Compilation of published comparative genomic hybridization studies

Cancer Genetics and Cytogenetics

Volumn 135, Issue 1, 2002, Pages 63-90

  Struski, Stéphanie ^a   Doco Fenzy, Martine ^b   Cornillet Lefebvre, Pascale ^a  

^a SERVICE DE DERMATOLOGIE   (France)

^b HÔPITAL MAISON BLANCHE   (France)

Author keywords

[No Author keywords available]

Indexed keywords

CANCER GENETICS; CHROMOSOME ABERRATION; COMPARATIVE GENOMIC HYBRIDIZATION; CYTOGENETICS; HUMAN; KARYOTYPE; ONCOGENE; PRIORITY JOURNAL; REVIEW; SOLID TUMOR;

EID: 0036275710     PISSN: 01654608     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0165-4608(01)00624-0     Document Type: Article

References (438)

1. Comparative genomic hybridization for molecular cytogenetic analysis of solid tumors
2. Comparative genomic hybridization analysis detects frequent, often high-level, overrepresentation of DNA sequences at 3q, 5p, 7p, and 8q in human non-small cell lung carcinomas
3. DNA gains in 3q occur frequently in squamous cell carcinoma of the lung, but not in adenocarcinoma
4. Comparison of DNA copy number changes in malignant mesothelioma, adenocarcinoma and large-cell anaplastic carcinoma of the lung
5. Identification of frequent novel genetic alterations in small cell lung carcinoma
6. Identification of novel regions of altered DNA copy number in small cell lung tumors
7. Chromosome 3 imbalances are the most frequent aberration found in non-small cell lung carcinoma
8. Molecular cytogenetic analysis of non-small cell lung carcinoma by spectral karyotyping and comparative genomic hybridization
9. Comparison of chromosomal imbalances in neuroendocrine and non-small-cell lung carcinomas
10. Patterns of chromosomal imbalances in adenocarcinoma and squamous cell carcinoma of the lung
11. Small-cell lung cancer is characterized by a high incidence of deletions on chromosomes 3p, 4q, 5q, 10q, 13q and 17p
12. Chromosomal alterations in the clonal evolution to the metastatic stage of squamous cell carcinomas of the lung
13. Mapping of multiple DNA gains and losses in primary small cell lung carcinomas by comparative genomic hybridization
14. Primary small-cell lung carcinomas and their metastases are characterized by a recurrent pattern of genetic alterations
15. Comparison of genetic changes in primary sarcomas and their pulmonary metastases
16. Typical and atypical carcinoid tumors of the lung are characterized by 11q deletions as detected by comparative genomic hybridization
17. Comparative genomic hybridization and loss of heterozygosity analyses identify a common region of deletion at 15q11.1-15 in human malignant mesothelioma
18. Recurrent DNA copy number changes in 1q, 4q, 6q, 9p, 13q, 14q and 22q detected by comparative genomic hybridization in malignant mesothelioma
19. Gains and losses of DNA sequences in malignant mesothelioma by comparative genomic hybridization
20. Comparative genomic hybridization study on pooled DNAs from tumors of one clinical-pathological entity
21. Comparative genomic hybridization analysis detects frequent over-representation of DNA sequences at 3q, 7p, and 8q in head and neck carcinomas
22. Distinct patterns of chromosomal alterations in high- and low-grade head and neck squamous cell carcinomas
23. Patterns of chromosomal alterations in metastasizing and nonmetastasizing primary head and neck carcinomas
24. Genomic alterations associated with malignancy in head and neck cancer
25. Frequent novel DNA copy number increase in squamous cell head and neck tumors
26. Pattern of genomic imbalances in oral squamous cell carcinomas with and without an increased copy number of 11q13
27. Relationship between cytogenetic aberrations by CGH coupled with tissue microdissection and DNA ploidy by laser scanning cytometry in head and neck squamous cell carcinoma
28. Assessment of chromosomal gains and losses in oral squamous cell carcinoma by comparative genomic hybridisation
29. Comparison of DNA copy numbers in original oral squamous cell carcinomas and corresponding cell lines by comparative genomic hybridization
30. Gain of DNA copy number on chromosomes 3q26-qter and 5p14-pter is a frequent finding in head and neck squamous cell carcinomas
31. Identification of genetic aberrations in cell lines from oral squamous cell carcinomas by comparative genomic hybridization
32. The relationship of genetic aberrations detected by comparative genomic hybridization to DNA ploidy and tumor size in human oral squamous cell carcinomas
33. A simple specific pattern of chromosomal aberrations at early stages of head and neck squamous cell carcinomas; PIK3CA but not p63 gene as a likely target of 3q26-qter gains
34. Comparative genomic hybridization detects novel deletions and amplifications in head and neck squamous cell carcinomas
35. Recurrent chromosomal imbalances detected in biopsy material from oral premalignant and malignant lesions by combined tissue microdissection, universal DNA amplification, and comparative genomic hybridization
36. Patterns of chromosomal aberrations in metastasizing and nonmetastasizing squamous cell carcinomas of the oropharynx and hypopharynx
37. Oral squamous cell carcinomas are characterized by a rather uniform pattern of genomic imbalances detected by comparative genomic hybridisation
38. Chromosomal aberrations in nasopharyngeal carcinoma analyzed by comparative genomic hybridization
39. Comparative genomic hybridization analysis of nasopharygeal carcinoma; consistent patterns of genetic aberrations and clinicopathological correlations
40. Frequent c-myc and Int-2 overrepresentations in nasopharyngeal carcinoma
41. Analysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization
42. Detection of recurrent chromosomal gains and losses in primary nasopharyngeal carcinoma by comparative genomic hybridisation
43. Analysis by comparative genomic hybridization of epithelial and spindle cell components in sarcomatoid carcinoma and carcinosarcoma; histogenetic aspects
44. DNA copy number losses are more frequent in primary larynx tumors with lymph node metastases than in tumors without metastases
45. Mapping of novel regions of DNA gain and loss by comparative genomic hybridization in esophageal carcinoma in the Black and Colored populations of South Africa
46. Frequent loss of copy number on the long arm of chromosome 21 in human esophageal squamous cell carcinoma
47. Comparative genomic hybridization of esophageal and gastroesophageal adenocarcinomas shows consensus areas of DNA gain and loss
48. Molecular cytogenetic fingerprinting of esophageal squamous cell carcinoma by comparative genomic hybridization reveals a consistent pattern of chromosomal alterations
49. Comparative genomic hybridization of squamous cell carcinoma of the esophagus; the possible involvement of the DPI gene in the 13q34 amplicon
50. Cytogenetic analysis of esophageal squamous cell carcinoma cell lines by comparative genomic hybridization; relationship of cytogenetic aberrations to in vitro cell growth
51. Gains of 8q23-qter and 20q and loss of 11q22-qter in esophageal squamous cell carcinoma associated with lymph node metastasis
52. Clonal analysis of a case of multifocal oesophageal (Barrett's) adenocarcinoma by comparative genomic hybridization
53. Chromosomal imbalances in Barrett's adenocarcinoma and the metaplasia-dysplasia-carcinoma sequence
54. CD44 is a potential target of amplification within the 11p13 amplicon detected in gastric cancer cell lines
55. Recurrent chromosome changes in 62 primary gastric carcinomas detected by comparative genomic hybridization
56. Chromosomal alterations in paired gastric adenomas and carcinomas
57. Changes in DNA copy number in primary gastric carcinomas by comparative genomic hybridization
58. 17q12-21 amplicon, a novel recurrent genetic change in intestinal type of gastric carcinoma; a comparative genomic hybridization study
59. Presence of high-level DNA copy number gains in gastric carcinoma and severely dysplastic adenomas but not in moderately dysplastic adenomas
60. Genetic alterations of gastric cancer. Comparative genomic hybridization and fluorescence in situ hybridization studies
61. Comparative genomic hybridization reveals differences in DNA copy number changes between sporadic gastric carcinomas and gastric carcinomas from patients with hereditary nonpolyposis colorectal cancer
62. Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2
63. Gains, losses, and amplifications of genomic materials in primary gastric cancers analyzed by comparative genomic hybridization
64. Helicobacter pylori-related and -non-related gastric cancers do not differ with respect to chromosomal aberrations
65. Correlation of histologic subtypes and replication error phenotype with comparative genomic hybridization in gastric cancer
66. DNA copy number losses in chromosome 1996;14:an early change in gastrointestinal stromal tumors
67. Putative chromosomal deletions on 9p, 9q and 22q occur preferentially in malignant gastrointestinal stromal tumors
68. Different patterns of DNA copy number changes in gastrointestinal stromal tumors, leiomyomas, and schwan- nomas
69. Comparative genomic hybridization of cancer of the gastroesophageal junction; deletion of 14Q31-32.1 discriminates between esophageal (Barrett's) and gastric cardia adenocarcinomas
70. Genomic alterations in distal bile duct carcinoma by comparative genomic hybridization and karyotype analysis
71. Genetic aberrations detected by comparative genomic hybridization in biliary tract cancers
72. Comparative genomic hybridization analysis of primary colorectal carcinomas and their synchronous metastases
73. Chromosomal alterations in ulcerative colitis-related and sporadic colorectal cancers by comparative genomic hybridization
74. Chromosomal gains and losses in primary colorectal carcinomas detected by CGH and their associations with tumour DNA ploidy, genotypes and phenotypes
75. Heterogeneity studies identify a subset of sporadic colorectal cancers without evidence for chromosomal or microsatellite instability
76. Chromosome arm 20q gains and other genomic alterations in colorectal cancer metastatic to liver, as analyzed by comparative genomic hybridization and fluorescence in situ hybridization
77. Progression from colorectal adenoma to carcinoma is associated with non-random chromosomal gains as detected by comparative genomic hybridisation
78. Genetic changes in primary colorectal cancer by comparative genomic hybridization
79. Genetic changes in colorectal carcinoma tumors with liver metastases analyzed by comparative genomic hybridization and DNA ploidy
80. Analysis of colorectal cancer by comparative genomic hybridization; evidence for induction of the metastatic phenotype by loss of tumor suppressor genes
81. Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors
82. Comparative genomic in situ hybridization of colon carcinomas with replication error
83. Chromosomal alterations in ulcerative colitis-related neoplastic progression
84. Genomic instability is an early event during the progression pathway of ulcerative-colitis-related neoplasia
85. A recurrent pattern of chromosomal aberrations and immunophenotypic appearance defines anal squamous cell carcinomas
86. Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1
87. Chromosomal changes and clonality relationship between primary and recurrent hepatocellular carcinoma
88. Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative genomic hybridization
89. Evaluation of the reliability of chromosomal imbalances detected by combined use of universal DNA amplification and comparative genomic hybridization
90. Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas; their relationship to clinicopathological features
91. Chromosomal abnormality in hepatocellular carcinoma by comparative genomic hybridisation in Taiwan
92. Recurrent chromosomal abnormalities in hepatocellular carcinoma detected by comparative genomic hybridization
93. Distinct chromosomal abnormality pattern in primary liver cancer of non-B, non-C patients
94. The association of chromosome 8p deletion and tumor metastasis in human hepatocellular carcinoma
95. Chromosomal aberrations in human hepatocellular carcinomas associated with hepatitis C virus infection detected by comparative genomic hybridization
96. Marked genetic similarities between hepatitis B virus-positive and hepatitis C virus-positive hepatocellular carcinomas
97. Differentiation of liver cell adenomas from well-differentiated hepatocellular carcinomas by comparative genomic hybridization
98. Assessment of genetic changes in hepatocellular carcinoma by comparative genomic hybridization analysis; relationship to disease stage, tumor size, and cirrhosis
99. Genomic aberrations in human hepatocellular carcinomas of differing etiologies
100. Molecular cytogenetic evaluation of virus-associated and non-viral hepatocellular carcinoma; analysis of 26 carcinomas and 12 concurrent dysplasias
101. Comparative genomic hybridization reveals population-based genetic alterations in hepatoblastomas
102. Comparative genomic hybridization analysis of hepatoblastomas
103. Comparative genomic hybridization analysis of hepatoblastomas; additional evidence for a genetic link with Wilms tumor and rhabdomyosarcoma
104. Adrenocortical carcinoma is characterized by a high frequency of chromosomal gains and high-level amplifications
105. Comparative genomic hybridization reveals frequent losses of chromosomes 1p and 3q in pheochromocytomas and abdominal paragangliomas, suggesting a common genetic etiology
106. Comparative genomic hybridization analysis of adrenocortical tumors of childhood
107. Highly consistent genetic alterations in childhood adrenocortical tumours detected by comparative genomic hybridization
108. Genetic aberrations in adrenocortical tumors detected using comparative genomic hybridization correlate with tumor size and malignancy
109. Analysis of genomic alterations in sporadic adrenocortical lesions. Gain of chromosome 17 is an early event in adrenocortical tumorigenesis
110. Frequent gain of copy number on the long arm of chromosome 20 in human pancreatic adenocarcinoma
111. Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer
112. Identification of frequent chromosomal aberrations in ductal adenocarcinoma of the pancreas by comparative genomic hybridization (CGH)
113. Mapping of chromosomal imbalances in pancreatic carcinoma by comparative genomic hybridization
114. Genetic differences in endocrine pancreatic tumor subtypes detected by comparative genomic hybridization
115. Chromosomal alterations in human pancreatic endocrine tumors
116. Pancreatic acinar carcinoma shows a distinct pattern of chromosomal imbalances by comparative genomic hybridization
117. From amplification to gene in thyroid cancer; a high-resolution mapped bacterial-artificial-chromosome resource for cancer chromosome aberrations guides gene discovery after comparative genome hybridization
118. Low frequency of numerical chromosomal aberrations in follicular thyroid tumors detected by comparative genomic hybridization
119. CGH alterations in medullary thyroid carcinomas in relation to the RET M918T mutation and clinical outcome
120. Comparison of benign and malignant follicular thyroid tumours by comparative genomic hybridization
121. DNA copy number changes in thyroid carcinoma
122. Comparative genomic hybridization defines frequent loss on 16p in human anaplastic thyroid carcinoma
123. Screening for genetic aberrations in papillary thyroid cancer by using comparative genomic hybridization
124. Frequent chromosomal DNA unbalance in thyroid oncocytic (Hurthle cell) neoplasms detected by comparative genomic hybridization
125. 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
126. Comparative genomic hybridization analysis of human parathyroid tumors
127. Alternative genetic pathways in parathyroid tumorigenesis
128. Patterns of chromosomal imbalances in parathyroid carcinomas
129. Novel chromosomal abnormalities identified by comparative genomic hybridization in parathyroid adenomas
130. Comparative genomic hybridization analysis of nonfunctioning pituitary tumors
131. Cytogenetic alterations in pituitary adenomas detected by comparative genomic hybridization
132. Detection of chromosomal imbalances in growth hormone-secreting pituitary tumors by comparative genomic hybridization
133. Multiple genetic aberrations including evidence of chromosome 11q13 rearrangement detected in pituitary adenomas by comparative genomic hybridization
134. Chromosomal aberrations in sporadic pituitary tumors
135. Comparative genomic hybridization in pineal germ cell tumors
136. Comparative genomic hybridization in pineal parenchymal tumors
137. Comparative genomic hybridization analysis of clear cell sarcoma of the kidney
138. Evaluation of the clonal relationship between primary and metastatic renal cell carcinoma by comparative genomic hybridization
139. The genetics of renal tumors in end-stage renal failure differs from those occurring in the general population
140. Comparison of DNA gains and losses in primary renal clear cell carcinomas and metastatic sites; importance of 1q and 3p copy number changes in metastatic events
141. Chromosomal abnormalities in renal cell neoplasms associated with acquired renal cystic disease. A series studied by comparative genomic hybridization and fluorescence in situ hybridization
142. Chromosomal imbalances in papillary renal cell carcinoma; genetic differences between histological subtypes
143. Genetic characterization of multifocal tumor growth in renal cell carcinoma
144. Genetic alterations in metastatic renal cell carcinoma detected by comparative genomic hybridization; correlation with clinical and histological data
145. Genetic aberrations detected by comparative genomic hybridization are associated with clinical outcome in renal cell carcinoma
146. Renal cell carcinoma genetic analysis by comparative genomic hybridization and restriction fragment length polymorphism analysis
147. Comparative genomic hybridization for genetic analysis of renal oncocytomas
148. Specific loss of chromosomes 1, 2, 6, 10, 13, 17, and 21 in chromophobe renal cell carcinomas revealed by comparative genomic hybridization
149. Identification of novel regions of deletion in familial Wilms' tumor by comparative genomic hybridization
150. Comparative genomic hybridization and its application to Wilms' tumorigenesis
151. Gain of 1q is associated with adverse outcome in favorable histology Wilms' tumors
152. Comparative genomic hybridization analysis of Wilms tumors
153. DNA copy number changes in schistosoma-associated and non-schistosoma-associated bladder cancer
154. Genetic alterations in primary bladder cancers and their metastases
155. Identification of gains and losses of DNA sequences in primary bladder cancer by comparative genomic hybridization
156. Detection of genetic alterations in bladder tumors by comparative genomic hybridization and cytogenetic analysis
157. Comparison of comparative genomic hybridization, fluorescence in situ hybridization and flow cytometry in urinary bladder cancer
158. Marked genetic differences between stage pTa and stage pT1 papillary bladder cancer detected by comparative genomic hybridization
159. Chromosomal imbalances are associated with a high risk of progression in early invasive (pT1) urinary bladder cancer
160. Chromosomal aberrations associated with invasion in papillary superficial bladder cancer
161. Patterns of chromosomal imbalances in muscle invasive bladder cancer
162. Cytogenetic analysis of multifocal bladder cancer supports a monoclonal origin and intraepithelial spread of tumor cells
163. Chromosomal imbalances in small cell carcinomas of the urinary bladder
164. Detection of chromosomal imbalances in transitional cell carcinoma of the bladder by comparative genomic hybridization
165. Chromosomal imbalances in noninvasive papillary bladder neoplasms (pTa)
166. Molecular genetic aspects of oligodendrogliomas including analysis by comparative genomic hybridization
167. The glial and mesenchymal elements of gliosarcomas share similar genetic alterations
168. Astroblastoma; clinicopathologic features and chromosomal abnormalities defined by comparative genomic hybridization
169. Comparative genomic hybridization reveals recurrent enhancements on chromosome 20 and in one case combined amplification sites on 15q24q26 and 20p11p12 in glioblastomas
170. Intratumoral cytogenetic heterogeneity detected by comparative genomic hybridization and laser scanning cytometry in human gliomas
171. Chromosomal abnormalities in glioblastoma multiforme by comparative genomic hybridization; correlation with radiation treatment outcome
172. Identification of subgroups of high-grade oligodendroglial tumors by comparative genomic hybridization
173. Subtyping of oligo-astrocytic tumours by comparative genomic hybridization
174. Evidence of focal genetic microheterogeneity in glioblastoma multiforme by area-specific CGH on microdissected tumor cells
175. Chromosomal abnormalities in glioblastoma multiforme tumors and glioma cell lines detected by comparative genomic hybridization
176. Genetic aberrations in oligodendroglial tumours; an analysis using comparative genomic hybridization
177. Molecular and cytogenetic analysis of glioblastoma multiforme
178. Chromosomal aberrations detected by comparative genomic hybridization (CGH) in human astrocytic tumors
179. Genetic analysis of glioblastoma multiforme provides evidence for subgroups within the grade
180. Oncogene amplification in human gliomas; a molecular cytogenetic analysis
181. Investigation of genetic alterations associated with the grade of astrocytic tumor by comparative genomic hybridization
182. Gliomas in families; chromosomal analysis by comparative genomic hybridization
183. Chromosome imbalances in familial gliomas detected by comparative genomic hybridization
184. Chromosomal imbalances in brain metastases of solid tumors
185. Chromosome arm 6q loss is the most common recurrent autosomal alteration detected in primary pediatric ependymoma
186. Accumulation of genetic changes is associated with poor prognosis in grade II astrocytomas
187. Low frequency of chromosomal imbalances in anaplastic ependymomas as detected by comparative genomic hybridization
188. Detection of complex genetic alterations in human glioblastoma multiforme using comparative genomic hybridization
189. Comparative genomic hybridization of human malignant gliomas reveals multiple amplification sites and nonrandom chromosomal gains and losses
190. Recurrent gain of chromosome arm 7q in low-grade astrocytic tumors studied by comparative genomic hybridization
191. Characterization of genomic alterations associated with glioma progression by comparative genomic hybridization
192. Clinically distinct subgroups of glioblastoma multiforme studied by comparative genomic hybridization
193. Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children
194. Molecular cytogenetic analysis of medulloblastomas and supratentorial primitive neuroectodermal tumors by using conventional banding, comparative genomic hybridization, and spectral karyotyping
195. Comparative genomic hybridization and histological variation in primitive neuroectodermal tumours
196. Genetic alterations in pediatric medulloblastomas detected by comparative genomic hybridization
197. Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization
198. Comparative genomic hybridization in patients with supratentorial and infratentorial primitive neuroectodermal tumors
199. Mapping of chromosomal gains and losses in primitive neuroectodermal tumors by comparative genomic hybridization
200. Novel regions of chromosomal loss in familial neuroblastoma by comparative genomic hybridization
201. Coordinate deletion of chromosome 3p and 11q in neuroblastoma detected by comparative genomic hybridization
202. Comparative genomic hybridization (CGH) analysis of neuroblastomas-an important methodological approach in paediatric tumour pathology
203. Comparative genomic hybridization and telomerase activity analysis identify two biologically different groups of 4s neuroblastomas
204. Numerical and structural aberrations in advanced neuroblastoma tumours by CGH analysis; survival correlates with chromosome 17 status
205. 1q23 gain is associated with progressive neuroblastoma resistant to aggressive treatment
206. Comparative genomic hybridization study of primary neuroblastoma tumors. United Kingdom Children's Cancer Study Group
207. Gain of chromosome 17 is the most frequent abnormality detected in neuroblastoma by comparative genomic hybridization
208. Comparative genomic hybridization (CGH) analysis of stage 4 neuroblastoma reveals high frequency of 11Q deletion in tumors lacking MYCN amplification
209. Genetic heterogeneity of neuroblastoma studied by comparative genomic hybridization
210. Sensitive and reliable detection of genomic imbalances in human neuroblastomas using comparative genomic hybridisation analysis
211. Comparative genomic hybridization reveals changes in DNA-copy number in poor-risk neuroblastoma
212. 1p and 3p deletions in meningiomas without detectable aberrations of chromosome 22 identified by comparative genomic hybridization
213. Chromosomal losses and gains in meningiomas; comparative genomic hybridization (CGH) study of the whole genome
214. Comparative genomic hybridization analysis of genetic alterations associated with malignant progression of meningioma
215. Analysis of genomic alterations in benign, atypical, and anaplastic meningiomas; toward a genetic model of meningioma progression
216. Gain of 17q24-qter detected by comparative genomic hybridization in malignant tumors from patients with von Recklinghausen's neurofibromatosis
217. Analysis of chromosomal imbalances in sporadic and NF1-associated peripheral nerve sheath tumors by comparative genomic hybridization
218. Genomic imbalances of 7p and 17q in malignant peripheral nerve sheath tumors are clinically relevant
219. Comparative genomic hybridization analysis of sporadic neuroendocrine tumors of the digestive system
220. Analysis of sporadic neuroendocrine tumours of the enteropancreatic system by comparative genomic hybridisation
221. Concomitant loss of chromosome 3 and whole arm losses and gains of chromosome 1, 6, or 8 in metastasizing primary uveal melanoma
222. Comparative genomic hybridization analysis of archival formalin-fixed paraffin-embedded uveal melanomas
223. Comparative genomic hybridization in the detection of DNA copy number abnormalities in uveal melanoma
224. Characterization of complex chromosomal abnormalities in uveal melanoma by fluorescence in situ hybridization, spectral karyotyping, and comparative genomic hybridization
225. Chromosomal gains and losses in uveal melanomas detected by comparative genomic hybridization
226. Identification of chromosomes 3, 6, and 8 aberrations in uveal melanoma by microsatellite analysis in comparison to comparative genomic hybridization
227. Marked differences in unilateral isolated retinoblastomas from young and older children studied by comparative genomic hybridization
228. Detection of chromosome imbalances in retinoblastoma by parallel karyotype and CGH analyses
229. Chromosomal gains and losses in primary cutaneous melanomas detected by comparative genomic hybridization
230. Molecular cytogenetic analysis of Spitz nevi shows clear differences to melanoma
231. Direct visualization of the clonal progression of primary cutaneous melanoma; application of tissue microdissection and comparative genomic hybridization
232. Comparative genomic hybridization (CGH) discloses chromosomal and subchromosomal copy number changes in Merkel cell carcinomas
233. Characteristic pattern of chromosomal gains and losses in Merkel cell carcinoma detected by comparative genomic hybridization
234. Intratumoral heterogeneity in breast carcinoma revealed by laser-microdissection and comparative genomic hybridization
235. Extensive ductal carcinoma in situ with small foci of invasive ductal carcinoma; evidence of genetic resemblance by CGH
236. Comparative genomic hybridization of ductal carcinoma in situ of the breast-evidence of multiple genetic pathways
237. Different genetic pathways in the evolution of invasive breast cancer are associated with distinct morphological subtypes
238. Genetic relation of lobular carcinoma in situ, ductal carcinoma in situ, and associated invasive carcinoma of the breast
239. Comparative genomic hybridization of fine needle aspirates from breast carcinomas
240. Comparative genomic hybridization analysis of breast tumors with predetermined profiles of DNA amplification
241. Molecular cytogenetic analysis of 11 new breast cancer cell lines
242. Genetic imbalances in pT2 breast cancers of southern Chinese women
243. Differences in genetic alterations between primary lobular and ductal breast cancers detected by comparative genomic hybridization
244. Genetic analysis of 53 lymph node-negative breast carcinomas by CGH and relation to clinical, pathological, morphometric, and DNA cytometric prognostic factors
245. Genetic aberrations detected by comparative genomic hybridization predict outcome in node-negative breast cancer
246. Genetic alterations in ERBB2-amplified breast carcinomas
247. Comparative genomic hybridisation of ductal carcinoma in situ of the breast; identification of regions of DNA amplification and deletion in common with invasive breast carcinoma
248. Detection and mapping of amplified DNA sequences in breast cancer by comparative genomic hybridization
249. Genetic heterogeneity and clonal evolution underlying development of asynchronous metastasis in human breast cancer
250. Genetic changes in intraductal breast cancer detected by comparative genomic hybridization
251. Comparative genomic hybridization reveals complex genetic changes in primary breast cancer tumors and their cell lines
252. Genetic changes associated with telomerase activity in breast cancer
253. Genetic changes in breast cancer detected by comparative genomic hybridization
254. Phyllodes tumors of the breast analyzed by comparative genomic hybridization and association of increased 1q copy number with stromal overgrowth and recurrence
255. Comparative genomic hybridization analysis of lobular carcinoma in situ and atypical lobular hyperplasia and potential roles for gains and losses of genetic material in breast neoplasia
256. Analysis of chromosomal aberrations in breast cancer by comparative genomic hybridization (CGH). Correlation with histoprognostic variables and c-erbB-2 immunoexpression
257. Widespread chromosomal abnormalities in high-grade ductal carcinoma in situ of the breast. Comparative genomic hybridization study of pure high-grade DCIS
258. Detection of DNA amplification in 17 primary breast carcinomas with homogeneously staining regions by a modified comparative genomic hybridization technique
259. Identification of amplified DNA sequences in breast cancer and their organization within homogeneously staining regions
260. Genetic alterations in lobular breast cancer by comparative genomic hybridization
261. Genetic alterations in primary breast cancers and their metastases; direct comparison using modified comparative genomic hybridization
262. Comparative genomic hybridization detects novel amplifications in fibroadenomas of the breast
263. Chromosomal aberrations in breast cancer; a comparison between cytogenetics and comparative genomic hybridization
264. Patterns of chromosomal imbalances in invasive breast cancer
265. Comparative genomic hybridization of formalin-fixed, paraffin-embedded breast tumors reveals different patterns of chromosomal gains and losses in fibroadenomas and diploid and aneuploid carcinomas
266. Comparative genomic hybridization of breast tumors stratified by histological grade reveals new insights into the biological progression of breast cancer
267. Chromosome alterations in breast carcinomas; frequent involvement of DNA losses including chromosomes 4q and 21q
268. Genetic aberrations in hypodiploid breast cancer; frequent loss of chromosome 4 and amplification of cyclin D1 oncogene
269. Distinct somatic genetic changes associated with tumor progression in carriers of BRCA1 and BRCA2 germ-line mutations
270. Molecular cytogenetics of primary breast cancer by CGH
271. Somatic genetic alterations in BRCA2-associated and sporadic male breast cancer
272. Genetic alterations on chromosome 16 and 17 are important features of ductal carcinoma in situ of the breast and are associated with histologic type
273. Chromosomal alterations in ductal carcinomas in situ and their in situ recurrences
274. Overrepresentation of 3q and 8q material and loss of 18q material are recurrent findings in advanced human ovarian cancer
275. Genetic analysis of benign, low-grade, and high-grade ovarian tumors
276. Comparative genomic hybridization detects genetic imbalances in primary ovarian carcinomas as correlated with grade of differentiation
277. Comparative genomic hybridization detects frequent overrepresentation of chromosomal material from 3q26, 8q24, and 20q13 in human ovarian carcinomas
278. Genetic aberrations detected by comparative genomic hybridization in ovarian clear cell adenocarcinomas
279. Evidence for divergence of DNA copy number changes in serous, mucinous and endometrioid ovarian carcinomas
280. Genetic changes in inherited and sporadic ovarian carcinomas by comparative genomic hybridization; extensive similarity except for a difference at chromosome 2q24-q32
281. Analysis of ovarian borderline tumors using comparative genomic hybridization and fluorescence in situ hybridization
282. Frequent gains and losses of specific chromosome segments in human ovarian carcinomas shown by comparative genomic hybridization
283. Distinct cytogenetic alterations in squamous intraepithelial lesions of the cervix revealed by laser-assisted microdissection and comparative genomic hybridization
284. Prognostic value of genomic alterations in invasive cervical squamous cell carcinoma of clinical stage IB detected by comparative genomic hybridization
285. Detection of DNA copy number changes in human endometriosis by comparative genomic hybridization
286. Gain of chromosome 3q defines the transition from severe dysplasia to invasive carcinoma of the uterine cervix
287. Advanced-stage cervical carcinomas are defined by a recurrent pattern of chromosomal aberrations revealing high genetic instability and a consistent gain of chromosome arm 3q
288. Human papilloma virus status and chromosomal imbalances in primary cervical carcinomas and tumour cell lines
289. Genetic imbalances in precursor lesions of endometrial cancer detected by comparative genomic hybridization
290. Comparative genomic hybridization reveals a recurrent pattern of chromosomal aberrations in severe dysplasia/carcinoma in situ of the cervix and in advanced-stage cervical carcinoma
291. Genomic changes and HPV type in cervical carcinoma
292. Distinct chromosomal imbalances in uterine serous and endometrioid carcinomas
293. Detection of DNA gains and losses in primary endometrial carcinomas by comparative genomic hybridization
294. Genetic aberrations detected by comparative genomic hybridization predict outcome in patients with endometrioid carcinoma
295. Frequent gains on chromosome arms 1q and/or 8q in human endometrial cancer
296. Loss in 3p and 4p and gain of 3q are concomitant aberrations in squamous cell carcinoma of the vulva
297. Genetic analysis of ovarian germ cell tumors by comparative genomic hybridization
298. Primary carcinoma of the fallopian tube; comparative genomic hybridization reveals high genetic instability and a specific, recurring pattern of chromosomal aberrations
299. Genomic alterations in fallopian tube carcinoma; comparison to serous uterine and ovarian carcinomas reveals similarity suggesting likeness in molecular pathogenesis
300. Detection of chromosomal DNA gains and losses in testicular germ cell tumors by comparative genomic hybridization
301. Comparative genomic hybridization of germ cell tumors of the adult testis; confirmation of karyotypic findings and identification of a 12p-amplicon
302. Comparative genomic and in situ hybridization of germ cell tumors of the infantile testis
303. Detection of chromosomal aberrations in seminomatous germ cell tumours using comparative genomic hybridization
304. Chromosomal amplification is associated with cisplatin resistance of human male germ cell tumors
305. Chromosomal gains and losses in testicular germ cell tumors of adolescents and adults investigated by a modified comparative genomic hybridization approach
306. Molecular cytogenetic analysis of adult testicular germ cell tumours and identification of regions of consensus copy number change
307. Comparative genomic hybridization, allelic imbalance, and fluorescence in situ hybridization on chromosome 8 in prostate cancer
308. Genetic alterations in untreated metastases and androgen-independent prostate cancer detected by comparative genomic hybridization and allelotyping
309. A similar pattern of chromosomal alterations in prostate cancers from African-Americans and Caucasian Americans
310. Discovery of new DNA amplification loci in prostate cancer by comparative genomic hybridization
311. Mapping of chromosomal gains and losses in prostate cancer by comparative genomic hybridization
312. Androgen receptor gene alterations and chromosomal gains and losses in prostate carcinomas appearing during finasteride treatment for benign prostatic hyperplasia
313. Genetic alterations in hormone-refractory recurrent prostate carcinomas
314. Genetic changes in familial prostate cancer by comparative genomic hybridization
315. Comparative genomic hybridization reveals DNA copy number gains to frequently occur in human prostate cancer
316. Microdissection, DOP-PCR, and comparative genomic hybridization of paraffin-embedded familial prostate cancers
317. Genetic changes in primary and recurrent prostate cancer by comparative genomic hybridization
318. Genetic heterogeneity in a prostatic carcinoma and associated prostatic intraepithelial neoplasia as demonstrated by combined use of laser-microdissection, degenerate oligonucleotide primed PCR and comparative genomic hybridization
319. Chromosomal changes during development and progression of prostate adenocarcinomas
320. Comparative genomic hybridization analysis of human sarcomas; II. Identification of novel amplicons at 6p and 17p in osteosarcomas
321. Isolation of osteosarcoma-associated amplified DNA sequences using representational difference analysis
322. Chromosomal regions involved in the pathogenesis of osteosarcomas
323. Ring chromosomes in parosteal osteosarcoma contain sequences from 12q13-15; a combined cytogenetic and comparative genomic hybridization study
324. Gains and losses of DNA sequences in osteosarcomas by comparative genomic hybridization
325. Comparative genomic hybridization of low-grade central osteosarcoma
326. DNA sequence copy number increase at 8q; a potential new prognostic marker in high-grade osteosarcoma
327. Gains, losses, and amplifications of DNA sequences evaluated by comparative genomic hybridization in chondrosarcomas
328. Clinical significance of genetic imbalances revealed by comparative genomic hybridization in chondrosarcomas
329. Recurrent gains of 1q, 8 and 12 in the Ewing family of tumours by comparative genomic hybridization
330. Clinical correlations of genetic changes by comparative genomic hybridization in Ewing sarcoma and related tumors
331. Assessment of genomic imbalances in malignant fibrous histiocytomas by comparative genomic hybridization
332. Comparative genomic hybridization of malignant fibrous histiocytoma reveals a novel prognostic marker
333. Loss of chromosome 13 is the most frequent genomic imbalance in malignant fibrous histiocytomas. A comparative genomic hybridization analysis of a series of 30 cases
334. Identification of a novel gene, MASL1, within an amplicon at 8p23.1 detected in malignant fibrous histiocytomas by comparative genomic hybridization
335. Frequent loss of 9p21 (p16(INK4A)) and other genomic imbalances in human malignant fibrous histiocytoma
336. Comparative genomic hybridization analysis of human sarcomas; I. Occurrence of genomic imbalances and identification of a novel major amplicon at 1q21-q22 in soft tissue sarcomas
337. Chromosomal analysis of renal angiomyolipoma by comparative genomic hybridization; evidence for clonal origin
338. DNA copy number changes in epithelioid sarcoma and its variants; a comparative genomic hybridization study
339. Comparative genomic hybridization reveals novel chromosome deletions in 90 primary soft tissue tumors
340. Comparative genomic hybridization as a tool to define two distinct chromosome 12-derived amplification units in well-differentiated liposarcomas
341. Gains and losses of DNA sequences in liposarcomas evaluated by comparative genomic hybridization
342. Overrepresentation of 1q21-23 and 12q13-21 in lipoma-like liposarcomas but not in benign lipomas; a comparative genomic hybridization study
343. DNA copy number changes in development and progression in leiomyosarcomas of soft tissues
344. Molecular cytogenetic analysis of uterine leiomyoma and leiomyosarcoma by comparative genomic hybridization
345. Analysis of genetic alterations in uterine leiomyomas and leiomyosarcomas by comparative genomic hybridization
346. Clinical importance of genomic imbalances in synovial sarcoma evaluated by comparative genomic hybridization
347. Genetic imbalances in 67 synovial sarcomas evaluated by comparative genomic hybridization
348. Novel genomic imbalances in embryonal rhabdomyosarcoma revealed by comparative genomic hybridization and fluorescence in situ hybridization; an intergroup rhabdomyosarcoma study
349. A novel and consistent amplicon at 13q31 associated with alveolar rhabdomyosarcoma
350. Application of comparative genomic hybridization, spectral karyotyping, and microarray analysis in the identification of subtype-specific patterns of genomic changes in rhabdomyosarcoma
351. Gains, losses, and amplification of genomic material in rhabdomyosarcoma analyzed by comparative genomic hybridization
352. Novel formation and amplification of the PAX7-FKHR fusion gene in a case of alveolar rhabdomyosarcoma
353. DNA copy number changes in alveolar soft part sarcoma; a comparative genomic hybridization study
354. Patterns of chromosomal imbalances in benign solitary fibrous tumours of the pleura
355. Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas
356. Ring chromosomes in dermatofibrosarcoma protuberans are composed of interspersed sequences from chromosomes 17 and 22
357. Ring 22 chromosomes in dermatofibrosarcoma protuberans are low-level amplifiers of chromosome 17 and 22 sequences
358. Chromosome band 1q21 is recurrently gained in desmoid tumors
359. Radiation-associated sarcomas are characterized by complex karyotypes with frequent rearrangements of chromosome arm 3p
360. Comparative genomic hybridization studies in hydatidiform moles and choriocarcinoma; amplification of 7q21-q31 and loss of 8p12-p21 in choriocarcinoma
361. Comparative genomic hybridization in chronic B-cell leukemias shows a high incidence of chromosomal gains and losses
362. Contribution of comparative genomic hybridization and fluorescence in situ hybridization to the detection of chromosomal abnormalities in b-cell chronic lymphocytic leukemia
363. Frequent loss of the 11q14-24 region in chronic lymphocytic leukemia; a study by comparative genomic hybridization. Tampere CLL Group
364. Genomic imbalances are rare in hairy cell leukemia
365. The relationship between typical and atypical B-cell chronic lymphocytic leukemia. A comparative genomic hybridization-based study
366. Chromosomal imbalances in adult T-cell leukemia revealed by comparative genomic hybridization; gains at 14q32 and 2p16-22 in cell lines
367. Identification by comparative genomic hybridization of genetic changes involved in tumoral progression of a T-cell non-Hodgkin lymphoma
368. High-level DNA amplifications are common genetic aberrations in B-cell neoplasms
369. Low number of DNA copy number changes in small lymphocytic lymphoma
370. Increased number of chromosomal imbalances and high-level DNA amplifications in mantle cell lymphoma are associated with blastoid variants
371. t(11;14)-positive mantle cell lymphomas exhibit complex karyotypes and share similarities with B-cell chronic lymphocytic leukemia
372. Gain of 3q and deletion of 11q22 are frequent aberrations in mantle cell lymphoma
373. Comparative genomic hybridization detects genomic abnormalities in 80% of follicular lymphomas
374. High incidence of chromosomal imbalances and gene amplifications in the classical follicular variant of follicle center lymphoma
375. Consistent copy number gain in chromosome 12 in primary diffuse large cell lymphomas of the stomach
376. Characteristic pattern of chromosomal gains and losses in marginal zone B cell lymphoma detected by comparative genomic hybridization
377. Novel genomic imbalances in b-cell splenic marginal zone lymphomas revealed by comparative genomic hybridization and cytogenetics
378. Gain of chromosome arm 9p is characteristic of primary mediastinal B-cell lymphoma (MLB); comprehensive molecular cytogenetic analysis and presentation of a novel MBL cell line
379. Primary mediastinal (thymic) B-cell lymphoma is characterized by gains of chromosomal material including 9p and amplification of the REL gene
380. Nonrandom chromosomal imbalances in primary mediastinal B-cell lymphoma detected by arbitrarily primed PCR fingerprinting
381. Characteristic pattern of chromosomal gains and losses in primary large B-cell lymphomas of the gastrointestinal tract
382. Distinct primary central nervous system lymphoma defined by comparative genomic hybridization and laser scanning cytometry
383. REL proto-oncogene is frequently amplified in extranodal diffuse large cell lymphoma
384. DNA copy number changes in diffuse large B-cell lymphoma-comparative genomic hybridization study
385. BCL2 overexpression associated with chromosomal amplification in diffuse large B-cell lymphoma
386. Chromosomal and gene amplification in diffuse large B-cell lymphoma
387. Chromosomal imbalances in primary lymphomas of the central nervous system
388. Characteristic chromosomal imbalances in primary central nervous system lymphomas of the diffuse large B-cell type
389. Lymphocyte predominance Hodgkin disease is characterized by recurrent genomic imbalances
390. Genomic imbalances including amplification of the tyrosine kinase gene JAK2 in CD30+ Hodgkin cells
391. Genetic analysis of sorted Hodgkin and Reed-Sternberg cells using comparative genomic hybridization
392. Among numerous DNA copy number changes, losses of chromosome 13 are highly recurrent in plasmacytoma
393. Molecular cytogenetic abnormalities in multiple myeloma and plasma cell leukemia measured using comparative genomic hybridization
394. Characterization of nonrandom chromosomal gains and losses in multiple myeloma by comparative genomic hybridization
395. Differences in genetic changes between multiple myeloma and plasma cell leukemia demonstrated by comparative genomic hybridization
396. Comparative genomic hybridization in the investigation of myeloid leukemias
397. Comparative genomic hybridization study of de novo myeloid neoplasia
398. Identification of amplified genes in a patient with acute myeloid leukemia and double minute chromosomes
399. Chromosomal breakpoints and changes in DNA copy number in refractory acute myeloid leukemia
400. Delimiting the use of comparative genomic hybridization in human myeloid neoplastic disorders
401. Microdissection based comparative genomic hybridization analysis (micro-CGH) of secondary acute myelogenous leukemias
402. Comparative genomic hybridization and conventional cytogenetic analyses in childhood acute myeloid leukemia
403. The application of comparative genomic hybridization as an additional tool in the chromosome analysis of acute myeloid leukemia and myelodysplastic syndromes
404. Comparison of fluorescein isothiocyanate- and Texas red-conjugated nucleotides for direct labeling in comparative genomic hybridization
405. Extrachromosomal gene amplification in acute myeloid leukemia; characterization by metaphase analysis, comparative genomic hybridization, and semi-quantitative PCR
406. Comparative genomic hybridization in acute myeloid leukemia. A comparison with G-banding and chromosome painting
407. Comparative genomic hybridization-aided unraveling of complex karyotypes in human hematopoietic neoplasias
408. Analysis of hematologic diseases using conventional karyotyping, fluorescence in situ hybridization (FISH), and comparative genomic hybridization (CGH)
409. 12p rearrangement and DNA amplification mapped by comparative genomic hybridization in a patient with secondary myeloid leukemia
410. Importance of using comparative genomic hybridization to improve detection of chromosomal changes in childhood acute lymphoblastic leukemia
411. Genetic aberrations in pediatric acute lymphoblastic leukemia by comparative genomic hybridization
412. Comparative genomic hybridization in childhood acute lymphoblastic leukemia
413. Comparative genomic hybridization in childhood acute lymphoblastic leukemia; correlation with interphase cytogenetics and loss of heterozygosity analysis
414. Detection of chromosome over- and underrepresentations in hyperdiploid acute lymphoblastic leukemia by comparative genomic hybridization
415. Comparative genomic hybridization analysis of natural killer cell lymphoma/leukemia. Recognition of consistent patterns of genetic alterations
416. Comparative analysis of G-banding, chromosome painting, locus-specific fluorescence in situ hybridization, and comparative genomic hybridization in chronic myeloid leukemia blast crisis
417. Chromosomal aberrations during progression of chronic myeloid leukemia identified by cytogenetic and molecular cytogenetic tools; implication of 1q12-21
418. Cytogenetic aberrations in myelodysplastic syndrome detected by comparative genomic hybridization and fluorescence in situ hybridization
419. DNA copy number amplifications in human neoplasms; review of comparative genomic hybridization studies
420. DNA copy number losses in human neoplasms
421. Comparative genomic hybridisation for the analysis of chromosomal imbalances in solid tumours and haematological malignancies
422. Optimizing comparative genomic hybridization for analysis of DNA sequence copy number changes in solid tumors
423. Quantitative mapping of amplicon structure by array CGH identifies CYP24 as a candidate oncogene
424. Matrix-based comparative genomic hybridization; biochips to screen for genomic imbalances
425. High resolution analysis of DNA copy number variation using comparative genomic hybridization to microarrays