Abstract
Auniversal aspect of cancer development is its multistage nature. Precancerous stages evolve to more advanced stages of malignancy and metastasis. This has been reviewed extensively by Foulds.1,2 Based on observations of karyotypic progression in hematopoietic and other neoplasms, Nowell3 proposed a clonal evolution model for tumor progression. In this model, variant cell clones which possess some growth advantage overgrow the other cells in the tumor.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Foulds L. The experimental study of Cancer Res 1954; 14: 317–39.
Foulds L. Neoplastic Development. 1969, 1975.
Nowell PC. The clonal evolution of ence (Washington DC) 1976; 194: 23
Nordling CO. A new theory on the tumor progression: a review. New York: Academic Press tumor cell populations. Sci-cancer-inducing mechanism. Br J Cancer 1953; 7: 68–72.
Armitage P, Doll R. The age distribution of cancer and a multistage theory of carcinogenesis. Br J Cancer 1954; 8: 1–12.
Ashley DJ. On the incidence of carcinoma of the prostate. J Pathol Bacteriol 1965; 90: 217–24.
Whittemore AS. Quantitative theories of oncogenesis. Adv Canc Res 1978; 27: 55–88.
Muir CS, Fraumeni JF Jr, Doll R. The interpretation of time trends. Cancer Surveys 1994; 19 /20: 5–21.
Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell 1990; 61: 759–67.
Vogelstein B, Kinzler KW. The multistep nature of cancer. Trends in Genetics 1993; 9: 138–41.
Wolfe HJ, Melvin KEW, Cervi-Skinner SJ et al. C-cell hyperplasia preceding medullary thyroid carcinoma. N Engl J Med 1973; 289: 437–41.
Gagel RF, Jackson CE, Block MA et al. Age-related probability of development of hereditary medullary thyroid carcinoma. J Pediatr 1982; 101: 941–6.
Ponder, BAJ, Coffey R, Gagel RF et al. Risk estimation and screening in families of patients with medullary thyroid carcinoma. Lancet 1988; 1: 397–400.
Boultwood J, Wynford-Thomas D, Richards GP et al. In-situ analysis of calcitonin and CGRP expression in medullary thyroid carcinoma. Clin Endocrinol 1990; 33: 381–90.
Williams ED, Ponder BAJ, Craig RK. Immunohistochemical study of calcitonin gene-related peptide in human medullary carcinoma and C cell hyperplasia. Clin Endocrinol 1987; 27: 107–14.
Lippman SM, Mendelsohn G, Trump DL et al. The prognostic and biologic significance of cellular heterogeneity in medullary thyroid carcinoma: A study of calcitonin, L-dopa decarboxylase, and histaminase. J Clin Endocrinol Metab 1982; 54: 233–40.
Saad MF, Ordonez NG, Guido JJ et al. The prognostic value of immunostaining in medullary carcinoma of the thyroid. J Clin Endocrinol Metab 1984; 59: 850–6.
Bergholm U, Adami H-O, Auer G et al. Histopathologic characteristics and nuclear DNA content as prognostic factors in medullary thyroid carcinoma. Cancer 1989; 64: 135–42.
Takami H, Bessho T, Kameya T et al. Immunohistochemical study of medullary thyroid carcinoma: Relationship of clinical features to prognostic factors in 36 patients. World J Surg 1988; 12: 572–9.
Riddell DA, Lampe HB, Cramer H et al. Medullary thyroid carcinoma: prognostic factors. J Otolaryngol 1993; 22: 180–3.
Pacini F, Basolo F, Ekisei R et al. Medullary thyroid cancer. An immunohistochemical and humoral study using six separate antigens. Am J Clin Pathol 1991; 95: 300–8.
Roncalli M, Viale G, Grimelius L et al. Prognostic value of N-myc immunoreactivity in medullary thyroid carcinoma. Cancer 1994; 74: 134–41.
Boultwood J, Wyllie FS, Williams ED et al. N-myc expression in neoplasia of human thyroid C-cells. Cancer Res 1988; 48: 4073–7.
Klimpfinger M, Ruhri C, Putz B et al. Oncogene expression in a medullary thyroid carcinoma. Virchows Arch B Cell Pathol Incl Mol Pathol 1988; 54: 256–9.
Neuhold N, Langle F, Gnant M et al. Relationship of CD15 immunoreactivity and prognosis in sporadic medullary thyroid carcinoma. J Cancer Res Clin Oncol 1992; 118: 629–34.
Langle F, Soliman T, Neuhold N et al. CD15 (LeuM1) immunoreactivity: Prognostic factor for sporadic and hereditary medullary thyroid cancer? Study Group on Multiple Endocrine Neoplasia of Austria. World J Surg 1994; 18: 583–7.
Takami H, Ito K. Calcitonin gene-related peptide as a tumor marker for medullary thyroid carcinoma. Int Surg 1992; 77: 181–5.
Skopelitou A, Korkolopoulou P, Papanikolaou A et al. Proliferating cell nuclear antigen (PCNA) in medullary thyroid carcinoma. J Cancer Res Clin Oncol 1993; 119: 379–81.
Komminoth P, Roth J, Saremaslani P et al. Polysialic acid of the neural cell adhesion molecule in the human thyroid: A marker for medullary thyroid carcinoma and primary C-cell hyperplasia. An immunohistochemical study on 79 thyroid lesions. Am J Surg Pathol 1994; 18: 399–411.
Vierbuchen M, Schroder S, Larene A et al. Native and sialic acid masked (a) antigen reactivity in medullary thyroid carcinoma. Distinct tumor-associated and prognostic relevant antigens. Virchows Archiv A Pathol Anat Histopathol 1994; 424: 205–11.
Neuhold N, Ullrich R. Secretogranin IV immunoreactivity in medullary thyroid carcinoma: An immunohistochemical study of 62 cases. Virchows Arch A Pathol Anat Histopathol 1993; 423: 85–9.
Harach HR, Wilander E, Grimelius L et al. Chromogranin A immunoreactivity compared with argyrophilia, calcitonin immunoreactivity, and amyloid as tumour markers in the histopathological diagnosis of medullary (C-cell) thyroid carcinoma. Pathol Res Pract 1992; 188: 123–30.
Pyke CM, Hay ID, Goellner JR et al. Prognostic significance of calcitonin immunoreactivity, amyloid staining, and flow cytometric DNA measurements in medullary thyroid carcinoma. Surgery 1991; 110: 964–70.
Sunday ME, Wolfe HJ, Roos BA et al. Gastrin-releasing peptide gene expression in developing, hyperplastic and neoplastic thyroid C-cells. Endocrinol 1988; 122: 1551–8.
Viale G, Roncalli M, Grimelius L et al. Prognostic value of BCL-2 immunoreactivity in medullary thyroid carcinoma. Human Path 1995; 26: 945–50.
Nelkin BD, Nakamura Y, White RW et al. Low incidence of loss of chromosome 10 in sporadic and hereditary human medullary thyroid carcinoma. Cancer Res 1989; 49: 4114–9.
Nelkin BD, Ball DW, Baylin SB. Molecular abnormalities in tumors associated with multiple endocrine neoplasia, type 2. Endocrinol Metab Clin North Amer 1994; 23: 187–213.
Fabien N, Paulin C, Santoro M et al. Expression of the RET proto-oncogene in normal human C-cells and adrenal medulla. Int J Onc 1994; 4: 623–6.
Tsuzuki T, Takahashi M, Asai N et al. Spatial and temporal expression of the ret proto-oncogene product in embryonic, infant and adult rat tissues. Oncogene 1995; 1005–17.
Höppener JWM. The human calcitonin genes. Ph.D. thesis. University of Utrecht. Utrecht, Netherlands 1988; 37–75.
Rosenfeld MG, Emeson RB, Yeakley JM et al. Calcitonin gene-related peptide: A neuropeptide generated as a consequence of tissue-specific, developmentally regulated alternative RNA processing events. Ann NY Acad Sci 1992; 657: 1–17.
Amara SG, Jonas V, Rosenfeld MG et al. Alternative RNA processing generates mRNAs encoding diffeent polypeptide products. Nature 1982; 298: 240–4.
Rosenfeld MG, Mermod J-J, Amara SG et al. Production of a novel neuropeptide encoded by the calcitonin gene via tissue-specific RNA processing. Nature 1983; 304: 129–35.
Sabate, MI, Stolarsky, LS, Polak JM et al. Regulation of neuroendocrine gene expression by alternative RNA processing. J Biol Chem 1985; 260: 2589–92.
Crenshaw EB III, Russo AF, Swanson LW et al. Neuron-specific alternative RNA processing in transgenic mice expressing a metallothionein-calcitonin fusion gene. Cell 1987; 49: 389–98.
Leff SE, Evans RM, Rosenfeld MG. Splice commitment dictates neuron-specific alternative RNA processing in calcitonin/CGRP gene expression. Cell 1987; 48: 517–24.
Emeson RB, Hedjran R, Yeakley JM et al. Alternative production of calcitonin and CGRP mRNA is regulated at the calcitonin-specific splice acceptor. Nature (London) 1989; 341: 76–80.
Bovenberg RAL, Adema GJ, Baas PD. Model for tissue specific calcitonin/CGRP-I RNA processing from in vitro experiments. Nucleic Acids Res 1988; 16: 7867–83.
Adema GJ, Bovenberg RAL, Baas PD. Unusual branch point selection involved in splicing of the alternatively processed calcitonin/ CGRP-I pre-mRNA. Nucleic Acids Res 1988; 16: 9513–26.
Amara SG, Evans RM, Rosenfeld MG. Calcitonin/calcitonin gene-related peptide transcription unit: tissue-specific expression involves selective use of alternative polyadenylation sites. Mol Cell Biol 1984; 4: 2151–60.
Moore MJ, Query CC, Sharp PA. Splicing of precursors to mRNAs by the spliceosome. In: Gesteland RF, Atkins JF, eds. The RNA World. Cold Spring Harbor: Cold Spring Harbor Laboratory Press, 1993: 303–357.
Cote GJ, Nguyen IN, Lips CJM et al. Validation of an in vitro RNA processing system for CT/CGRP precursor mRNA. Nucleic Acids Res 1991; 19: 3601–6.
Cote GJ, Stolow, DT, Peleg S et al. Identification of exon sequences and an exon binding protein involved in alternative RNA splicing of calcitonin/CGRP. Nucleic Acids Res 1992; 20: 2361–6.
Cote GJ. Alternative RNA splicing of calcitonin/calcitonin gene-related peptide minigene transcripts in a thyroid C-cell line. Biochem Biophys Res Commun 1994; 200: 993–8.
Roesser JR, Litschwager K, Leff SE. Regulation of tissue-specific splicing of the calcitonin/CGRP gene by RNA binding proteins. J. Biol. Chem. 1993; 268: 8366–75.
van Oers CCM, Adema GJ, Zandberg H et al. Two different sequence elements within exon 4 are necessary for calcitonin-specific splicing of the human calcitonin/calcitonin gene-related peptide I pre-mRNA. Mol Cell Biol 1994; 14: 951–960.
Yeakley JM, Hedjran F, Morfin J-P et al. Control of calcitonin/ calcitonin gene-related paptide pre-mRNA processing by constitutive intron and exon elements. Mol Cell Biol 1993; 13: 5999–6011.
Adema GJ, van Hulst KL, Baas PD. Uridine branch acceptor is a cis-acting element involved in regulation of the alternative processing of calcitonin/CGRP-I pre-mRNA. Nucleic Acids Res 1990; 18: 5365–73
Adema GJ, Baas PD. Deregulation of alternative processing of calcitonin/CGRP-I pre-mRNA by a single point mutation. Biochem Biophys Res Commun 1991; 178: 985–92.
Trump DL, Mendelsohn G, Baylin SB. Discordance between plasma calcitonin and tumor-cell mass in medullary thyroid carcinoma. New Engl J Med 1979; 301: 253–5.
Le Guellec P, Dumas S, Volle GE et al. An efficient method to detect calcitonin mRNA in normal and neoplastic rat C-cells (medullary thyroid carcinoma) by in situ hybridization using a digoxigenin-labeled synthetic oligodeoxyribonucleotide probe. J Histochem Cytochem 1993; 41: 389–95.
Saad MF, Ordonez NG, Rashid RK et al. Medullary carcinoma of the thyroid. A study of the clinical features and prognostic factors in 161 patients. Medicine 1984; 63: 319–42.
Brodeur GM, Seeger RC, Schwab M et al. Amplification of Nmyc in untreated human neuroblastomas correlates with advanced disease stage. Science 1984; 224: 1121–4.
Nakagawara A, Arima-Nakagawara M, Scavarda NJ et al. Association between high levels of expression of the TRK gene and favorable outcome in human neuroblastoma. N Engl J Med 1993; 328: 847–54.
Nakagawara A, Azar CG, Scavarda NJ et al. Expression and function of TRK-B and BDNF in human neuroblastomas. Mol Cell Biol 1994; 14: 759–67.
Larcher JC, Basseville M, Vayssiere JL et al. Growth inhibition of N1E-115 mouse neuroblastoma cells by c-myc or N-myc antisense oligodeoxynucleotides causes limited differentiation but is not coupled to neurite formation. Biochem Biophys Res Commun 1992; 185: 915–24.
Schmidt ML, Salwen HR, Manohar CF et al. The biological effects of antisense N-myc expression in human neuroblastoma. 1994; 5: 171–8.
Matsushima H, Bogenmann E. Expression of trkA cDNA in neuroblastomas mediates differentiation in vitro and in vivo. Mol Cell Biol 1993; 13: 7447–56.
Azar CG, Scavarda NJ, Reynolds CP et al. Multiple defects of the nerve growth factor receptor in human neuroblastomas. Cell Growth Differ 1990; 1: 421–8.
Matsumoto K, Wada RK, Yamashiro JM et al. Constitutive Nmyc gene expression inhibits trkA mediated neuronal differentiation. Oncogene 1995; 10: 1915–25.
Thiele C, Matsumoto K, Lucarelli E et al. Brain derived neurotrophic factor (BDNF) stimulates NMYC transcription in human neuroblastoma cells. Proc Amer Assoc for Cancer Res 1995; 36: 559.
Leong SS, Horoszewicz JS, Shimaoka K, et al. A new cell line for study of human medullary thyroid carcinoma. In: Andreoli M, Monaco F, Robbins J, eds. Advances in Thyroid Neoplasia. Rome, Italy: Field Eductional Italia 1981; 95–108.
Carlomagno F, Salvatore D, Santoro M. Expression of brain-derived neurotrophic factor and p145TrkB affects survival, differentiation, and invasiveness of human neuroblastoma cells. Cancer Res 1995; 55: 1798–806.
Nakagawa T, Mabry M, de Bustros A et al. Introduction of Harvey v-ras oncogene induces differentiation of cultured human medullary thyroid carcinoma cells. Proc Natl Acad Sci USA 1987; 84: 5923–7.
Samuels ML, Weber MJ, Bishop JM et al. Conditional transformation of cells and rapid activation of the mitogen-activated protein kinase cascade by an estradiol-dependent human raf-1 protein kinase. Mol Cell Biol 1993; 13: 6241–52.
Carson EB, McMahon M, Baylin SB et al. Ret gene silencing is associated with raf-l-induced medullary thyroid carcinoma cell differentiation. Cancer Res 1995; 55: 2048–52.
Nelkin BD, Chen KY, de Bustros A et al. Changes in calcitonin gene RNA processing during growth of a human medullary thyroid carcinoma cell line. Cancer Res 1989; 49: 6949–52.
Chesa PG, Rettig WJ, Melamed MR et al. Expression of p21 ras in normal and malignant human tissues: lack of association with proliferation and malignancy. Proc Natl Acad Sci 1987; 84: 3234–8.
Furth ME, Aldrich TH, Cordon-Cardo C. Expression of ras proto-oncogene proteins in normal human tissues. Oncogene 1987; 1: 47–58.
Rights and permissions
Copyright information
© 1996 Springer-Verlag Berlin Heidelberg
About this chapter
Cite this chapter
Nelkin, B.D. (1996). Progression of Medullary Thyroid Carcinoma. In: Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2. Medical Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-21948-5_8
Download citation
DOI: https://doi.org/10.1007/978-3-662-21948-5_8
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-662-21950-8
Online ISBN: 978-3-662-21948-5
eBook Packages: Springer Book Archive