4. / ENDOCRINE GLANDS
Total number of publications: 58
Total number of cases: 1406
Total number of amplifications: 275
Tumor / Loss / Amplicon / Percentage
(number of cases) / Amplified genes (studied from the same cases) / Reference
4.1 / Pituitary tumor, non-functioning / NA / ?/23 / 1
4.1 / PITUITARY TUMOR, SOMATOMAMMOTROPIC (?/4 cases)
Comment: Amplifications were not determined.
Pack SD, Kirschner LS, Pak E, Zhuang Z, Carney JA, Stratakis CA: Genetic and histologic studies of somatomammotropic pituitary tumors in patients with the ''complex of spotty skin pigmentation, myxomas, endocrine overactivity and schwannomas'' (Carney complex). J Clin Endocrinol Metab 2000, 85:3860-3865.
4.1 / PITUITARY TUMOR, SPORADIC (0/75 cases)
Trautmann K, Thakker RV, Ellison DW, Ibrahim A, Lees PD, Harding B, Fischer C, Popp S, Bartram CR, Jauch A: Chromosomal aberrations in sporadic pituitary tumors. Int J Cancer 2001, 91:809-814.
4.1 / Pituitary adenoma / 1q21-q23 / 8 (1/12) / 2
7q11 / 8 (1/12) / 2
13q14 / 42 (5/12) / 2
13q21-q31 / 30 (3/10) / 3
None / 0 (0/10) / 3
4.1 / PITUITARY ADENOMA (1/8 cases)
amp(7,9)
Rickert CH, Dockhorn-Dworniczak B, Busch G, Moskopp D, Albert FK, Rama B, Paulus W: Increased chromosomal imbalances in recurrent pituitary adenomas. Acta Neuropathol 2001, 102:615-620.
4.1 / PITUITARY ADENOMA (4/38 cases)
amp(5p15.1pter,5q31qter,6p21.1pter,6q25qter,9q22qter,14q22qter,16,19)/amp(19)/amp(19p)/amp(9q33qter,19)
Fan X, Paetau A, Aalto Y, Välimäki M, Sane T, Poranen A, Castresana JS, Knuutila S: Gain of chromosome 3 and loss of 13q are frequent alterations in pituitary adenomas. Cancer Genet Cytogenet 2001, 128:97-103.
4.1 / PITUITARY ADENOMA (?/52 cases)
Comment: Amplifications were not determined.
Metzger AK, Mohapatra G, Minn YA, Bollen AW, Lamborn K, Waldman FM, Wilson CB, Feuerstein BG: Multiple genetic aberrations including evidence of chromosome 11q13 rearrangement detected in pituitary adenomas by comparative genomic hybridization. J Neurosurg 1999, 90:306-314.
4.1 / PITUITARY CARCINOMA (3/4 cases)
amp(1q,3p,8,14)/amp(13q22qter)/amp(9p,13,14,21)
Rickert CH, Scheithauer BW, Paulus W: Chromosomal aberrations in pituitary carcinoma metastases. Acta Neuropathol 2001, 102:117-120.
4.1 / Pituitary tumors: 31 amplifications out of 222 cases

4.2 / Adrenocortical adenoma / None / 0 (0/14) / 4
4.2 / Benign adrenocortical lesions / None / 5
4.3 / Adrenocortical carcinoma / 2p22.2-pter / 38 (3/8) / 4
2q21.3-p22.2 / 50 (4/8) / 4
2q22-qter / 38 (3/8) / 4
6q / 38 (3/8) / 4
8p / 38 (3/8) / 4
9p / 38 (3/8) / 4
11q21.1-qter / 50 (4/8) / 4
17p / 50 (4/8) / 4
17q / 38 (3/8) / 4
18q / 38 (3/8) / 4
22 / 38 (3/8) / 4
4.3 / Adrenocortical carcinoma / 1p21-p31 / 67 (8/12) / 5
1q22-q41 / 33 (4/12) / 5
2p21-pter / 33 (4/12) / 5
2qcen-q35 / 42 (5/12) / 5
3p / 50 (6/12) / 5
4p16 / 8 (1/12) / 5
4q25-qter / 25 (3/12) / 5
5p15 / 8 (1/12) / 5
5p23-p24 / 25 (3/12) / 5
5q13 / 17 (2/12) / 5
5q32-qter / 8 (1/12) / 5
6q16-q21 / 42 (5/12) / 5
8p / 25 (3/12) / 5
8q24 / 8 (1/12) / 5
9p23-p24 / 58 (7/12) / 5
9q32-qter / 8 (1/12) / 5
11p13-p14 / 25 (3/12) / 5
11q14-qter / 42 (5/12) / 5
12q13-q14 / 17 (2/12) / 5
13q12.2-q31 / 25 (3/12) / 5
18q / 33 (4/12) / 5
4.3 / ADRENOCORTICAL CARCINOMA (7/22 cases)
amp(1p34.3pter,1q22q25,3p24pter,17q24q25,19q)/amp(7p11.2p14)/amp(19p13.3)/amp(19p13.3)/amp (19)/amp(19p)/amp(19q13.4)
Dohna M, Reincke M, Mincheva A, Allolio B, Solinas-Toldo S, Lichter P: Adrenocortical carcinoma is characterized by a high frequency of chromosomal gains and high-level amplifications. Genes Chromosomes Cancer 2000, 28:145-152.
4.3 / Adrenocortical tumours, childhood / 1p32-pter / 18 (2/11) / 6
2q21-q32 / 36 (4/11) / 6
3pcen-p14 / 27 (3/11) / 6
3q13-q26 / 27 (3/11) / 6
4q21-q28 / 64 (7/11) / 6
5q34-qter / 9 (1/11) / 6
6q16-q22 / 27 (3/11) / 6
7p21-pter / 9 (1/11) / 6
7p22 / 18 (2/11) / 6
7q33-qter / 9 (1/11) / 6
7q36 / 18 (2/11) / 6
9q34 / 64 (7/11) / 6
11p13-p14 / 46 (5/11) / 6
11q12-q13 / 9 (1/11) / 6
11q21 / 36 (4/11) / 6
13q21-q31 / 36 (4/11) / 6
17q24-qter / 9 (1/11) / 6
19 / 73 (8/11) / 6
22q / 18 (2/11) / 6
18q12 / 73 (8/11) / 6
Xp
/ 46 (5/11) / 6
Xq21-q25 / 46 (5/11) / 6
4.3 / Adrenocortical tumors, childhood / 2q22-q33 / 44 (4/9) / 7
4q / 56 (5/9) / 7
6p21.3 / 22 (2/9) / 7
9q34 / 67 (6/9) / 7
11q13 / 11 (1/9) / 7
12q11-q21 / 11 (1/9) / 7
13q22-qter / 11 (1/9) / 7
16 / 11 (1/9) / 7
4.3 / ADRENOCORTICAL TUMOR (3/35 cases)
amp(5q32qter,12q13q15)/amp(5p15)/amp(4p15pter,12q12q15,20q)
Zhao J, Roth J, Bode-Lesniewska B, Pfaltz M, Heitz PU, Komminoth P: Combined comparative genomic hybridization and genomic microarray for detection of gene amplifications in pulmonary artery intimal sarcomas and adrenocortical tumors. Genes Chromosomes Cancer 2002, 34:48-57.
4.3 / ADRENOCORTICAL TUMOR (?/32 cases)
Comment: Amplifications were not determined.
Sidhu S, Marsh DJ, Theodosopoulos G, Philips J, Bambach CP, Campbell P, Magarey CJ, Russell CFJ, Schulte K-M, Roher H-D, Delbridge L, Robinson BG: Comparative genomic hybridization analysis of adrenocortical tumors. J Clin Endocrinol Metab 2002, 87:3467-3474.
4.3 / ADRENOCORTICAL TUMOR, CHILDHOOD
ADDITIONAL LITERATURE
Figueiredo BC, Ribeiro RC, Zambetti G, Haddad B, Pianovsky MD, Pereira RM, DeLacerda L, Sandrini R: Amplification of 9q34 in childhood adrenocortical tumors: a specific feature unrelated to ethnic origin or living conditions. Braz J Med Biol Res 2000, 33:1217-1224.
4.3 / Adrenocortical carcinoma: 66 amplifications out of 129 cases

4.4 / Pancreatic adenocarcinoma / 1p32-p34 / 4 (1/27) / 8
1cen-p32 / 50 (3/6) / 9
4q31.1-pter / 50 (3/6) / 9
6q / 23 (3/13) / 10
6q21 / 15 (4/27) / 8
6q24 / 11 (3/27) / 8
6q24 / 4 (1/27) / CMYB / 8,11
7q22 / 4 (1/27) / 8
9p21.1-22 / 15 (4/27) / 8
9p22-pter / 50 (3/6) / 9
9p23-pter / 30 (8/27) / 8
9cen-p21 / 23 (3/13) / 10
12p13 / 4 (1/27) / 8
13q22-32 / 11 (3/27) / 8
17p / 23 (3/13) / 10
18p / 23 (3/13) / 10
18q / 42 (8/19) / 9,10
18q23 / 11 (3/27) / 8
22 / 7 (2/27) / 8
Y / 50 (3/6) / 9
4.4 / PANCREATIC ADENOCARCINOMA (7/8 cases)
amp(8q,10q,15q21qter,22)/amp(8q24qter,15q24qter,20q12qter)/amp(1q12qter,3q25q27,6p21.1p22,7p13pter,8p23pter)/amp(1q32qter,8p23pter,16p,16q23qter,20q13.1qter)/amp(8q24qter,Xq26qter)/amp(7p,7q11.2q22,16q,20q)/amp(7p,7q11.2q21,8q23qter,11,14q21qter,16,20)
Armengol G, Knuutila S, Lluis F, Capella G, Miro R, Caballin MR: DNA copy number changes and evaluation of MYC, IGF1R, and FES amplification in xenografts of pancreatic adenocarcinoma. Cancer Genet Cytogenet 2000, 116:133-141.
4.4 / PANCREATIC ADENOCARCINOMA, DUCTAL (?/33 cases)
Comment: Number of cases was not clearly defined, but high-level amplifications were observed at 5p, 8q13q24.1, 8q22qter, 12p11.2p12, 19q12q13.2, and 20q.
Schleger C, Arens N, Zentgraf H, Bley U, Verbeke C: Identification of frequent chromosomal aberrations in ductal adenocarcinoma of the pancreas by comparative genomic hybridization. J Pathol 2000, 191:27-32.
4.4 / Pancreatic cancer / None / 0 (0/24) / 10
6q / 23 (3/13) / 10
9cen-p21 / 23 (3/13) / 10
17p / 23 (3/13) / 10
18p / 23 (3/13) / 10
18q / 31 (4/13) / 10
4.4 / PANCREATIC CANCER (?/27 cases)
Comment: Number of cases was not clearly defined, but amplifications were found at 3q26.3qter, 5p, 7q21q31, 8q, 8q22.1qter, 11q14.1q23.3, 12p11.2pter, 19q13.1qter, 20p11.2pter, and 20q12qter.
Shiraishi K, Okita K, Kusano N, Harada T, Kondoh S, Okita S, Ryozawa S, Ohmura R, Noguchi T, Iida Y, Akiyama T, Oga A, Fukumoto Y, Furuya T, Kawauchi S, Sasaki K: A comparison of DNA copy number changes detected by comparative genomic hybridization in malignancies of the liver, biliary tract and pancreas. Oncology 2001, 60:151-161.
4.4 / PANCREATIC CANCER (?/32 cases)
Comment: Number of cases was not clearly defined, but amplifications were found at 1q12qter, 1q31qter, 1p22.3pter, 2q23qter, 2p23p24, 3q23qter, 3q24qter, 5p, 6q, 7,7q21.1q31.2, 8q11.21qter, 8q22.1qter, 8q24, 11q13.1q14.1, 11q13.3q23.3, 12p, 14q, 15q, 18q11.2pter, 19q13, 20q11.2qter, 20, 22q11.2qter, Xp11.21pter, Xq13qter, and Xq25q28.
Harada T, Okita K, Shiraishi K, Kusano N, Furuya T, Oga A, Kawauchi S, Kondoh S, Sasaki K: Detection of genetic alterations in pancreatic cancers by comparative genomic hybridization coupled with tissue microdissection and degenerate oligonucleotide primed polymerase chain reaction. Oncology 2002, 62:251-258.
4.4 / PANCREATIC CARCINOMA (12/20 cases)
amp(8q,Xq25qter)/amp(3q24qter,8q22qter,11q13q23,12q22qter)/amp(5p,12p11p12,13q14q32)/amp(8q)/amp(1q24qter,2q21q34)/amp(12p12pter,15q24qter)/amp(5p12p14,5q14q23,7p,8q)/amp(8q)/amp(20q)/amp(5p11p14,18p)/amp(12p)/amp(5p)
Harada T, Okita K, Shiraishi K, Kusano N, Kondoh S, Sasaki K: Interglandular cytogenetic heterogeneity detected by comparative genomic hybridization in pancreatic cancer. Cancer Res 2002, 62:835-839.
4.4 / PANCREATIC CARCINOMA, ACINAR (?/6 cases)
Comment: Amplifications were not determined.
Taruscio D, Paradisi S, Zamboni G, Rigaud G, Falconi M, Scarpa A: Pancreatic acinar carcinoma shows a distinct pattern of chromosomal imbalances by comparative genomic hybridization. Genes Chromosomes Cancer 2000, 28:294-299.
4.4 / Pancreatic tumor, endocrine / 1p21-p22 / 21 (9/44) / 12
1qcen-q22 / 16 (7/44) / 12
2q23-q36 / 21 (9/44) / 12
3qcen-q21 / 25 (11/44) / 12
3q22-q26 / 27 (12/44) / 12
4pcen-p14 / 7 (3/44) / 12
4q13.3-q24 / 7 (3/44) / 12
6q21-q22 / 39 (17/44) / 12
8q21.3-qter / 23 (10/44) / 12
9p22-pter / 9 (4/44) / 12
10p13-pter / 18 (8/44) / 12
10q22-q25 / 23 (10/44) / 12
11p13 / 30 (13/44) / 12
11q14-q22 / 34 (15/44) / 12
13q21.1 / 16 (7/44) / 12
13q22-q31 / 16 (7/44) / 12
15q24-qter / 14 (6/44) / 12
16p / 7 (3/44) / 12
16q21-q22 / 9 (4/44) / 12
21q21 / 18 (8/44) / 12
22q12-qter / 9 (4/44) / 12
Xp22 / 18 (8/44) / 12
Xq22-q23 / 25 (11/44) / 12
None / 0 (0/44) / 12
4.4 / Pancreatic tumor, endocrine / 1p22-p31 / 13 (3/23) / 13
1q32-q44 / 13 (3/23) / 13
5 / 4 (1/23) / 13
6q15-q22 / 22 (5/23) / 13
7p11.2-q11.2 / 4 (1/23) / 13
7p11.2-q31 / 4 (1/23) / 13
7 / 9 (2/23) / 13
8q11.2 / 17 (4/23) / 13
8q23 / 17 (4/23) / 13
9p12-q21 / 4 (1/23) / 13
9p13-q34 / 4 (1/23) / 13
9q11-q12 / 4 (1/23) / 13
9q32-qter / 4 (1/23) / 13
11p14-p15.3 / 26 (6/23) / 13
11q21-q22 / 35 (8/23) / 13
12p11.2-q13 / 4 (1/23) / 13
12 / 4 (1/23) / 13
13q21-q31 / 13 (3/23) / 13
16 / 4 (1/23) / 13
17p11.2-q25 / 4 (1/23) / 13
17 / 35 (8/23) / 13
18q12-q23 / 13 (3/23) / 13
19 / 48 (11/23) / 13
20p11.2-q13 / 9 (2/23) / 13
20q11-q13 / 9 (2/23) / 13
21q22 / 4 (1/23) / 13
X / 26 (6/23) / 13
4.4 / PANCREATIC TUMOR, ENDOCRINE (?/93 cases)
Comment: Amplifications were not determined
Barghorn A, Speel EJM, Farspour B, Saremaslani P, Schmid S, Perren A, Roth J, Heitz PU, Komminoth P: Putative tumor suppressor loci at 6q22 and 6q23-q24 are involved in the malignant progression of sporadic endocrine pancreatic tumors. Am J Pathol 2001, 158:1903-1911.
4.4 / PANCREATIC TUMOR, ENDOCRINE (0/38 cases: 28 functioning and 10 nonfunctioning endocrine pancreatic tumors)
Speel EJM, Scheidweiler AF, Zhao J, Matter C, Saremaslani P, Roth J, Heitz PU, Komminoth P: Genetic evidence for early divergence of small functioning and nonfunctioning endocrine pancreatic tumors: gain of 9q34 is an early event in insulinomas. Cancer Res 2001, 61:5186-5192.
4.4 / PANCREATIC TUMOR, ENDOCRINE (0/45 cases: 17 primary metastatic and 28 nonmetastatic)
Zhao J, Moch H, Scheidweiler AF, Baer A, Schäffer AA, Speel EJM, Roth J, Heitz PU, Komminoth P: Genomic imbalances in the progression of endocrine pancreatic tumors. Genes Chromosomes Cancer 2001, 32:364-372.
4.4 / ENTEROPANCREATIC TUMOR, NEUROENDOCRINE (0/26 cases: 12 foregut tumours and 14 midgut tumours)
Tonnies H, Toliat MR, Ramel C, Pape UF, Neitzel H, Berger W, Wiedenmann B: Analysis of sporadic neuroendocrine tumours of the enteropancreatic system by comparative genomic hybridisation. Gut 2001, 48:536-541.
4.4 / PANCREATIC CANCER
ADDITIONAL LITERATURE
Armengol G, Capella G, Farre L, Peinado MA, Miro R, Caballin MR: Genetic evolution in the metastatic progression of human pancreatic cancer studied by CGH. Lab Invest 2001, 81:1703-1707.
4.4 / PANCREATIC ADENOCARCINOMA, DUCTAL
ADDITIONAL LITERATURE
Schleger C, Verbeke C, Hildenbrand R, Zentgraf H, Bleyl U: c-MYC activation in primary and metastatic ductal adenocarcinoma of the pancreas: incidence, mechanisms, and clinical significance. Mod Pathol 2002, 15:462-469.
4.4 / Pancreatic adenocarcinoma: 149 amplifications out of 446 cases

4.5 / Gastroenteropancreatic endocrine tumor / 17q11 / 5 (1/20) / 14
19q13 / 5 (1/20 / 14
4.5 / Bile duct carcinoma, primary / 3q / 13 (1/8) / 15
6q16-qter / 38 (3/8) / 15
8p / 38 (3/8) / 15
8q21.1-qter / 13 (1/8) / 15
8q / 38 (3/8) / 15
11 / 13 (1/8) / 15
12p / 13 (1/8) / 15
13q / 25 (2/8) / 15
17q11.1-q21 / 13 (1/8) / 15
18q21-qter / 50 (4/8) / 15
4.5 / Gastroenteropancreatic tumor: 12 amplifications out of 28 cases

4.6 / Thyroid adenoma / (22) / 7 (2/29) / 16
4.6 / Thyroid adenoma, follicular / None / None / 18
4.7 / Thyroid carcinoma, follicular / 1p / 31 (4/13) / 16
14q11.2-q22 / 5 (1/20) / 17
18q12.1-q21 / 5 (1/20) / 17
22 / 46 (6/13) / 16
4.7 / Thyroid carcinoma, follicular / 1p21-p22 / 20 (4/20) / 17
9q13-q21.3 / 23 (3/13) / 18
13q21-q22 / 25 (5/20) / 17
14q11.2-q22 / 5 (1/20) / 17
18q12.1-q21 / 5 (1/20) / 17
22q12.3-qter / 40 (8/20) / 17
None / 18
4.7 / Thyroid carcinoma, papillary / None / 0 (0/26) / 17
4.7 / THYROID CARCINOMA, PAPILLARY (1/25 cases)
amp(1q25qter)
Kjellman P, Lagercrantz S, Hoog A, Wallin G, Larsson C, Zedenius J: Gain of 1q and loss of 9q21.3-q32 are associated with a less favorable prognosis in papillary thyroid carcinoma. Genes Chromosomes Cancer 2001, 32:43-49.
4.7 / THYROID CANCER, PAPILLARY (0/21 cases)
Singh B, Lim D, Cigudosa JC, Ghossein R, Shaha AR, Poluri A, Wreesmann VB, Tuttle M, Shah JP, Rao PH: Screening for genetic aberrations in papillary thyroid cancer by using comparative genomic hybridization. Surgery 2000, 128:888-894.
4.7 / THYROID CANCER, PAPILLARY (?/17 cases)
Comment: Amplifications were not determined.
Bauer AJ, Cavalli LR, Rone JD, Francis GL, Burch HB, Tuttle RM, Ringel MD, Stratakis CA, Haddad BR: Evaluation of adult papillary thyroid carcinomas by comparative genomic hybridization and microsatellite instability analysis. Cancer Genet Cytogenet 2002, 135:182-186.
4.7 / THYROID CARCINOMA, ANAPLASTIC (?/9cases)
Comment: Amplifications were not determined, but FISH indicated amp(8q21,5p12) in some cases.
Wilkens L, Benten D, Tchinda J, Brabant G, Potter E, von Wasielewski RHD: Aberrations of chromosomes 5 and 8 as recurrent cytogenetic events in anaplastic carcinoma of the thyroid as detected by fluorescence in situ hybridisation and comparative genomic hybridisation. Virchows Arch 2000, 436:312-318.
4.7 / THYROID CARCINOMA, MEDULLARY (0/23 cases)
Frisk T, Zedenius J, Lundberg J, Wallin G, Kytola S, Larsson C: CGH alterations in medullary thyroid carcinomas in relation to the RET M918T mutation and clinical outcome. Int J Oncol 2001, 18:1219-1225.
4.7 / THYROID CANCER (?/42 cases: 15 WDTC, 12 PDTC, 15ATC)
Comment: Number of cases not clearly defined, but amplifications were found at 3p14q13, 3q23q25, and 17q24q25.
Wreesmann BV, Ghossein RA, Patel SG, Harris CP, Schnaser EA, Shaha AR, Tuttle MR, Shah JP, Rao PH, Singh B: Genome-wide appraisal of thyroid cancer progression. Am J Pathol 2002, 161:1549-1556.
4.7 / Thyroid carcinoma: 10 amplifications out of 196 cases

4.8 / Thyroid oncocytic tumors, Hürthle cell / None / 0 (0/11) / 19
Not determined / 19
4.8 / HÜRTHLE CELL THYROID CARCINOMA (?/28 cases)
Comment: Amplifications were not determined.
Wada N, Duh QY, Miura D, Brunaud L, Wong MG, Clark OH: Chromosomal aberrations by comparative genomic hybridization in Hurthle cell thyroid carcinomas are associated with tumor recurrence. J Clin Endocrinol Metab 2002, 87:4595-4601.
4.9 / Medullary carcinoma / None / 0 (0/10) / 17
4.10 / Anaplastic carcinoma / None / 0 (0/13) / 17
4.11 / Parathyroid adenoma / None / 0 (0/63) / 20,21
1p / 11 (6/53) / 20
4 / 10 (1/10) / 21
5 / 10 (1/10) / 21
6q26-qter / 11 (6/53) / 20
11p / 25 (13/53) / 20
11cen-q22 / 30 (16/53) / 20
11q23-qter / 34 (18/53) / 20
13cen-q12 / 11 (6/53) / 20
13q14-qter / 17 (9/53) / 20
14q / 10 (1/10) / 21
15q14-25 / 15 (8/53) / 20
15q26 / 13 (7/53) / 20
4.11 / PARATHYROID ADENOMA (1/44 cases)
amp(7q21q35,8p12p22,8q21.2qter)
Hemmer S, Wasenius V-M, Haglund C, Zhu Y, Knuutila S, Franssila K, Joensuu H: Deletion of 11q23 and cyclin D1 overexpression are frequent aberrations in parathyroid adenomas. Am J Pathol 2001, 158:1355-1362.
4.11 / PARATHYROID CARCINOMA (?/29 cases)
Comment: Amplifications were not determined.
Kytölä S, Farnebo F, Obara T, Isola J, Grimelius L, Farnebo L-O, Sandelin K, Larsson C: Patterns of chromosomal imbalances in parathyroid carcinomas. Am J Pathol 2000, 157:579-586.
4.11 / Parathyroid adenoma, sporadic / 1p34-pter / 19 (5/26) / 22
11 / 39 (10/26) / 22
15q15-qter / 27 (7/26) / 22
18q / 12 (3/26) / 22
Not determined / 22
4.11 / PARATHYROID ADENOMA, SPORADIC (0/14 cases)
García JL, Tardío JC, Gutiérrez NC, González MB, Polo JR, Hernández JM, Menárguez J: Chromosomal imbalances identified by comparative genomic hybridization in sporadic parathyroid adenomas. Eur J Endocrinol 2002, 146:209-213.
4.11 / Parathyroid adenoma, irradiation associated / 1pcen-p22 / 30 (3/10) / 22
1p32 / 40 (4/10) / 22
6q16-q26 / 30 (3/10) / 22
11p12-p14 / 40 (4/10) / 22
11q / 50 (5/10) / 22
18q / 30 (3/10) / 22
22q / 30 (3/10) / 22
4.11 / PARATHYROID TUMORS, MULTIPLE (0/5 cases)
Dwight T, Nelson AE, Theodosopoulos G, Richardson AL, Learoyd DL, Philips J, Delbridge L, Zedenius J, Teh BT, Larsson C, Marsh DJ, Robinson BG: Independent genetic events associated with the development of multiple parathyroid tumors in patients with primary hyperparathyroidism. Am J Pathol 2002, 161:1299-1306.
4.11 / PARATHYROID TUMORS (?/12 cases)
Comment: Amplifications were not determined.
Dwight T, Kytölä S, Teh BT, Theodosopoulos G, Richardson AL, Philips J, Twigg S, Delbridge L, Marsh DJ, Nelson AE, Larsson C, Robinson BG: Genetic analysis of lithium-associated parathyroid tumors. Eur J Endocrinol 2002, 146:619-627.
4.11 / Parathyroid adenoma: 6 amplifications out of 213 cases

4.12 / MULTIPLE ENDOCRINE NEOPLASM (?/5 cases)
Comment: Amplifications were not determined.
Pourani J, Kaserer K, Pfragner R: Cytogenetic and molecular analyses of multiple endocrine neoplasias of the MEN1 syndrome. Int J Oncol 2002, 20:971-976.
4.13 / Thymoma, medullary / None / None / 23
4.14 / Thymic carcinoma, well-differentiated, type B3 thymoma / 6q / 38 (6/16) / 23
8p12 / 6 (1/16) / 23
13q21-q32 / 31 (5/16) / 23
4.14 / Thymic squamous cell carcinoma, primary, type C thymoma / 6q / 44 (4/9) / 23
16q13-q24 / 67 (6/9) / 23
17p13 / 33 (3/9) / 23

Concerning Losses: 10% of the cases must be aberrant and the number of aberrant cases at least three; findings in parentheses are examples of highly frequent aberrations that fail to meet the 3 cases/10% criteria; Boldface indicates that more than 30% of the cases detected in a study of at least 10 cases were aberrant;

*Description of a region, e.g. 6q21-q22, implies that in a variety of cases the loss was located within the area but it did not necessarily affect the whole area in all cases. The described regions may therefore not be considered analogous with minimal overlapping area. Furthermore, in some single cases the loss area may extend beyond the region described. As a whole, the description should be considered a flexible way to summarize critical areas of recurrent DNA copy number changes in that particular tumor type. Description without an asterisk indicates minimal overlapping areas.

Concerning Amplicons: Boldface indicates recurrent established amplicons (at least three cases and frequency more than 5%).

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