58
1406
275

Tumor Loss Amplicon Percentage
(number of cases)
Amplified genes
(studied from the same cases)
Reference
4.1 Pituitary tumor, nonfunctioning
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)
4.1
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.
Pituitary adenoma 1q21-q23 8 (1/12)
13q14
13q21-q31
7q11
None
8 (1/12)
42 (5/12)
30 (3/10)
0 (0/10)
2
2
2
3
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(9q3
3qter,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
4.2 Benign adrenocortical lesions
4.3 Adrenocortical carcinoma 2p22.2-pter
None
2q21.3-p22.2
2q22-qter
6q
8p
9p
11q21.1-qter
17p
17q
18q
22
4.3 Adrenocortical carcinoma 1p21-p31
1q22-q41
2p21-pter
2qcen-q35
3p
4p16
4q25-qter
5p23-p24
6q16-q21
8p
9p23-p24
5p15
5q13
5q32-qter
8q24
9q32-qter
0 (0/14)
50 (6/12)
8 (1/12)
25 (3/12)
8 (1/12)
25 (3/12)
17 (2/12)
8 (1/12)
42 (5/12)
25 (3/12)
8 (1/12)
58 (7/12)
8 (1/12)
38 (3/8)
50 (4/8)
38 (3/8)
38 (3/8)
38 (3/8)
38 (3/8)
50 (4/8)
50 (4/8)
38 (3/8)
38 (3/8)
38 (3/8)
67 (8/12)
33 (4/12)
33 (4/12)
42 (5/12)
4
5
5
5
5
5
5
5
5
5
5
5
5
5
5
5
5
4
4
4
4
5
4
4
4
4
4
4
4

11p13-p14
11q14-qter
13q12.2-q31
18q
12q13-q14
25 (3/12)
42 (5/12)
17 (2/12)
25 (3/12)
33 (4/12)
5
5
5
5
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
3pcen-p14
3q13-q26
4q21-q28
6q16-q22
11p13-p14
11q21
13q21-q31
5q34-qter
7p21-pter
7p22
7q33-qter
7q36
9q34
11q12-q13
17q24-qter
19
22q
36 (4/11)
27 (3/11)
27 (3/11)
64 (7/11)
9 (1/11)
27 (3/11)
9 (1/11)
18 (2/11)
9 (1/11)
18 (2/11)
64 (7/11)
46 (5/11)
9 (1/11)
36 (4/11)
36 (4/11)
9 (1/11)
73 (8/11)
18 (2/11)
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6

4.3 Adrenocortical tumors, childhood
18q12
Xp
Xq21-q25
2q22-q33
73 (8/11)
46 (5/11)
46 (5/11)
44 (4/9)
6
6
6
7
4q
6p21.3
9q34
11q13
12q11-q21
13q22-qter
16
56 (5/9)
22 (2/9)
67 (6/9)
11 (1/9)
11 (1/9)
11 (1/9)
11 (1/9)
7
7
7
7
7
7
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 1p32-p34 4 (1/27) 8 adenocarcinoma
1cen-p32
4q31.1-pter
6q
6q21
6q24
9p21.1-22
9p22-pter
9p23-pter
9cen-p21
13q22-32
17p
18p
18q
18q23
Y
6q24
7q22
12p13
22
50 (3/6)
50 (3/6)
23 (3/13)
15 (4/27)
11 (3/27)
4 (1/27)
4 (1/27)
15 (4/27)
50 (3/6)
30 (8/27)
23 (3/13)
4 (1/27)
11 (3/27)
23 (3/13)
23 (3/13)
42 (8/19)
11 (3/27)
7 (2/27)
50 (3/6)
CMYB
9
8
10
8
8
10
10
9,10
9
9
10
8
8
8,11
8
8
8
8
9
4.4 PANCREATIC ADENOCARCINOMA (7/8 cases) amp(8q,10q,15q21qter,22)/amp(8q24qter,15q24qter,20q12qter)/amp(1q12qter,3q25q27,6p21.1p22,7p1
3pter,8p23pter)/amp(1q32qter,8p23pter,16p,16q23qter,20q13.1qter)/amp(8q24qter,Xq26qter)/amp(7p,7 q11.2q22,16q,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
6q
9cen-p21
17p
18p
18q
None 0 (0/24)
23 (3/13)
23 (3/13)
23 (3/13)
23 (3/13)
31 (4/13)
10
10
10
10
10
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
1qcen-q22
21 (9/44)
16 (7/44)
12
2q23-q36
3qcen-q21
3q22-q26
4pcen-p14
4q13.3-q24
6q21-q22
8q21.3-qter
9p22-pter
10p13-pter
10q22-q25
11p13
11q14-q22
13q21.1
13q22-q31
15q24-qter
16p
21 (9/44)
25 (11/44)
27 (12/44)
7 (3/44)
7 (3/44)
39 (17/44)
23 (10/44)
9 (4/44)
18 (8/44)
23 (10/44)
30 (13/44)
34 (15/44)
16 (7/44)
16 (7/44)
14 (6/44)
7 (3/44)
12
12
12
12
12
12
12
12
12
12
12
12
12
12
12
12
12

4.4 Pancreatic tumor, endocrine
16q21-q22
21q21
22q12-qter
Xp22
Xq22-q23
1p22-p31
None
9 (4/44)
18 (8/44)
9 (4/44)
18 (8/44)
25 (11/44)
0 (0/44)
13 (3/23)
1q32-q44
6q15-q22
8q11.2
8q23
5
13 (3/23)
4 (1/23)
22 (5/23)
7p11.2-q11.2 4 (1/23)
7p11.2-q31 4 (1/23)
7 9 (2/23)
9p12-q21
17 (4/23)
17 (4/23)
4 (1/23)
9p13-q34
9q11-q12
11p14-p15.3
9q32-qter
11q21-q22
13q21-q31
12p11.2-q13
12
4 (1/23)
4 (1/23)
4 (1/23)
26 (6/23)
35 (8/23)
4 (1/23)
4 (1/23)
13 (3/23)
18q12-q23
16
17
4 (1/23)
17p11.2-q25 4 (1/23)
35 (8/23)
13 (3/23)
19 48 (11/23)
20p11.2-q13 9 (2/23)
20q11-q13 9 (2/23)
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
13
12
12
12
12
12
12
13

X
21q22 4 (1/23)
26 (6/23)
13
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
4.5 Bile duct carcinoma, primary
6q16-qter
8p
18q21-qter
17q11
19q13
3q
5 (1/20)
5 (1/20
13 (1/8)
38 (3/8)
38 (3/8)
8q21.1-qter 13 (1/8)
8q
11
12p
13q
38 (3/8)
13 (1/8)
13 (1/8)
25 (2/8)
17q11.1-q21 13 (1/8)
50 (4/8)
14
14
15
15
15
15
15
15
15
15
15
15

4.5 Gastroenteropancreatic tumor: 12 amplifications out of 28 cases

4.6 Thyroid adenoma
4.6 Thyroid adenoma, follicular
4.7 Thyroid carcinoma, follicular
(22)
None
1p
None
7 (2/29)
31 (4/13)
16
18
16
22
13q21-q22
14q11.2-q22
18q12.1-q21
5 (1/20)
5 (1/20)
46 (6/13)
25 (5/20)
14q11.2-q22 5 (1/20)
17
17
16
17 4.7 Thyroid carcinoma, follicular
1p21-p22
9q13-q21.3
22q12.3-qter
18q12.1-q21
20 (4/20)
23 (3/13)
5 (1/20)
40 (8/20)
18
17
17
17
17
18
17 4.7 Thyroid carcinoma, papillary
None
None 0 (0/26)
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 9q21.3q32 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
4.8 HÜRTHLE CELL THYROID CARCINOMA (?/28 cases)
Comment: Amplifications were not determined.
19
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
4.10 Anaplastic carcinoma
4.11 Parathyroid adenoma
None
None
None
0 (0/10)
0 (0/13)
0 (0/63)
17
17
1p
6q26-qter
11p
11cen-q22
11q23-qter
13cen-q12
13q14-qter
15q14-25
15q26
4
5
14q
11 (6/53)
10 (1/10)
10 (1/10)
11 (6/53)
25 (13/53)
30 (16/53)
34 (18/53)
11 (6/53)
17 (9/53)
10 (1/10)
15 (8/53)
13 (7/53)
20,21
20
21
21
20
20
20
20
20
20
21
20
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, 1p34-pter 19 (5/26) sporadic
22
11
15q15-qter
18q
Not determined
39 (10/26)
27 (7/26)
12 (3/26)
22
22
22
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
1p32
30 (3/10)
40 (4/10)
22
6q16-q26
11p12-p14
11q
18q
22q
30 (3/10)
40 (4/10)
50 (5/10)
30 (3/10)
30 (3/10)
22
22
22
22
22
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, welldifferentiated, type B3 thymoma
6q 38 (6/16) 23
4.14 Thymic squamous cell carcinoma, primary, type
C thymoma
13q21-q32
6q
8p12 6 (1/16)
31 (5/16)
44 (4/9)
23
23
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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