Skip to main content
Top
Published in: Pathology & Oncology Research 2/2012

01-04-2012 | Research

Amplification of Thymosin Beta 10 and AKAP13 Genes in Metastatic and Aggressive Papillary Thyroid Carcinomas

Authors: Liliána Z. Fehér, Gábor Pocsay, László Krenács, Ágnes Zvara, Enikő Bagdi, Réka Pocsay, Géza Lukács, Ferenc Győry, Andrea Gazdag, Erzsébet Tarkó, László G. Puskás

Published in: Pathology & Oncology Research | Issue 2/2012

Login to get access

Abstract

Papillary thyroid carcinoma (PTC) is the most common well-differentiated thyroid cancer. Although the great majority of the cases exhibit an indolent clinical course, some of them develop local invasion with distant metastasis, and a few cases transform into undifferentiated/anaplastic thyroid carcinoma with a rapidly lethal course. To identify gene copy number alterations predictive of metastatic potential or aggressive transformation, array-based comparative genomic hybridization (CGH-array) was performed in 43 PTC cases. Formalin-fixed and paraffin-embedded samples from primary tumours of 16 cases without metastasis, 14 cases with only regional lymph node metastasis, and 13 cases with distant metastasis, recurrence or extrathyroid extension were analysed. The CGH-array and confirmatory quantitative real-time PCR results identified the deletion of the EIF4EBP3 and TRAK2 gene loci, while amplification of thymosin beta 10 (TB10) and Tre-2 oncogene regions were observed as general markers for PTC. Although there have been several studies implicating TB10 as a specific marker based on gene expression data, our study is the first to report on genomic amplification. Although no significant difference could be detected between the good and bad prognosis cases in the A-kinase anchor protein 13 (AKAP13) gene region, it was discriminative markers for metastasis. Amplification in the AKAP13 region was demonstrated in 42.9% and 15.4% of the cases with local or with distant metastasis, respectively, while no amplification was detected in non-metastatic cases. AKAP13 and TB10 regions may represent potential new genomic markers for PTC and cancer progression.
Literature
1.
go back to reference Hundahl SA, Fleming ID, Fremgen AM et al (1998) A National Cancer Data Base report on 53,856 cases of thyroid carcinoma treated in the U.S., 1985–1995. Cancer 83:2638–2646PubMedCrossRef Hundahl SA, Fleming ID, Fremgen AM et al (1998) A National Cancer Data Base report on 53,856 cases of thyroid carcinoma treated in the U.S., 1985–1995. Cancer 83:2638–2646PubMedCrossRef
2.
go back to reference Samaan NA, Schultz PN, Hickey RC et al (1992) The results of various modalities of treatment of well differentiated thyroid carcinomas: a retrospective review of 1599 patients. J Clin Endocrinol Metab 75:714–720PubMedCrossRef Samaan NA, Schultz PN, Hickey RC et al (1992) The results of various modalities of treatment of well differentiated thyroid carcinomas: a retrospective review of 1599 patients. J Clin Endocrinol Metab 75:714–720PubMedCrossRef
3.
go back to reference Mazzaferri EL, Jhiang SM (1994) Long-term impact of initial surgical and medical therapy on papillary and follicular thyroid cancer. Am J Med 97:418–428PubMedCrossRef Mazzaferri EL, Jhiang SM (1994) Long-term impact of initial surgical and medical therapy on papillary and follicular thyroid cancer. Am J Med 97:418–428PubMedCrossRef
4.
go back to reference Gilliland FD, Hunt WC, Morris DM et al (1997) Prognostic factors for thyroid carcinoma. A population-based study of 15,698 cases from the Surveillance, Epidemiology and End Results (SEER) program 1973–1991. Cancer 79:564–573PubMedCrossRef Gilliland FD, Hunt WC, Morris DM et al (1997) Prognostic factors for thyroid carcinoma. A population-based study of 15,698 cases from the Surveillance, Epidemiology and End Results (SEER) program 1973–1991. Cancer 79:564–573PubMedCrossRef
5.
go back to reference Sherman SI, Brierley JD, Sperling M et al (1998) Prospective multicenter study of thyroid carcinoma treatment: initial analysis of staging and outcome. National Thyroid Cancer Treatment Cooperative Study Registry Group. Cancer 83:1012–1021PubMedCrossRef Sherman SI, Brierley JD, Sperling M et al (1998) Prospective multicenter study of thyroid carcinoma treatment: initial analysis of staging and outcome. National Thyroid Cancer Treatment Cooperative Study Registry Group. Cancer 83:1012–1021PubMedCrossRef
6.
go back to reference Tsang RW, Brierley JD, Simpson WJ et al (1998) The effects of surgery, radioiodine, and external radiation therapy on the clinical outcome of patients with differentiated thyroid carcinoma. Cancer 82:375–388PubMedCrossRef Tsang RW, Brierley JD, Simpson WJ et al (1998) The effects of surgery, radioiodine, and external radiation therapy on the clinical outcome of patients with differentiated thyroid carcinoma. Cancer 82:375–388PubMedCrossRef
7.
go back to reference Nikiforova MN, Kimura ET, Gandhi M et al (2003) BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab 88:5399–5404PubMedCrossRef Nikiforova MN, Kimura ET, Gandhi M et al (2003) BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab 88:5399–5404PubMedCrossRef
8.
go back to reference Fagin JA (2004) Challenging dogma in thyroid cancer molecular genetics-role of RET/PTC and BRAF in tumour initiation. J Clin Endocrinol Metab 89:4264–4266PubMedCrossRef Fagin JA (2004) Challenging dogma in thyroid cancer molecular genetics-role of RET/PTC and BRAF in tumour initiation. J Clin Endocrinol Metab 89:4264–4266PubMedCrossRef
10.
go back to reference Xing M, Westra WH, Tufano RP et al (2005) BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer. J Clin Endocrinol Metab 90:6373–6379PubMedCrossRef Xing M, Westra WH, Tufano RP et al (2005) BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer. J Clin Endocrinol Metab 90:6373–6379PubMedCrossRef
11.
go back to reference Kondo T, Ezzat S, Asa SL (2006) Pathogenetic mechanisms in thyroid follicular-cell neoplasia. Nat Rev Cancer 6:292–306PubMedCrossRef Kondo T, Ezzat S, Asa SL (2006) Pathogenetic mechanisms in thyroid follicular-cell neoplasia. Nat Rev Cancer 6:292–306PubMedCrossRef
12.
go back to reference Adeniran AJ, Zhu Z, Gandhi M et al (2006) Correlation between genetic alterations and microscopic features, clinical manifestations, and prognostic characteristics of thyroid papillary carcinomas. Am J Surg Pathol 30:216–222PubMedCrossRef Adeniran AJ, Zhu Z, Gandhi M et al (2006) Correlation between genetic alterations and microscopic features, clinical manifestations, and prognostic characteristics of thyroid papillary carcinomas. Am J Surg Pathol 30:216–222PubMedCrossRef
13.
go back to reference Giannini R, Ugolini C, Lupi C et al (2007) The heterogeneous distribution of BRAF mutation supports the independent clonal origin of distinct tumour foci in multifocal papillary thyroid carcinoma. J Clin Endocrinol Metab 92:3511–3516PubMedCrossRef Giannini R, Ugolini C, Lupi C et al (2007) The heterogeneous distribution of BRAF mutation supports the independent clonal origin of distinct tumour foci in multifocal papillary thyroid carcinoma. J Clin Endocrinol Metab 92:3511–3516PubMedCrossRef
14.
go back to reference Ciampi R, Nikiforov YE (2007) RET/PTC rearrangements and BRAF mutations in thyroid tumorigenesis. Endocrinology 148:936–941PubMedCrossRef Ciampi R, Nikiforov YE (2007) RET/PTC rearrangements and BRAF mutations in thyroid tumorigenesis. Endocrinology 148:936–941PubMedCrossRef
15.
go back to reference Suarez HG (1998) Genetic alterations in human epithelial thyroid tumours. Clin Endocrinol (Oxf) 8:531–546CrossRef Suarez HG (1998) Genetic alterations in human epithelial thyroid tumours. Clin Endocrinol (Oxf) 8:531–546CrossRef
16.
go back to reference Garcia-Rostan G, Zhao H, Camp RL et al (2003) Ras mutations are associated with aggressive tumour phenotypes and poor prognosis in thyroid cancer. J Clin Oncol 1:3226–3235CrossRef Garcia-Rostan G, Zhao H, Camp RL et al (2003) Ras mutations are associated with aggressive tumour phenotypes and poor prognosis in thyroid cancer. J Clin Oncol 1:3226–3235CrossRef
17.
go back to reference Ciampi R, Knauf JA, Kerler R et al (2005) Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer. J Clin Invest 115:94–101PubMed Ciampi R, Knauf JA, Kerler R et al (2005) Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer. J Clin Invest 115:94–101PubMed
18.
go back to reference Santoro M, Papotti M, Chiappetta G et al (2002) RET activation and clinicopathologic features in poorly differentiated thyroid tumours. J Clin Endocrinol Metab 87:370–379PubMedCrossRef Santoro M, Papotti M, Chiappetta G et al (2002) RET activation and clinicopathologic features in poorly differentiated thyroid tumours. J Clin Endocrinol Metab 87:370–379PubMedCrossRef
19.
go back to reference Tallini G, Santoro M, Helie M et al (1998) RET/PTC oncogene activation defines a subset of papillary thyroid carcinomas lacking evidence of progression to poorly differentiated or undifferentiated tumour phenotypes. Clin Cancer Res 4:287–294PubMed Tallini G, Santoro M, Helie M et al (1998) RET/PTC oncogene activation defines a subset of papillary thyroid carcinomas lacking evidence of progression to poorly differentiated or undifferentiated tumour phenotypes. Clin Cancer Res 4:287–294PubMed
21.
go back to reference Greco A, Miranda C, Pagliardini S et al (1997) Chromosome 1 rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid-specific TRK oncogenes. Genes Chromosomes Cancer 19:112–123PubMedCrossRef Greco A, Miranda C, Pagliardini S et al (1997) Chromosome 1 rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid-specific TRK oncogenes. Genes Chromosomes Cancer 19:112–123PubMedCrossRef
22.
go back to reference Beimfohr C, Klugbauer S, Demidchik EP et al (1999) NTRK1 re-arrangement in papillary thyroid carcinomas of children after the Chernobyl reactor accident. Int J Cancer 80:842–847PubMedCrossRef Beimfohr C, Klugbauer S, Demidchik EP et al (1999) NTRK1 re-arrangement in papillary thyroid carcinomas of children after the Chernobyl reactor accident. Int J Cancer 80:842–847PubMedCrossRef
23.
go back to reference Ito T, Seyama T, Mizuno T et al (1992) Unique association of p53 mutations with undifferentiated but not with differentiated carcinomas of the thyroid gland. Cancer Res 52:1369–1371PubMed Ito T, Seyama T, Mizuno T et al (1992) Unique association of p53 mutations with undifferentiated but not with differentiated carcinomas of the thyroid gland. Cancer Res 52:1369–1371PubMed
24.
go back to reference Fagin JA, Matsuo K, Karmakar A et al (1993) High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas. J Clin Invest 91:179–184PubMedCrossRef Fagin JA, Matsuo K, Karmakar A et al (1993) High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas. J Clin Invest 91:179–184PubMedCrossRef
25.
go back to reference Asakawa H, Kobayashi T (2002) Multistep carcinogenesis in anaplastic thyroid carcinoma: a case report. Pathology 34:94–97PubMedCrossRef Asakawa H, Kobayashi T (2002) Multistep carcinogenesis in anaplastic thyroid carcinoma: a case report. Pathology 34:94–97PubMedCrossRef
26.
go back to reference Garcia-Rostan G, Camp RL, Herrero A et al (2001) Beta-catenin dysregulation in thyroid neoplasms: down-regulation, aberrant nuclear expression, and CTNNB1 exon 3 mutations are markers for aggressive tumor phenotypes and poor prognosis. Am J Pathol 158:987–996PubMedCrossRef Garcia-Rostan G, Camp RL, Herrero A et al (2001) Beta-catenin dysregulation in thyroid neoplasms: down-regulation, aberrant nuclear expression, and CTNNB1 exon 3 mutations are markers for aggressive tumor phenotypes and poor prognosis. Am J Pathol 158:987–996PubMedCrossRef
27.
go back to reference Huang Y, Prasad M, Lemon WJ et al (2001) Gene expression in papillary thyroid carcinoma reveals highly consistent profiles. Proc Natl Acad Sci USA 98:15044–15049PubMedCrossRef Huang Y, Prasad M, Lemon WJ et al (2001) Gene expression in papillary thyroid carcinoma reveals highly consistent profiles. Proc Natl Acad Sci USA 98:15044–15049PubMedCrossRef
28.
go back to reference Puskas LG, Juhasz F, Zarva A et al (2005) Gene profiling identifies genes specific for well-differentiated epithelial thyroid tumors. Cell Mol Biol (Noisy-le-grand) 51:177–186 Puskas LG, Juhasz F, Zarva A et al (2005) Gene profiling identifies genes specific for well-differentiated epithelial thyroid tumors. Cell Mol Biol (Noisy-le-grand) 51:177–186
29.
30.
go back to reference Gunn SR, Robetorye RS, Mohammed MS et al (2007) Comparative genomic hybridization arrays in clinical pathology: progress and challenges. Mol Diagn Ther 11:73–77PubMed Gunn SR, Robetorye RS, Mohammed MS et al (2007) Comparative genomic hybridization arrays in clinical pathology: progress and challenges. Mol Diagn Ther 11:73–77PubMed
31.
go back to reference Hemmer S, Wasenius VM, Knuutila S et al (1999) DNA copy number changes in thyroid carcinoma. Am J Pathol 154:1539–1547PubMedCrossRef Hemmer S, Wasenius VM, Knuutila S et al (1999) DNA copy number changes in thyroid carcinoma. Am J Pathol 154:1539–1547PubMedCrossRef
32.
go back to reference Kjellman P, Lagercrantz S, Hoog A et al (2001) Gain of 1q and loss of 9q21.3-q32 are associated with a less favorable prognosis in papillary thyroid carcinoma. Genes Chromosomes Cancer 32:43–49PubMedCrossRef Kjellman P, Lagercrantz S, Hoog A et al (2001) Gain of 1q and loss of 9q21.3-q32 are associated with a less favorable prognosis in papillary thyroid carcinoma. Genes Chromosomes Cancer 32:43–49PubMedCrossRef
33.
go back to reference Rodrigues R, Roque L, Espadinha C et al (2007) Comparative genomic hybridization, BRAF, RAS, RET, and oligo-array analysis in aneuploid papillary thyroid carcinomas. Oncol Rep 18:917–926PubMed Rodrigues R, Roque L, Espadinha C et al (2007) Comparative genomic hybridization, BRAF, RAS, RET, and oligo-array analysis in aneuploid papillary thyroid carcinomas. Oncol Rep 18:917–926PubMed
34.
go back to reference Lee JJ, Au AY, Foukakis T et al (2008) Array-CGH identifies cyclin D1 and UBCH10 amplicons in anaplastic thyroid carcinoma. Endocr Relat Cancer 15:801–815PubMedCrossRef Lee JJ, Au AY, Foukakis T et al (2008) Array-CGH identifies cyclin D1 and UBCH10 amplicons in anaplastic thyroid carcinoma. Endocr Relat Cancer 15:801–815PubMedCrossRef
35.
go back to reference Finn S, Smyth P, O’Regan E et al (2007) Low-level genomic instability is a feature of papillary thyroid carcinoma: an array comparative genomic hybridization study of laser capture microdissected papillary thyroid carcinoma tumors and clonal cell lines. Arch Pathol Lab Med 131:65–73PubMed Finn S, Smyth P, O’Regan E et al (2007) Low-level genomic instability is a feature of papillary thyroid carcinoma: an array comparative genomic hybridization study of laser capture microdissected papillary thyroid carcinoma tumors and clonal cell lines. Arch Pathol Lab Med 131:65–73PubMed
36.
go back to reference Wreesmann VB, Sieczka EM, Socci ND et al (2004) Genome-wide profiling of papillary thyroid cancer identifies MUC1 as an independent prognostic marker. Cancer Res 64:3780–3789PubMedCrossRef Wreesmann VB, Sieczka EM, Socci ND et al (2004) Genome-wide profiling of papillary thyroid cancer identifies MUC1 as an independent prognostic marker. Cancer Res 64:3780–3789PubMedCrossRef
37.
go back to reference Unger K, Malisch E, Thomas G et al (2008) Array CGH demonstrates characteristic aberration signatures in human papillary thyroid carcinomas governed by RET/PTC. Oncogene 27:4592–4602PubMedCrossRef Unger K, Malisch E, Thomas G et al (2008) Array CGH demonstrates characteristic aberration signatures in human papillary thyroid carcinomas governed by RET/PTC. Oncogene 27:4592–4602PubMedCrossRef
38.
go back to reference Kitamura Y, Shimizu K, Tanaka S et al (2000) Association of allelic loss on 1q, 4p, 7q, 9p, 9q, and 16q with postoperative death in papillary thyroid carcinoma. Clin Cancer Res 6:1819–1825PubMed Kitamura Y, Shimizu K, Tanaka S et al (2000) Association of allelic loss on 1q, 4p, 7q, 9p, 9q, and 16q with postoperative death in papillary thyroid carcinoma. Clin Cancer Res 6:1819–1825PubMed
39.
go back to reference Pacini F, Schlumberger M, Harmer C et al (2005) Post-surgical use of radioiodine 131I in patients with papillary and follicular thyroid cancer and the issue of remnant ablation: a consensus report. Eur J Endocrinol 153:651–659PubMedCrossRef Pacini F, Schlumberger M, Harmer C et al (2005) Post-surgical use of radioiodine 131I in patients with papillary and follicular thyroid cancer and the issue of remnant ablation: a consensus report. Eur J Endocrinol 153:651–659PubMedCrossRef
40.
go back to reference Pacini F, Schlumberger M, Dralle G et al (2006) European consensus for the management of patients with differentiated thyroid carcinoma of the follicular epithelium. Eur J Endocrinol 154:767–803CrossRef Pacini F, Schlumberger M, Dralle G et al (2006) European consensus for the management of patients with differentiated thyroid carcinoma of the follicular epithelium. Eur J Endocrinol 154:767–803CrossRef
41.
go back to reference Feher LZ, Balazs M, Kelemen JZ et al (2006) Improved DOP-PCR-based representational whole-genome amplification using quantitative real-time PCR. Diagn Mol Pathol 15:43–48PubMedCrossRef Feher LZ, Balazs M, Kelemen JZ et al (2006) Improved DOP-PCR-based representational whole-genome amplification using quantitative real-time PCR. Diagn Mol Pathol 15:43–48PubMedCrossRef
42.
go back to reference Telenius H, Carter NP, Bebb CE et al (1992) Degenerate oligonucleotide-primed PCR: general amplification of target DNA by a single degenerate primer. Genomics 13:718–725PubMedCrossRef Telenius H, Carter NP, Bebb CE et al (1992) Degenerate oligonucleotide-primed PCR: general amplification of target DNA by a single degenerate primer. Genomics 13:718–725PubMedCrossRef
43.
go back to reference Nagy J, Feher LZ, Sonkodi I et al (2005) A second field metachronous Merkel cell carcinoma of the lip and the palatine tonsil confirmed by microarray-based comparative genomic hybridisation. Virchows Arch 446:278–286PubMedCrossRef Nagy J, Feher LZ, Sonkodi I et al (2005) A second field metachronous Merkel cell carcinoma of the lip and the palatine tonsil confirmed by microarray-based comparative genomic hybridisation. Virchows Arch 446:278–286PubMedCrossRef
44.
go back to reference Yang YH, Dudoit S, Luu P et al (2002) Normalization for cDNA microarray data: a robust composite method addressing single and multiple slide systematic variation. Nucleic Acids Res 30:e15PubMedCrossRef Yang YH, Dudoit S, Luu P et al (2002) Normalization for cDNA microarray data: a robust composite method addressing single and multiple slide systematic variation. Nucleic Acids Res 30:e15PubMedCrossRef
45.
go back to reference Pfaffl MW (2001) A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res 29:e45PubMedCrossRef Pfaffl MW (2001) A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res 29:e45PubMedCrossRef
46.
go back to reference Onno M, Nakamura T, Mariage-Samson R et al (1993) Human TRE17 oncogene is generated from a family of homologous polymorphic sequences by single-base changes. DNA Cell Biol 12:107–118PubMedCrossRef Onno M, Nakamura T, Mariage-Samson R et al (1993) Human TRE17 oncogene is generated from a family of homologous polymorphic sequences by single-base changes. DNA Cell Biol 12:107–118PubMedCrossRef
47.
go back to reference Martinu L, Masuda-Robens JM, Robertson SE et al (2004) The TBC (Tre-2/Bub2/Cdc16) domain protein TRE17 regulates plasma membrane-endosomal trafficking through activation of Arf6. Mol Cell Biol 24:9752–9762PubMedCrossRef Martinu L, Masuda-Robens JM, Robertson SE et al (2004) The TBC (Tre-2/Bub2/Cdc16) domain protein TRE17 regulates plasma membrane-endosomal trafficking through activation of Arf6. Mol Cell Biol 24:9752–9762PubMedCrossRef
48.
go back to reference Masuda-Robens JM, Kutney SN, Qi H et al (2003) The TRE17 oncogene encodes a component of a novel effector pathway for Rho GTPases Cdc42 and Rac1 and stimulates actin remodeling. Mol Cell Biol 23:2151–2161PubMedCrossRef Masuda-Robens JM, Kutney SN, Qi H et al (2003) The TRE17 oncogene encodes a component of a novel effector pathway for Rho GTPases Cdc42 and Rac1 and stimulates actin remodeling. Mol Cell Biol 23:2151–2161PubMedCrossRef
49.
go back to reference Smith MJ, Pozo K, Brickley K et al (2006) Mapping the GRIF-1 binding domain of the kinesin, KIF5C, substantiates a role for GRIF-1 as an adaptor protein in the anterograde trafficking of cargoes. J Biol Chem 281:27216–27228PubMedCrossRef Smith MJ, Pozo K, Brickley K et al (2006) Mapping the GRIF-1 binding domain of the kinesin, KIF5C, substantiates a role for GRIF-1 as an adaptor protein in the anterograde trafficking of cargoes. J Biol Chem 281:27216–27228PubMedCrossRef
50.
go back to reference Brickley K, Smith MJ, Beck M et al (2005) GRIF-1 and OIP106, members of a novel gene family of coiled-coil domain proteins: association in vivo and in vitro with kinesin. J Biol Chem 280:14723–14732PubMedCrossRef Brickley K, Smith MJ, Beck M et al (2005) GRIF-1 and OIP106, members of a novel gene family of coiled-coil domain proteins: association in vivo and in vitro with kinesin. J Biol Chem 280:14723–14732PubMedCrossRef
51.
go back to reference Yasuhara T, Okamoto A, Kitagawa T et al (2005) FGF7-like gene is associated with pericentric inversion of chromosome 9, and FGF7 is involved in the development of ovarian cancer. Int J Oncol 26:1209–1216PubMed Yasuhara T, Okamoto A, Kitagawa T et al (2005) FGF7-like gene is associated with pericentric inversion of chromosome 9, and FGF7 is involved in the development of ovarian cancer. Int J Oncol 26:1209–1216PubMed
52.
go back to reference Hishikawa Y, Tamaru N, Ejima K et al (2004) Expression of keratinocyte growth factor and its receptor in human breast cancer: its inhibitory role in the induction of apoptosis possibly through the overexpression of Bcl-2. Arch Histol Cytol 67:455–464PubMedCrossRef Hishikawa Y, Tamaru N, Ejima K et al (2004) Expression of keratinocyte growth factor and its receptor in human breast cancer: its inhibitory role in the induction of apoptosis possibly through the overexpression of Bcl-2. Arch Histol Cytol 67:455–464PubMedCrossRef
53.
go back to reference Firth JD, Putnins EE (2004) Keratinocyte growth factor 1 inhibits wound edge epithelial cell apoptosis in vitro. J Invest Dermatol 122:222–231PubMedCrossRef Firth JD, Putnins EE (2004) Keratinocyte growth factor 1 inhibits wound edge epithelial cell apoptosis in vitro. J Invest Dermatol 122:222–231PubMedCrossRef
54.
go back to reference Diviani D, Abuin L, Cotecchia S et al (2004) Anchoring of both PKA and 14-3-3 inhibits the Rho-GEF activity of the AKAP-Lbc signaling complex. EMBO J 23:2811–2820PubMedCrossRef Diviani D, Abuin L, Cotecchia S et al (2004) Anchoring of both PKA and 14-3-3 inhibits the Rho-GEF activity of the AKAP-Lbc signaling complex. EMBO J 23:2811–2820PubMedCrossRef
55.
go back to reference Shibolet O, Giallourakis C, Rosenberg I et al (2007) AKAP13, a RhoA GTPase-specific guanine exchange factor, is a novel regulator of TLR2 signaling. J Biol Chem 282:35308–35317PubMedCrossRef Shibolet O, Giallourakis C, Rosenberg I et al (2007) AKAP13, a RhoA GTPase-specific guanine exchange factor, is a novel regulator of TLR2 signaling. J Biol Chem 282:35308–35317PubMedCrossRef
56.
go back to reference Wirtenberger M, Tchatchou S, Hemminki K et al (2006) Association of genetic variants in the Rho guanine nucleotide exchange factor AKAP13 with familial breast cancer. Carcinogenesis 27:593–598PubMedCrossRef Wirtenberger M, Tchatchou S, Hemminki K et al (2006) Association of genetic variants in the Rho guanine nucleotide exchange factor AKAP13 with familial breast cancer. Carcinogenesis 27:593–598PubMedCrossRef
57.
go back to reference Chiappetta G, Pentimalli F, Monaco M et al (2004) Thymosin beta-10 gene expression as a possible tool in diagnosis of thyroid neoplasias. Oncol Rep 12:239–243PubMed Chiappetta G, Pentimalli F, Monaco M et al (2004) Thymosin beta-10 gene expression as a possible tool in diagnosis of thyroid neoplasias. Oncol Rep 12:239–243PubMed
58.
go back to reference Takano T, Hasegawa Y, Miyauchi A et al (2002) Quantitative analysis of thymosin beta-10 messenger RNA in thyroid carcinomas. Jpn J Clin Oncol 32:229–232PubMedCrossRef Takano T, Hasegawa Y, Miyauchi A et al (2002) Quantitative analysis of thymosin beta-10 messenger RNA in thyroid carcinomas. Jpn J Clin Oncol 32:229–232PubMedCrossRef
59.
go back to reference Hall AK (1995) Thymosin beta-10 accelerates apoptosis. Cell Mol Biol Res 41:167–180PubMed Hall AK (1995) Thymosin beta-10 accelerates apoptosis. Cell Mol Biol Res 41:167–180PubMed
60.
go back to reference Maelan AE, Rasmussen TK, Larsson LI (2007) Localization of thymosin beta10 in breast cancer cells: relationship to actin cytoskeletal remodeling and cell motility. Histochem Cell Biol 127:109–113PubMedCrossRef Maelan AE, Rasmussen TK, Larsson LI (2007) Localization of thymosin beta10 in breast cancer cells: relationship to actin cytoskeletal remodeling and cell motility. Histochem Cell Biol 127:109–113PubMedCrossRef
61.
go back to reference Califano D, Monaco C, Santelli G et al (1998) Thymosin beta-10 gene overexpression correlated with the highly malignant neoplastic phenotype of transformed thyroid cells in vivo and in vitro. Cancer Res 58:823–828PubMed Califano D, Monaco C, Santelli G et al (1998) Thymosin beta-10 gene overexpression correlated with the highly malignant neoplastic phenotype of transformed thyroid cells in vivo and in vitro. Cancer Res 58:823–828PubMed
62.
go back to reference Santelli G, Califano D, Chiappetta G et al (1999) Thymosin beta-10 gene overexpression is a general event in human carcinogenesis. Am J Pathol 155:799–804PubMedCrossRef Santelli G, Califano D, Chiappetta G et al (1999) Thymosin beta-10 gene overexpression is a general event in human carcinogenesis. Am J Pathol 155:799–804PubMedCrossRef
63.
go back to reference Lee SH, Son MJ, Oh SH et al (2005) Thymosin {beta}(10) inhibits angiogenesis and tumour growth by interfering with Ras function. Cancer Res 65:137–148PubMed Lee SH, Son MJ, Oh SH et al (2005) Thymosin {beta}(10) inhibits angiogenesis and tumour growth by interfering with Ras function. Cancer Res 65:137–148PubMed
64.
go back to reference Santelli G, Bartoli PC, Giuliano A et al (2002) Thymosin beta-10 protein synthesis suppression reduces the growth of human thyroid carcinoma cells in semisolid medium. Thyroid 12:765–772PubMedCrossRef Santelli G, Bartoli PC, Giuliano A et al (2002) Thymosin beta-10 protein synthesis suppression reduces the growth of human thyroid carcinoma cells in semisolid medium. Thyroid 12:765–772PubMedCrossRef
65.
go back to reference Huff T, Muller CS, Otto AM et al (2001) beta-Thymosins, small acidic peptides with multiple functions. Int J Biochem Cell Biol 33:205–220PubMedCrossRef Huff T, Muller CS, Otto AM et al (2001) beta-Thymosins, small acidic peptides with multiple functions. Int J Biochem Cell Biol 33:205–220PubMedCrossRef
Metadata
Title
Amplification of Thymosin Beta 10 and AKAP13 Genes in Metastatic and Aggressive Papillary Thyroid Carcinomas
Authors
Liliána Z. Fehér
Gábor Pocsay
László Krenács
Ágnes Zvara
Enikő Bagdi
Réka Pocsay
Géza Lukács
Ferenc Győry
Andrea Gazdag
Erzsébet Tarkó
László G. Puskás
Publication date
01-04-2012
Publisher
Springer Netherlands
Published in
Pathology & Oncology Research / Issue 2/2012
Print ISSN: 1219-4956
Electronic ISSN: 1532-2807
DOI
https://doi.org/10.1007/s12253-011-9467-7

Other articles of this Issue 2/2012

Pathology & Oncology Research 2/2012 Go to the issue
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine