Gains of 8q23-qter and 20q and loss of 11q22-qter in esophageal squamous cell carcinoma associated with lymph node metastasis

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is associated with poor prognosis and lymph node metastasis is one of the critical prognostic factors. Although it is important to elucidate the genetic aberrations underlying its lymph node metastasis, to the authors' knowledge little is known regarding alterations in the primary ESCC that are linked with ESCC metastasis to the lymph nodes. METHODS: To elucidate genetic aberrations involved in the lymph node metastasis of ESCC, comparative genomic hybridization analysis was applied to 36 ESCC specimens, from 12 cases with no lymph node metastasis and 24 cases with lymph node metastasis. RESULTS: Copy number gains frequently were detected at 3q (75%), 8q23-qter (50%), 11q13 (44%), 5p14-pter (25%), 20q (25%), 7q (22%), 2p (19%), 12p (17%), and 20p (17%) and losses were detected at 18q (58%), 3p (50%), 9p (44%), 5q14-23 (39%), 4q (33%), 13q (22%), and 11q22-qter (19%). DNA amplifications were detected at four loci: 11q13, 2q12, 7q21, and 20q11.2 It is interesting to note that the gains of 8q23-qter (P < 0.0005) and 20q (P < 0.02) and loss of 11q22-qter (P < 0.05) were observed in tumors metastatic to the lymph nodes. The gains of 3q and 11q13 and losses of 18q, 3p, 9p, 5q14-23, and 4q were detected in both early and advanced stage ESCCs. CONCLUSIONS: These observations suggest that gains of 8q23-qter and 20q and loss of 11q22-qter allow the prediction of lymph node metastasis, and that gains of 3q and 11q13 and losses of 18q, 3p, 9p, 5q14-23, and 4q are associated with the development of ESCC.     

Chromosomal aberrations detected by comparative genomic hybridization predict outcome in patients with colorectal carcinoma

To obtain comprehensive information regarding the correlation between genomic changes and clinicopathological parameters such as disease stage, metastases, and survival, we investigated genomic changes by comparative genomic hybridization (CGH) in 73 patients with colorectal cancer (CRC), and assessed the associations of such charges with clinicopathological parameters. Gains of 8q21-22, 13q21-31 and 20q12-qter and loss of 17p12-pter were detected in >50% of stage I tumors. Gain of 8q23-qter and losses of 8p12-pter and 18q12-qter were observed more frequently in stage III/IV tumors than in stage I tumors (all P<0.05). Loss of 8p12-pter and gain of 8q23-qter were linked to nodal metastasis (all P<0.05). Loss of 18q12-qter and gain of 8q23-qter were associated with distant organ metastasis at diagnosis and/or recurrence after surgery (all P<0.05). Moreover, losses of 8p12-pter and 18q12-qter and gains of 8q23 and 8q24-qter were associated significantly with unfavorable prognosis (all P<0.05). Furthermore, combined examination of the above four changes can provide a more accurate assessment for patient's prognosis. Specifically, 11 of 19 patients with these four changes died, but only 1 of 21 cases without these four changes died during the follow-up period (P<0.0001). Multivariate analysis revealed that loss of 18q12-qter is an independent prognostic marker (P=0.031). Our findings indicate that genetic aberrations detected by CGH may predict outcome in patients with CRC.     

Gain of 5p15 detected by comparative genomic hybridization as an independent marker of poor prognosis in patients with esophageal squamous cell carcinoma.

Comparative genomic hybridization was applied to 51 primary esophageal squamous cell carcinomas (ESCCs) to clarify the relation between DNA sequence copy number aberrations (DSCNAs) and the clinicopathology of the disease. The average number of DSCNAs was 10.9 DSCNAs/tumor (6.1 gains and 4.9 losses), ranging from 1-30 DSCNAs/tumor. Gain of 3q26-qter and loss of 18q22-qter were detected in >60% of stage I tumors and considered to play an important role in the development of ESCC. Whereas gain of 8q24-qter was observed in 82.6% (19 of 23) of stage III and IV cancers, it was seen in 27.3% (3 of 11) of stage I tumors. It is suggested that gain of 8q24-qter plays an important role in tumor progression. Gains of 8q24-qter and 20q12-qter and loss of 11q22-23 were linked to nodal metastasis (P = 0.0006, 0.002, and 0.02, respectively). Gains of 5p15 and 14q21 were associated with distant organ metastasis after surgery (P = 0.006 and 0.02, respectively). These observations suggest that nodal and distant organ metastases involve different genes. Gains of 5p15, 8q24-qter, and 14q21 were significantly associated with unfavorable prognosis (P = 0.0002, 0.007, and 0.04, respectively). Multivariate analysis revealed the 5p15 gain to be an independent prognostic marker with a higher significance than that of nodal status (risk ratio = 5.95; P = 0.001). The present findings indicate that comparative genomic hybridization analysis may be used to predict the likelihood of a poor or favorable outcome in cases of ESCC.     

大肠癌染色体组DNA拷贝数异常的临床病理学意义

目的分析大肠癌染色体组DNA拷贝数异常区域与患者临床病理特征的关系。方法应用比较基因组杂交技术（CGH）检测73例大肠癌患者的标本。结果大肠癌染色体8p12-pter丢失和8q23-qter扩增与淋巴结转移显著相关;而8q23-qter扩增和18q12-qter丢失与远处器官转移和（或）术后复发显著相关;8q23-qter扩增、8p12-pter和18q12-qter丢失,与大肠癌患者不良预后密切相关。Cox多因素分析表明,18q12-qter丢失在大肠癌是一个独立的不良预后生物学指标。结论采用CGH法检测染色体组DNA拷贝数异常能预测大肠癌患者的预后,并为临床治疗提供有意义的信息。     

Frequent gains of 20q and losses of 18q are associated with lymph node metastasis in intestinal-type gastric cancer

BACKGROUND: The genetic aberrations associated with development and progression of gastric carcinomas (GCs) are poorly understood. The aim of this study was to identify chromosomal aberrations associated with the development and/or progression of intestinal-type GC. MATERIALS AND METHODS: Comparative genomic hybridization (CGH) analysis was applied to 36 intestinal-type GCs. We compared chromosomal aberrations detected by CGH analysis with clinicopathological parameters. RESULTS: Frequent gains of DNA copy number were found on 8q, 13q, 20q, 3q, 6q and losses were found on 17p, 18q in intestinal-type GCs. No significant differences were observed in the chromosomal aberrations between tumor stage, tumor location, peritoneal dissemination, liver metastasis or other distant metastasis. However, the frequencies of 20q12-13 gain and 18q21-22 loss were significantly higher in tumors with lymph node metastasis than in those without metastasis. CONCLUSION: Gains of 20q and losses of 18q may contribute to lymph node metastasis and the malignant phenotype in intestinal-type GCs.     

Chromosomal abnormalities associated with neck nodal metastasis in nasopharyngeal carcinoma.

Neck lymphatic metastasis represents the single most important clinical prognostic factor in nasopharyngeal carcinoma (NPC), but underlying genetic mechanisms remain ill defined. In this study 23 samples of primary tumor (PT) and 9 of neck lymph node metastasis (NLNM) obtained from NPC patients were analyzed by comparative genomic hybridization (CGH) coupled with tissue microdissection and degenerate oligonucleotide primer-polymerase chain reaction (DOP-PCR). A similar pattern of chromosomal abnormalities was seen in PT and NLNM, the common aberrations were gains on 5p, 12p, 12q and 18p and deletions on 1p, 3p, 9q, 14q, 17p and 16q. However, NLNMs, but not PTs, also exhibited frequent losses on 9p, 16p, 17q, 20q, 21p, 21q and 22q and gains on 8q and 8p. The most frequent unique aberration in NLNMs was loss on 16p, observed in 100% (9/9) NLNMs tested, as well as loss of 20q, observed in 77.8% of tumors tested. For the first time, we report that a gain on 8p and a loss at 20q is common to NLNMs. The analysis furthermore suggests that specific alterations, e.g. losses of 9p, 16p, 7q, 20q, 21p, 21q, 22q and gains on 8q and 8p are associated with NLNM of NPC, and that these alterations may be involved in the onset and/or progression of a metastatic phenotype.     

Gains in chromosomes 7, 8q, 15q and 17q are characteristic changes in malignant but not in benign peripheral nerve sheath tumors from patients with Recklinghausen's disease

In order to investigate typical genomic alterations in patients with Recklinghausen's disease (NF1) we studied one from each of the six patients with NF1 several benign and/or malignant tumors. By means of comparative genomic hybridization (CGH) gained results from six benign neurofibromas and 14 malignant peripheral nerve sheath tumors (MPNSTs) were compared with four benign peripheral nerve sheath tumors (BPNSTs) from patients without NF1. In all 14 MPNSTs DNA sequence copy number changes were detected with a mean value of 13.5 imbalances per sample. The most frequent gains were in 8q, 17q (12 tumors each), 7p, 15q (ten tumors each), and 7q (nine tumors). We found ten high-level amplifications in nine of the 14 samples. In two cases, the high-level amplification involved 7p14-pter and 17q24-qter as well. The most frequent loss was in 17p (seven tumors). The benign neurofibromas from NF1-patients and the sporadic BPNSTs revealed only partially DNA sequence copy number changes without any distinct pattern. The gains of #7, 8q, 15q, and 17q were found exclusively in MPNSTs but not in neurofibromas and are supposed to be associated with malignant tumor progression. In comparison of the results of the 14 MPNSTs from NF1-patients with the results of previously published 20 sporadic MPNSTs, we found that the gain of 8q occurs most frequently in both tumor groups. Of course additionally in the sporadic MPNSTs there were more frequent gains of 5p, #6, and statistically significant gains of 20q. On the other hand in the MPNSTs from NF1-patients the most frequent gains were found in #7, and statistically significant in 15q, and 17q.     

食管癌原发灶与淋巴结转移灶细胞染色体变化特征的比较

背景与目的:食管癌早期可发生局部淋巴或血行转移,这是导致复发和预后差的主要原因。但是,食管癌转移发生的分子机制尚不清楚。本研究旨在分析食管癌原发灶和淋巴结转移灶肿瘤细胞染色体变化的特征,寻找或定位与食管癌转移相关基因,加深对其转移机制的了解。方法:应用比较基因组杂交技术(comparativegenomichybridization,CGH)分析15例食管癌患者原发灶和其对应的淋巴结转移灶的染色体基因组改变。结果:最常见染色体DNA拷贝数增加的部位是3q,8q,6p,20p,5p,18p,2p,2q,1q;常见的染色体DNA拷贝数丢失的部位是10p,10q,17p,18q,4p,13q。其中,最有意义的发现是6p增加(原发灶:2/15,13%,转移灶:7/15,47%),20p增加(原发灶:5/15,33.3%,转移灶:11/15,73.3%)。第二个发现是10p丢失(原发灶:2/15,13.3%,转移灶:8/15,53%),10q丢失(原发灶:2/15,13.3%,转移灶:7/15,46.6%)。结论:食管癌原发灶和淋巴结转移灶细胞染色体基因组改变最显著的部位是6p,20p的增加和10p,10q的丢失;这些部位可能存在与食管癌细胞淋巴结转移相关的基因。     

Chromosomal alterations in the clonal evolution to the metastatic stage of squamous cell carcinomas of the lung

Comparative genomic hybridization (CGH) was applied to squamous cell carcinomas (SCC) of the lung to define chromosomal imbalances that are associated with the metastatic phenotype. In total, 64 lung SCC from 50 patients were investigated, 25 each with or without evidence of metastasis formation. The chromosomal imbalances summarized by a CGH histogram of the 50 cases revealed deletions most frequently on chromosomes 1p21-p31, 2q34-q36, 3p, 4p, 4q, 5q, 6q14-q24, 8p, 9p, 10q, 11p12-p14, 13q13-qter, 18q12-qter and 21q21. DNA over-representations were most pronounced for chromosomes 1q11-q25, 1q32-q41, 3q, 5p, 8q22-qter, 11q13, 12p, 17q21-q22, 17q24-q25, 19, 20q and 22q. In ten cases, paired samples of primaries and at least one metastasis were analysed. The comparison revealed a considerable chromosomal instability and genetic heterogeneity; however, the CGH pattern indicated a clonal relationship in each case. The difference in histograms from the metastatic and non-metastatic tumour groups was most useful in pinpointing chromosomal imbalances associated with the metastatic phenotype, indicating that the deletions at 3p12-p14, 3p21, 4p15-p16, 6q24-qter, 8p22-p23, 10q21-qter and 21q22, as well as the over-representations at 1q21-q25, 8q, 9q34, 14q12 and 15q12-q15, occurred significantly more often in the metastatic tumour group. The comparison of the paired samples confirmed these findings in individual cases and suggested distinct genetic changes, in particular the extension of small interstitial deletions, during tumour progression. Importantly, metastasis-associated lesions were frequently detectable in the primary tumour providing a method of identifying patients at risk for tumour dissemination. Individual profiles and histograms are accessible at our web site http://amba.charite.de/cgh.     

Detection of chromosomal alterations in bladder transitional cell carcinomas from Northern China by comparative genomic hybridization

To identify chromosome alterations in Chinese bladder cancer, forty-six transitional cell carcinomas of the bladder were analyzed by comparative genomic hybridization. Frequent gains of DNA copy number were observed on 1p (13/46), 1q (13/46), 5p (8/46), 6p (9/46), 7p (7/46), 8q (12/46), 11q (8/46), 17q (11/46), 19q (7/46), 20q (8/46) and Yq (8/46), with minimal overlapping regions at 1p32-pter (10/46), 1q21-q24 (12/46), 5p (8/46), 6p22-p23 (7/46), 7p11.2-p14 (7/46), 8q22-q24 (12/46), 11q13-q14 (8/46), 17q22-qter (11/46), 19q11-13.2 (7/46), 20q11-q13.2 (8/46) and Yq11 (8/46). Losses were predominantly found on 2q (16/46), 5q (8/46), 8p (7/46), 9p (8/46), 9q (13/46), 11p (7/46), 13q (7/46), 17p (12/46), 18q (7/46), Xp (18/46) and Xq (19/46), with smallest overlapping regions at 2q32-qter (16/46), 5q12-q31 (8/46), 8p12-pter (7/46), 9p21-pter (10/46), 9q (13/46), 11p (7/46), 13q13-q22 (7/46), 17p (12/46), 18q21-qter (7/46), Xp (18/46) and Xq (19/46). There were significantly higher frequencies of gains of 1q21-q24 and 17q22-qter in moderately differentiated tumors as compared with those in well-differentiated tumors, indicating a possible association of these two abnormalities with the dedifferentiation of tumor cells. Gains of 1p32-pter, 5p, 6p22-p23, 11q13-q14, 17q22-qter and losses of 2q32-qter, 9q, 17p were more frequent in pT1 as compared with those in pTa carcinomas. Gains at 1q21-q24, 7p11.2-p14, 8q22-q24, 19q, 20q11-q13.2 and losses at 5q12-q31, 8p12-pter, 9p21-pter, 11p, 13q13-q22 and 18q21-qter were unique to pT1 and higher stage tumors, suggesting that genes responsible for the invasion and progression of bladder cancer might be located at these chromosomal regions. In multiple tumors from the same patients, consistent alterations such as gains of 8q, 11q13-q14, 12q13-q15, 13q12, 20q and losses of 2q32-qter, 8p, 9, 11p, 11q21-qter, 13q13-qter, X were detected. These abnormalities were possibly earlier events, which might play a critical role during the genesis of the tumors. Further detailed studies to the recurrent aberration regions may lead to the identification of oncogenes and tumor suppressor genes involved in the development and progression of Chinese bladder cancer.     

Characterization of genetic rearrangements in esophageal squamous carcinoma cell lines by a combination of M-FISH and array-CGH: further confirmation of some split genomic regions in primary tumors

ABSTRACT: BACKGROUND: Chromosomal and genomic aberrations are common features of human cancers. However, chromosomal numerical and structural aberrations, breakpoints and disrupted genes have yet to be identified in esophageal squamous cell carcinoma (ESCC). METHODS: Using multiplex-fluorescence in situ hybridization (M-FISH) and oligo array-based comparative hybridization (array-CGH), we identified aberrations and breakpoints in six ESCC cell lines. Furthermore, we detected recurrent breakpoints in primary tumors by dual-color FISH. RESULTS: M-FISH and array-CGH results revealed complex numerical and structural aberrations. Frequent gains occurred at 3q26.33-qter, 5p14.1-p11, 7pter-p12.3, 8q24.13-q24.21, 9q31.1-qter, 11p13-p11, 11q11-q13.4, 17q23.3-qter, 18pter-p11, 19 and 20q13.32-qter. Losses were frequent at 18q21.1-qter. Breakpoints that clustered within 1 or 2 Mb were identified, including 9p21.3, 11q13.3-q13.4, 15q25.3 and 3q28. By dual-color FISH, we observed that several recurrent breakpoint regions in cell lines were also present in ESCC tumors. In particular, breakpoints clustered at 11q13.3-q13.4 were identified in 43.3% (58/134) of ESCC tumors. Both 11q13.3-q13.4 splitting and amplification were significantly correlated with lymph node metastasis (LNM) (P = 0.004 and 0.022) and advanced stages (P = 0.004 and 0.039). Multivariate logistic regression analysis revealed that only 11q13.3-q13.4 splitting was an independent predictor for LNM (P = 0.026). CONCLUSIONS: The combination of M-FISH and array-CGH helps produce more accurate karyotypes. Our data provide significant, detailed information for appropriate uses of these ESCC cell lines for cytogenetic and molecular biological studies. The aberrations and breakpoints detected in both the cell lines and primary tumors will contribute to identify affected genes involved in the development and progression of ESCC.     

Comparative genomic hybridization of esophageal squamous cell carcinoma: correlations between chromosomal aberrations and disease progression/prognosis.

BACKGROUND: Esophageal carcinoma is a major cause of cancer-related deaths among males in Taiwan. However, to date, the genetic alterations that accompany this lethal disease are not understood. METHODS: Chromosomal aberrations of 46 samples of esophageal squamous cell carcinoma (EC-SCC) were analyzed by comparative genomic hybridization (CGH), and their correlations with pathologic staging and prognosis were analyzed statistically. RESULTS: In total, 321 gains and 252 losses were found in 46 tumor samples; thus, the average gains and losses per patient were 6.98 and 5.47, respectively. Frequent gain abnormalities were found on chromosome arms 1q, 2q, 3q, 5p, 7p, 7q, 8q, 11q, 12p, 12q, 14q, 17q, 20q, and Xq. Frequent deletions were found on chromosome arms 1p, 3p, 4p, 5q, 8p, 9p, 9q, 11q, 13q, 16p, 17p, 18q, 19p, and 19q. It was found that deletions of 4p and 13q12-q14 and gain of 5p were significantly correlated with pathologic staging. Losses of 8p22-pter and 9p also were found more frequently in patients with advanced disease. Gain of 8q24-qter was seen more frequently in patients with Grade 3 tumors. A univariate analysis found that pathologic staging; gains of 5p and 7q; and deletions of 4p, 9p, and 11q were significant prognostic factors. However, pathologic staging became the only significant factor in a multivariate analysis. CONCLUSIONS: CGH not only revealed novel chromosomal aberrations in EC-SCC, but also found possible genotypic changes associated with disease progression. Despite all of the possible associations of chromosomal aberrations with disease progression, the most important prognostic factor for patients with EC-SCC was pathologic staging.     

Gain of chromosome 8q23-24 is a predictive marker for lymph node positivity in colorectal cancer.

PURPOSE: The prognosis of patients with colorectal cancer is largely determined by tumor stage. In this respect, colorectal cancers with lymph node metastases indicate a worse prognosis versus lymph node-negative tumors. Accordingly, there is considerable clinical interest in understanding the genetic mechanisms underlying metastasis formation. Furthermore, sensitive and specific biomarkers are needed to predict the metastatic phenotype at the time of diagnosis. EXPERIMENTAL DESIGN: Fifty colorectal cancers with or without lymph node metastases were assessed for genomic imbalances by comparative genomic hybridization. Particular interest was focused on whether specific chromosomal alterations exist in primary tumors that might be indicative and specific for the metastatic phenotype. RESULTS: The analysis revealed that lymph node-positive colorectal cancers show a higher degree of chromosomal instability than lymph node-negative cancers (average number of chromosomal copy alterations, 9.8 versus 7.5). Chromosomal alterations commonly described in colorectal cancers such as gain of 20q or loss of 18q21 were not different. However, the gain of chromosomal region 8q23-24 was seen in the vast majority of lymph node-positive cancers, whereas it was rather rare in lymph node-negative carcinomas (P = 0.0016). CONCLUSIONS: These data suggest that genes located at 8q23-24 might favor the development of lymphatic metastases in colorectal cancers. Additionally, the gain of this region could be used to predict the metastatic potential of primary colorectal cancers.     

Frequent gains and losses of specific chromosome segments in human ovarian carcinomas shown by comparative genomic hybridization

Total genomic DNA obtained from 24 ovarian carcinomas was examined for genomic imbalances by comparative genomic hybridization (CGH). A varying number of gains and losses (1 up to 31) of specific chromosomal segments was detected per tumor. Chromosomal segments which were most often present in increased copy numbers were (in decreasing order): 1q21, 8q24, 8q23, 3q26, 12p12-p13, 20q, 7q31, and 7q33-qter. Loss of material was found most frequently at 16q12, 13q13-q14, Xq, 8p21-p22, 5q13-q14, and 5q21. All these chromosomal segments involved in gains and losses may carry gene loci playing a more or less causal role in the process of ovarian malignancies. Based on these findings CGH can be regarded as a valuable tool for rapid screening of genomic imbalances in human tumors.     

Genetic differences between primary larynx and pharynx carcinomas and their matched lymph node metastases by multiplex ligation-dependent probe amplification

Lymph nodes metastasis is a major risk factor related to poor survival in larynx and pharynx carcinomas. The aim of this study is to search for markers of lymph node involvement analyzing the genetic differences between primary larynx and pharynx squamous cell carcinomas and their corresponding lymph node metastases. Twenty-five primary tumors and their corresponding lymph node metastases were examined. DNA copy number changes of 37 genes were analyzed by multiplex ligation-dependent probe amplification (MLPA). Loss of CDKN2A (9p21) occurred in 14 out of 25 pairs (56%) of primary tumor and lymph node metastases. Loss of LMNA (1q21) was exclusively detected in 8 lymph node samples (32%). Loss of CTNNB1 (3p22) and gain of CDKN2D (19p13) were also significantly more frequent in lymph node metastases. Other aberrations related to lymph node metastases were loss of MFHAS1 (8p23), RECQL4 (8q24) and gain of N33 (8p22) and TP53 (17p13). Primary tumor and corresponding lymph node metastases showed common genetic changes. However, the lymph node metastases presented with a number of additional alterations. Acquisition of these alterations may play a role in lymphatic metastasis development.     

Comparative Genomic Hybridization (CGH) Analysis of Chromosomal Aberrations in Iranian Patients with Invasive Ductal Carcinoma Breast Cancer.

Introduction: Breast cancer is one of the most common cancers in women; however, due to the complexity of chromosomal changes, limited data are available regarding chromosomal constitution. Materials and Methods: In this study, Comparative Genomic Hybridization (CGH) was used on 16 Iranian patients diagnosed with invasive ductal breast carcinomas. Results: 12 samples had abnormal CGH results (75%), including 21 types of chromosomal imbalance. The most prevalent were chromosomal gain of +1q, +17q, +8q and chromosomal loss of -13q. All three cases with DNA loss at chromosome 13q (-13q) had lymph node metastasis. Conclusions: CGH is able to detect chromosomal abnormalities which are difficult to identify by conventional cytogenetic techniques. More studies on a larger sample size may help to confirm or rule out any possible correlation between 13q monosomy and lymph node metastasis, which could result in establishing new strategies for prevention and early detection of invasive breast tumors.     

Recurrent DNA copy number changes in 1q, 4q, 6q, 9p, 13q, 14q and 22q detected by comparative genomic hybridization in malignant mesothelioma.

Comparative genomic hybridization (CGH) analyses were performed on 27 human pleural mesothelioma tumour specimens, consisting of 18 frozen tumours and nine paraffin-embedded tumours, to screen for gains and losses of DNA sequences. Copy number changes were detected in 15 of the 27 specimens with a range from one to eight per specimen. On average, more losses than gains of genetic material were observed. The loss of DNA sequences occurred most commonly in the short arm of chromosome 9 (p21-pter), in 60% of the abnormal specimens. Other losses among the abnormal specimens were frequently detected in the long arms of chromosomes 4 (q31.1-qter, 20%), 6 (q22-q24, 33%), 13 (33%),14 (q24-qter, 33%) and 22 (q13, 20%). A gain in DNA sequences was found in the long arm of chromosome 1 (cen-qter) in 33% of the abnormal specimens. Our analysis is the first genome-wide screening for gains and losses of DNA sequences using comparative genomic hybridization in malignant pleural mesothelioma tumours. The recurrent DNA sequence changes detected in this study suggest that the corresponding chromosomal areas most probably contain genes important for the initiation and progression of mesothelioma.     

Genetic aberrations detected by comparative genomic hybridization in ovarian clear cell adenocarcinomas

Genetic abnormalities were detected by comparative genomic hybridization (CGH) in 12 ovarian clear cell adenocarcinomas. DNA sequence copy number abnormalities (CNAs) occurring in more than 20% of the cancers included increased copy numbers of 8q11-q13, 8q21-q22, 8q23, 8q24-qter, 17q25-qter, 20q13-qter and 21q22-qter and reduced copy numbers of 19p. Increases in copy numbers of 8q11-q13, 8q21-q22, 8q23 and 8q24-qter occurred more frequently in disease-free patients than in recurrent/non-surviving patients (p < 0.05). However, increases in copy numbers of 17q25-qter and 20q13-qter occurred more frequently in recurrent/non-surviving patients than in disease-free patients (p < 0.05). Furthermore, increases in copy numbers of 17q25-qter and 20q13-qter occurred together (p < 0.05). Additionally, there were negative correlations between increases in copy numbers of 8q21-q22 and 17q25-qter, and between 8q21-q22 and 20q13-qter (p < 0.05). It appears that ovarian clear cell adenocarcinomas can be classified into two subtypes, one being cancer with an increase in copy numbers of 8q and the other being cancer with increases in copy numbers of 17q25-qter and 20q13-qter.     

Breast cancer in young women (< or = 35 years): Genomic aberrations detected by comparative genomic hybridization

Sporadic breast cancer in young women is different from the one in older patients regarding pathological features and aggressiveness of the tumors, but the spectrum of genetic alterations are largely unknown. We used comparative genomic hybridization (CGH) to analyze DNA copy number changes in 88 tumor samples from women 相似文献