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Genomic Profiling of Submucosal-Invasive Gastric Cancer by Array-Based Comparative Genomic Hybridization  [PDF]
Akiko Kuroda,Yoshiyuki Tsukamoto,Lam Tung Nguyen,Tsuyoshi Noguchi,Ichiro Takeuchi,Masahiro Uchida,Tomohisa Uchida,Naoki Hijiya,Chisato Nakada,Tadayoshi Okimoto,Masaaki Kodama,Kazunari Murakami,Keiko Matsuura,Masao Seto,Hisao Ito,Toshio Fujioka,Masatsugu Moriyama
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0022313
Abstract: Genomic copy number aberrations (CNAs) in gastric cancer have already been extensively characterized by array comparative genomic hybridization (array CGH) analysis. However, involvement of genomic CNAs in the process of submucosal invasion and lymph node metastasis in early gastric cancer is still poorly understood. In this study, to address this issue, we collected a total of 59 tumor samples from 27 patients with submucosal-invasive gastric cancers (SMGC), analyzed their genomic profiles by array CGH, and compared them between paired samples of mucosal (MU) and submucosal (SM) invasion (23 pairs), and SM invasion and lymph node (LN) metastasis (9 pairs). Initially, we hypothesized that acquisition of specific CNA(s) is important for these processes. However, we observed no significant difference in the number of genomic CNAs between paired MU and SM, and between paired SM and LN. Furthermore, we were unable to find any CNAs specifically associated with SM invasion or LN metastasis. Among the 23 cases analyzed, 15 had some similar pattern of genomic profiling between SM and MU. Interestingly, 13 of the 15 cases also showed some differences in genomic profiles. These results suggest that the majority of SMGCs are composed of heterogeneous subpopulations derived from the same clonal origin. Comparison of genomic CNAs between SMGCs with and without LN metastasis revealed that gain of 11q13, 11q14, 11q22, 14q32 and amplification of 17q21 were more frequent in metastatic SMGCs, suggesting that these CNAs are related to LN metastasis of early gastric cancer. In conclusion, our data suggest that generation of genetically distinct subclones, rather than acquisition of specific CNA at MU, is integral to the process of submucosal invasion, and that subclones that acquire gain of 11q13, 11q14, 11q22, 14q32 or amplification of 17q21 are likely to become metastatic.
CGI: Java Software for Mapping and Visualizing Data from Array-based Comparative Genomic Hybridization and Expression Profiling
Joyce Xiuweu-Xu Gu,Michael Yang Wei,Pulivarthi H. Rao,Ching C. Lau
Gene Regulation and Systems Biology , 2007,
Abstract: With the increasing application of various genomic technologies in biomedical research, there is a need to integrate these data to correlate candidate genes/regions that are identified by different genomic platforms. Although there are tools that can analyze data from individual platforms, essential software for integration of genomic data is still lacking. Here, we present a novel Java-based program called CGI (Cytogenetics-Genomics Integrator) that matches the BAC clones from array-based comparative genomic hybridization (aCGH) to genes from RNA expression profiling datasets. The matching is computed via a fast, backend MySQL database containing UCSC Genome Browser annotations. This program also provides an easy-to-use graphical user interface for visualizing and summarizing the correlation of DNA copy number changes and RNA expression patterns from a set of experiments. In addition, CGI uses a Java applet to display the copy number values of a specifi c BAC clone in aCGH experiments side by side with the expression levels of genes that are mapped back to that BAC clone from the microarray experiments. The CGI program is built on top of extensible, reusable graphic components specifically designed for biologists. It is cross-platform compatible and the source code is freely available under the General Public License.
Genomic Profiling of Oral Squamous Cell Carcinoma by Array-Based Comparative Genomic Hybridization  [PDF]
Shunichi Yoshioka, Yoshiyuki Tsukamoto, Naoki Hijiya, Chisato Nakada, Tomohisa Uchida, Keiko Matsuura, Ichiro Takeuchi, Masao Seto, Kenji Kawano, Masatsugu Moriyama
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056165
Abstract: We designed a study to investigate genetic relationships between primary tumors of oral squamous cell carcinoma (OSCC) and their lymph node metastases, and to identify genomic copy number aberrations (CNAs) related to lymph node metastasis. For this purpose, we collected a total of 42 tumor samples from 25 patients and analyzed their genomic profiles by array-based comparative genomic hybridization. We then compared the genetic profiles of metastatic primary tumors (MPTs) with their paired lymph node metastases (LNMs), and also those of LNMs with non-metastatic primary tumors (NMPTs). Firstly, we found that although there were some distinctive differences in the patterns of genomic profiles between MPTs and their paired LNMs, the paired samples shared similar genomic aberration patterns in each case. Unsupervised hierarchical clustering analysis grouped together 12 of the 15 MPT-LNM pairs. Furthermore, similarity scores between paired samples were significantly higher than those between non-paired samples. These results suggested that MPTs and their paired LNMs are composed predominantly of genetically clonal tumor cells, while minor populations with different CNAs may also exist in metastatic OSCCs. Secondly, to identify CNAs related to lymph node metastasis, we compared CNAs between grouped samples of MPTs and LNMs, but were unable to find any CNAs that were more common in LNMs. Finally, we hypothesized that subpopulations carrying metastasis-related CNAs might be present in both the MPT and LNM. Accordingly, we compared CNAs between NMPTs and LNMs, and found that gains of 7p, 8q and 17q were more common in the latter than in the former, suggesting that these CNAs may be involved in lymph node metastasis of OSCC. In conclusion, our data suggest that in OSCCs showing metastasis, the primary and metastatic tumors share similar genomic profiles, and that cells in the primary tumor may tend to metastasize after acquiring metastasis-associated CNAs.
Genome profiling of ovarian adenocarcinomas using pangenomic BACs microarray comparative genomic hybridization
Donatella Caserta, Moncef Benkhalifa, Marina Baldi, Francesco Fiorentino, Mazin Qumsiyeh, Massimo Moscarini
Molecular Cytogenetics , 2008, DOI: 10.1186/1755-8166-1-10
Abstract: We applied microarray comparative genomic hybridization (A-CGH) using one mega base BAC arrays to investigate chromosomal disorders in ovarian adenocarcinoma in patients with familial history.Our data on 10 cases of ovarian cancer revealed losses of 6q (4 cases mainly mosaic loss), 9p (4 cases), 10q (3 cases), 21q (3 cases), 22q (4 cases) with association to a monosomy X and gains of 8q and 9q (occurring together in 8 cases) and gain of 12p. There were other abnormalities such as loss of 17p that were noted in two profiles of the studied cases. Total or mosaic segmental gain of 2p, 3q, 4q, 7q and 13q were also observed. Seven of 10 patients were investigated by FISH to control array CGH results. The FISH data showed a concordance between the 2 methods.The data suggest that A-CGH detects unique and common abnormalities with certain exceptions such as tetraploidy and balanced translocation, which may lead to understanding progression of genetic changes as well as aid in early diagnosis and have an impact on therapy and prognosis.A number of strategies have been used for early detection of ovarian cancer and follow-up. CA-125 tumor marker investigation and trans vaginal ultrasound are the most common used procedures [1,2]. An increase of CA-125 marker has been shown to predate clinical or scan evidence of relapse in approximately 70% of patient with ovarian cancer [3]. For Genome disorders investigation classical cytogenetic, fluorescence in situ hybridization and comparative genome hybridization methods were applied in cancers [4-6]. Recent studies suggest that genomic changes can be useful for cancer grading [7]. For example, a study by Simon et al. [8] showed that breakpoints in regions 1p3 and 11p1 are important early events and distinguish a class of tumors associated with poor prognosis in ovarian adenocarcinoma. Genomic changes in ovarian cancers were investigated by using various techniques, each with its own limitations. For example fluorescence in situ hybrid
Genomic profiling using array comparative genomic hybridization define distinct subtypes of diffuse large b-cell lymphoma: a review of the literature  [cached]
Tirado Carlos A,Chen Weina,García Rolando,Kohlman Kelly A
Journal of Hematology & Oncology , 2012, DOI: 10.1186/1756-8722-5-54
Abstract: Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin Lymphoma comprising of greater than 30% of adult non-Hodgkin Lymphomas. DLBCL represents a diverse set of lymphomas, defined as diffuse proliferation of large B lymphoid cells. Numerous cytogenetic studies including karyotypes and fluorescent in situ hybridization (FISH), as well as morphological, biological, clinical, microarray and sequencing technologies have attempted to categorize DLBCL into morphological variants, molecular and immunophenotypic subgroups, as well as distinct disease entities. Despite such efforts, most lymphoma remains undistinguishable and falls into DLBCL, not otherwise specified (DLBCL-NOS). The advent of microarray-based studies (chromosome, RNA, gene expression, etc) has provided a plethora of high-resolution data that could potentially facilitate the finer classification of DLBCL. This review covers the microarray data currently published for DLBCL. We will focus on these types of data; 1) array based CGH; 2) classical CGH; and 3) gene expression profiling studies. The aims of this review were three-fold: (1) to catalog chromosome loci that are present in at least 20% or more of distinct DLBCL subtypes; a detailed list of gains and losses for different subtypes was generated in a table form to illustrate specific chromosome loci affected in selected subtypes; (2) to determine common and distinct copy number alterations among the different subtypes and based on this information, characteristic and similar chromosome loci for the different subtypes were depicted in two separate chromosome ideograms; and, (3) to list re-classified subtypes and those that remained indistinguishable after review of the microarray data. To the best of our knowledge, this is the first effort to compile and review available literatures on microarray analysis data and their practical utility in classifying DLBCL subtypes. Although conventional cytogenetic methods such as Karyotypes and FISH have played a major role in classification schemes of lymphomas, better classification models are clearly needed to further understanding the biology, disease outcome and therapeutic management of DLBCL. In summary, microarray data reviewed here can provide better subtype specific classifications models for DLBCL.
Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization (aCGH): revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma
Chung-Che Chang, Xiaobo Zhou, Jesalyn J Taylor, Wan-Ting Huang, Xianwen Ren, Federico Monzon, Yongdong Feng, Pulivarthi H Rao, Xin-Yan Lu, Facchetti Fabio, Susan Hilsenbeck, Chad J Creighton, Elaine S Jaffe, Ching-Ching Lau
Journal of Hematology & Oncology , 2009, DOI: 10.1186/1756-8722-2-47
Abstract: Examination of genomic data in PL revealed that the most frequent segmental gain (> 40%) include: 1p36.11-1p36.33, 1p34.1-1p36.13, 1q21.1-1q23.1, 7q11.2-7q11.23, 11q12-11q13.2 and 22q12.2-22q13.3. This correlated with segmental gains occurring in high frequency in DLBCL (AIDS-related and non AIDS-related) cases. There were some segmental gains and some segmental loss that occurred in PL but not in the other types of lymphoma suggesting that these foci may contain genes responsible for the differentiation of this lymphoma. Additionally, some segmental gains and some segmental loss occurred only in PL and AIDS associated DLBCL suggesting that these foci may be associated with HIV infection. Furthermore, some segmental gains and some segmental loss occurred only in PL and PCM suggesting that these lesions may be related to plasmacytic differentiation.To the best of our knowledge, the current study represents the first genomic exploration of PL. The genomic aberration pattern of PL appears to be more similar to that of DLBCL (AIDS-related or non AIDS-related) than to PCM. Our findings suggest that PL may remain best classified as a subtype of DLBCL at least at the genome level.Plasmablastic lymphoma (PL), one of the most frequent oral malignancies in human immunodeficiency virus (HIV) infected patients, was first characterized by Delecluse et al [1]. They proposed that this constituted a new subtype of diffuse large B cell lymphoma (DLBCL); it was suggested as a distinct entity based on its blastic morphology, its clinical behavior involving predominantly extramedullary sites (particularly oral cavity), and its limited antigenic phenotype data suggesting differentiation toward plasmacytic differentiation (CD20-, CD79a+ and VS38c+). The incidence of PL has increased following the introduction of highly active antiretroviral therapy (HAART) [2,3]. By WHO Classification, PL is categorized as a subtype of DLBCL associated with HIV and Epstein-Barr virus [1,4,5].Recent morph
Genomic profiling distinguishes familial multiple and sporadic multiple meningiomas
Yiping Shen, Fabio Nunes, Anat Stemmer-Rachamimov, Marianne James, Gayatry Mohapatra, Scott Plotkin, Rebecca A Betensky, David A Engler, Jennifer Roy, Vijaya Ramesh, James F Gusella
BMC Medical Genomics , 2009, DOI: 10.1186/1755-8794-2-42
Abstract: We compared 73 meningiomas presenting as sporadic solitary (64), sporadic multiple (5) and familial multiple (4) tumors using genomic profiling by array comparative genomic hybridization (array CGH).Sporadic solitary meningiomas revealed genomic rearrangements consistent with at least two mechanisms of tumor initiation, as unsupervised cluster analysis readily distinguished tumors with chromosome 22 deletion (associated with loss of the NF2 tumor suppressor) from those without chromosome 22 deletion. Whereas sporadic meningiomas without chromosome 22 loss exhibited fewer chromosomal imbalance events overall, tumors with chromosome 22 deletion further clustered into two major groups that largely, though not perfectly, matched with their benign (WHO Grade I) or advanced (WHO Grades II and III) histological grade, with the latter exhibiting a significantly greater degree of genomic imbalance (P < 0.001). Sporadic multiple meningiomas showed a frequency of genomic imbalance events comparable to the atypical grade solitary tumors. By contrast, familial multiple meningiomas displayed no imbalances, supporting a distinct mechanism for the origin for these tumors.Genomic profiling can provide an unbiased adjunct to traditional meningioma classification and provides a basis for exploring the different genetic underpinnings of tumor initiation and progression. Most importantly, the striking difference observed between sporadic and familial multiple meningiomas indicates that genomic profiling can provide valuable information for differential diagnosis of subjects with multiple meningiomas and for considering the risk for tumor occurrence in their family members.Meningiomas, which arise from arachnoidal cap cells of the leptomeninges, display an annual incidence 5.5 per 100,000, accounting for ~20% of all primary intracranial tumors [1,2]. They may be classified histologically into three grades, according to World Health Organization (WHO) criteria [3]: WHO grade I meningiomas
Microarray Profiling of Mononuclear Peripheral Blood Cells Identifies Novel Candidate Genes Related to Chemoradiation Response in Rectal Cancer  [PDF]
Pablo Palma, Marta Cuadros, Raquel Conde-Muí?o, Carmen Olmedo, Carlos Cano, Inmaculada Segura-Jiménez, Armando Blanco, Pablo Bueno, J. Antonio Ferrón, Pedro Medina
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074034
Abstract: Preoperative chemoradiation significantly improves oncological outcome in locally advanced rectal cancer. However there is no effective method of predicting tumor response to chemoradiation in these patients. Peripheral blood mononuclear cells have emerged recently as pathology markers of cancer and other diseases, making possible their use as therapy predictors. Furthermore, the importance of the immune response in radiosensivity of solid organs led us to hypothesized that microarray gene expression profiling of peripheral blood mononuclear cells could identify patients with response to chemoradiation in rectal cancer. Thirty five 35 patients with locally advanced rectal cancer were recruited initially to perform the study. Peripheral blood samples were obtained before neaodjuvant treatment. RNA was extracted and purified to obtain cDNA and cRNA for hybridization of microarrays included in Human WG CodeLink bioarrays. Quantitative real time PCR was used to validate microarray experiment data. Results were correlated with pathological response, according to Mandard′s criteria and final UICC Stage (patients with tumor regression grade 1–2 and downstaging being defined as responders and patients with grade 3–5 and no downstaging as non-responders). Twenty seven out of 35 patients were finally included in the study. We performed a multiple t-test using Significance Analysis of Microarrays, to find those genes differing significantly in expression, between responders (n = 11) and non-responders (n = 16) to CRT. The differently expressed genes were: BC 035656.1, CIR, PRDM2, CAPG, FALZ, HLA-DPB2, NUPL2, and ZFP36. The measurement of FALZ (p = 0.029) gene expression level determined by qRT-PCR, showed statistically significant differences between the two groups. Gene expression profiling reveals novel genes in peripheral blood samples of mononuclear cells that could predict responders and non-responders to chemoradiation in patients with locally advanced rectal cancer. Moreover, our investigation added further evidence to the importance of mononuclear cells’ mediated response in the neoadjuvant treatment of rectal cancer.
Surgical resection of rectal adenoma: A rapid review  [cached]
Damian Casadesus
World Journal of Gastroenterology , 2009,
Abstract: Transanal excision (TE), endoscopic transanal resection (ETAR) and transanal endoscopic microsurgery (TEM) can be used to remove adenomatous polyps. However, their use is limited by the size or location of the tumor. TE is limited to the lower rectum, TEM offers better access to lesions in the middle and upper rectum, and ETAR is used less frequently than it deserves for resection of rectal lesions.
Genomic alterations in rectal tumors and response to neoadjuvant chemoradiotherapy: an exploratory study
Chiara Molinari, Michela Ballardini, Nazario Teodorani, Massimo Giannini, Wainer Zoli, Ermanno Emiliani, Enrico Lucci, Alessandro Passardi, Paola Rosetti, Luca Saragoni, Massimo Guidoboni, Dino Amadori, Daniele Calistri
Radiation Oncology , 2011, DOI: 10.1186/1748-717x-6-161
Abstract: Forty-eight candidates for neoadjuvant chemoradiotherapy were recruited and their pretherapy biopsies analyzed by array Comparative Genomic Hybridization (aCGH). Pathologic response was evaluated by tumor regression grade.Both Hidden Markov Model and Smoothing approaches identified similar alterations, with a prevalence of DNA gains. Non responsive patients had a different alteration profile from responsive ones, with a higher number of genome changes mainly located on 2q21, 3q29, 7p22-21, 7q21, 7q36, 8q23-24, 10p14-13, 13q12, 13q31-34, 16p13, 17p13-12 and 18q23 chromosomal regions.This exploratory study suggests that an in depth characterization of chromosomal alterations by aCGH would provide useful predictive information on response to neoadjuvant chemoradiotherapy and could help to optimize therapy in rectal cancer patients.The data discussed in this study are available on the NCBI Gene Expression Omnibus [GEO: GSE25885].The benefits of neoadjuvant chemoradiotherapy (NCRT) in rectal cancer are well documented. In particular, preoperative treatment is indicated to downsize tumors in order to achieve tumor-free margins, reduce tumor burden and increase the possibility of conservative surgery, which results in a high rate of sphincter preservation and significant improvement in local disease control and survival [1,2]. However, although complete pathologic response rates of 10-25% can be achieved, more than one third of patients either do not respond or show only modest response to treatment [3].Whilst numerous studies have analyzed the correlation between expression levels of candidate genes and response to therapies [4,5], the predictive role of such genes is controversial and there is still no firm evidence upon which to base treatment strategies [6]. The gene expression profile evaluated by cDNA microarray has recently been found to provide indications about response of rectal tumors to NCRT [7-9], but such preliminary findings require confirmation in larger pa
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