Article  PubMed  CAS  Google Scholar 

  71. Bounacer A, Schlumberger M, Wicker R, et al. Search for NTRK1 proto-oncogene rearrangements in human thyroid tumours originated after therapeutic radiation. Br J Cancer 2000; 82:308–314.

    Article  PubMed  CAS  Google Scholar 

  72. Greco A, Pierotti MA, Bongarzone I, et al. Trk-T1 is a novel oncogene formed by the fusion of tpr and trk genes in human papillary thyroid carcinomas. Oncogene 1992; 7:237–242.

    PubMed  CAS  Google Scholar 

  73. Pierotti MA, Bongarzone I, Borrello MG, et al. Cytogenetics and molecular genetics of carcinomas arising from thyroid epithelial follicular cells. Genes Chromosomes Cancer 1996; 16:1–14.

    Article  PubMed  CAS  Google Scholar 

  74. Di Renzo MF, Olivero M, Ferro S. Overexpression of the c-MET/HGF receptor gene in human thyroid carcinomas. Oncogene 1992; 7:2549–2553.

    PubMed  Google Scholar 

  75. Belfiori A, Gamgemi P, Santomocito MG. Prognostic value of c-MET expression in papillary thyroid carcinoma. Thyroid 1995; 5:5–13.

    Google Scholar 

  76. Ruco LP, Ranalli T, Marzullo A, et al. Expression of Met protein in thyroid tumours. J Pathol 1996; 180:266–270.

    Article  PubMed  CAS  Google Scholar 

  77. Belfiori A, Gangemi P, Costantino A, et al. Negative/low expression of the Met/hepatocyte growth factor receptor identifies papillary thyroid carcinomas with high risk of distant metastases. J Clin Endocrinol Metab 1997; 82:2322–2328.

    Article  Google Scholar 

  78. Trovato M, Villari D, Bartolone L, et al. Expression of the hepatocyte growth factor and c-met in normal thyroid, non-neoplastic, and neoplastic nodules. Thyroid 1998; 8:125–131.

    PubMed  CAS  Google Scholar 

  79. Oyama T, Ichimura E, Sano T, et al. c-Met expression of thyroid tissue with special reference to papillary carcinoma. Pathol Int 1998; 48:763–768.

    PubMed  CAS  Google Scholar 

  80. Zanetti A, Stoppacciaro A, Marzullo A, et al. Expression of Met protein and urokinase-type plasminogen activator receptor (uPA-R) in papillary carcinoma of the thyroid. J Pathol 1998; 186:287–291.

    Article  PubMed  CAS  Google Scholar 

  81. de Luca A, Arena N, Sena LM, Medico E. Met overexpression confers HGF-dependent invasive phenotype to human thyroid carcinoma cells in vitro. J Cell Physiol 1999; 180:365–371.

    Article  PubMed  Google Scholar 

  82. Ramirez R, Hsu D, Patel A, et al. Over-expression of hepatocyte growth factor/scatter factor (HGF/SF) and the HGF/SF receptor (cMET) are associated with a high risk of metastasis and recurrence for children and young adults with papillary thyroid carcinoma. Clin Endocrinol 2000; 53:635–644.

    Article  CAS  Google Scholar 

  83. Nikiforova MN, Kimura ET, Gandhi M, et al. BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab 2003; 88:5399–5404.

    Article  PubMed  CAS  Google Scholar 

  84. Kimura ET, Nikiforova MN, Zhu A, et al. High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma. Cancer Res 2003; 63:1454–1457.

    PubMed  CAS  Google Scholar 

  85. Cohen Y, Xing M, Mambo E, et al. BRAF mutation in papillary thyroid carcinoma. J Natl Cancer Inst 2003; 95:625–627.

    Article  PubMed  CAS  Google Scholar 

  86. Xu X, Quiros RM, Gattuso P, et al. High prevalence of BRAF gene mutation in papillary thyroid carcinomas and thyroid tumor cell lines. Cancer Res 2003; 63:4561–4567.

    PubMed  CAS  Google Scholar 

  87. Soares P, Trovisco V, Rocha AS, et al. BRAF mutations and RET/PTC rearrangements are alternative events in the etiopathogenesis of PTC. Oncogene 2003; 22:4578–4580.

    Article  PubMed  CAS  Google Scholar 

  88. Fukushima T, Suzuki S, Mashiko M, et al. BRAF mutations in papillary carcinomas of the thyroid. Oncogene 2003; 22:6455–6457.

    Article  PubMed  CAS  Google Scholar 

  89. Lane DP: p53, guardian of the genome. Nature 1992; 358:15–16.

    Article  PubMed  CAS  Google Scholar 

  90. Marx J. How p53 suppresses cell growth. Science 1993; 262:1644–1645.

    Article  PubMed  CAS  Google Scholar 

  91. Frebourg T. Cancer risks from germline p53 mutations. J Clin Invest 1992; 90:1637–1641.

    PubMed  CAS  Google Scholar 

  92. Harris CC. Medical progress: clinical implications of the p53 tumor suppressor gene. N Engl J Med 1993; 329:1318–1327.

    Article  PubMed  CAS  Google Scholar 

  93. Greenblat MS, Bennet WP, Hollstein M, et al. Mutations in the p53 tumor suppressor gene: Clues to cancer aetiology and molecular pathogenesis. Cancer Res 1994; 54:4855–4878.

    Google Scholar 

  94. Dobashi Y, Sakamoto A, Sugimura H, et al. Overexpression of p53 as a possible prognostic factor in human thyroid carcinoma. Am J Surg Pathol 1993; 17:375–381.

    Article  PubMed  CAS  Google Scholar 

  95. Dobashi Y, Sugimura H, Sakamoto A, et al. Stepwise participation of p53 gene mutation during dedifferentiation of human thyroid carcinomas. Diagn Mol Pathol 1994; 3:9–14.

    PubMed  CAS  Google Scholar 

  96. Nakamura T, Yana I, Kobayashi T, et al. p53 gene mutations associated with anaplastic transformation of human thyroid carcinomas. Jpn J Cancer Res 1992; 83:1293–1298.

    PubMed  CAS  Google Scholar 

  97. Ito T, Seyma T, Mizuno T, et al. Unique association of p53 mutations with undifferentiated but not with differentiated carcinoma of the thyroid. Cancer Res 1992; 52:1369–1371.

    PubMed  CAS  Google Scholar 

  98. Fagin JA, Matsuo K, Karmakar A, et al. High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas. J Clin Invest 1993; 91:179–184.

    PubMed  CAS  Google Scholar 

  99. Donghi R, Longoni A, Pilotti S, et al. Gene p53 mutations are restricted to poorly differentiated and undifferentiated carcinomas of the thyroid gland. J Clin Invest 1993; 91:1753–1760.

    Article  PubMed  CAS  Google Scholar 

  100. Zedenius J, Larsson C, Wallin G, et al. Alterations of p53 and expression of WAF1/p21 in human thyroid tumors. Thyroid 1996; 6:1–9.

    PubMed  CAS  Google Scholar 

  101. Zou M, Shi Y, Farid NR. p53 mutations in all stages of thyroid carcinomas. J Clin Endocrinol Metab 1993; 77:1054–1058.

    Article  PubMed  CAS  Google Scholar 

  102. Doree M, Galas S. The cyclin-dependent protein kinases and the control of cell division. FASEB J 1994; 8:1114–1121.

    PubMed  CAS  Google Scholar 

  103. Morgan DO. Principles of CDK regulation. Nature 1995; 374:131–134.

    Article  PubMed  CAS  Google Scholar 

  104. Hartwell L. Defects in the cell cycle checkpoint may be responsible for genomic instability of cancer cells. Cell 1992; 71:543–546.

    Article  PubMed  CAS  Google Scholar 

  105. Kamb A, Gravis S, Weaver-Feldheus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science 1994; 264:436–440.

    Article  PubMed  CAS  Google Scholar 

  106. Cyrns VL, Thor A, Xu H-J, et al. Loss of the retinoblastoma tumorsuppressor gene in parathyroid carcinoma. N Engl J Med 1994; 330:757–761.

    Article  Google Scholar 

  107. Farid NR, Zou M, Shi Y. Genetics of follicular thyroid cancer. Endocrinol Metab Clin NA 1995; 24:865–883.

    CAS  Google Scholar 

  108. Haber DA. Telomeres, cancer and immortality. N Engl J Med 1995; 332:955–956.

    Article  PubMed  CAS  Google Scholar 

  109. Greider CW, Blackburn EH. Telomeres, telomerase and cancer. Sci Am 1996; 274:92–97.

    PubMed  CAS  Google Scholar 

  110. Haugen BR, Nawaz S, Markham et al. Telomerase activity in benign and malignant thyroid tumors. San Diego, CA: The 69th Annual Meeting of the American Thyroid Association 1996, Nov 14–17.

    Google Scholar 

  111. Folkman J. Fighting cancer by attacking its blood supply. Sci Am 1996; 275:150–154.

    PubMed  CAS  Google Scholar 

  112. Cuevas P, Gonzalez A-M, Carceller F, Baird A. Vascular response to basic fibroblast growth factor when infused onto normal adventitia or into the injured media of the rat carotid artery. Circ Res 1991; 69:360–369.

    PubMed  CAS  Google Scholar 

  113. Bernstein LR, Liotta LA. Molecular mediators of interactions with extracellular matrix components in metastasis and angiogenesis. Cur Opin Oncol 1994; 6:106–113.

    Article  CAS  Google Scholar 

  114. Ruoslahti E, Reed JC. Anchorage dependence, integrins and apoptosis. Cell 1994; 77:477–478.

    Article  PubMed  CAS  Google Scholar 

  115. Akiyama SK, Olden K, Yamada KM. Fibronectin and integrins in invasion and metastasis. Cancer Metastasis Rev 1996; 14:173–189.

    Article  Google Scholar 

  116. Ruoslahti E. How Cancer Spreads. Sci Am 1996; 275:72–77.

    PubMed  CAS  Google Scholar 

  117. Scheumann GFW, Hoang-Vu C, Cetin Y, et al. Clinical significance of E-cadherin as a prognostic marker in thyroid carcinomas. J Clin Endocrinol Metab 1995; 80:2168–2172.

    Article  Google Scholar 

  118. Oliff A, Gibbs JB, McCormick F: New molecular targets for cancer therapy. Sci Am 1996; 275:144–149.

    Article  PubMed  CAS  Google Scholar 

  119. Old LJ. Immunotherapy for cancer. Sci Am 1996; 275:136–143.

    PubMed  CAS  Google Scholar 

  120. Bassi V, Vitale M, Feliciello A, et al. Retinoic acid induces intercellular adhesion molecule-1 hyperexpression in human thyroid carcinoma cell lines. J Clin Endocrinol Metab 1995; 80:1129–1135.

    Article  PubMed  CAS  Google Scholar 

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  1. S/M Endocrinology/Metabolism/Diabetes Disease, University of Colorado Hospital, Aurora, CO

    Katherine B. Weber MD & Michael T. McDermott MD (Professor of Medicine, Practice Director)

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  1. Katherine B. Weber MD
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  2. Michael T. McDermott MD
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  1. Washington Hospital Center, Washington, DC

    Leonard Wartofsky MD, MPH, MACP  & Douglas Van Nostrand MD, FACP, FACNP  & 

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Weber, K.B., McDermott, M.T. (2006). Oncogenes in Thyroid Cancer. In: Wartofsky, L., Van Nostrand, D. (eds) Thyroid Cancer. Humana Press. https://doi.org/10.1007/978-1-59259-995-0_5

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