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Results for “expression profiling”

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PubMed2006

Relationship between classic Hodgkin lymphoma and overlapping large cell lymphoma investigated by comparative expressed sequence hybridization expression profiling.

There is a diagnostic grey zone between classic Hodgkin lymphoma (cHL) and some non-Hodgkin lymphoma (NHL), including primary mediastinal B cell lymphoma, diffuse large B cell lymphoma, and anaplastic large cell lymphoma. They all have some morphological and/or phenotypic features in common. To investigate this, we undertook an expression profiling study of these lymphomas using comparative expressed sequence hybridization. This technique detects chromosomal regions that are differentially expressed between a test and a reference tissue in a manner similar to comparative genomic hybridization, and is particularly suitable when the number of informative biopsies is limited. Using this approach, we identified a unique expression profile for all lymphoma types investigated. Unsupervised hierarchical cluster analysis of the acquired data showed that cHL separates from all investigated NHLs, including ALCL-like HL. Moreover, anaplastic lymphoma kinase (ALK)-negative ALCL clustered in a separate branch together with ALCL-like HL. Thus, analysing the neoplastic cells concurrently with their microenvironment, ALK-negative ALCL and ALCL-like HL seem to be related to each other, while cHL constitutes a separate lymphoma entity.

Adolescent↗

PubMed2004

[Alteration of gene expression profiles of cultured embryo rat cortex induced by phenylalanine].

To have more insight into the mechanism of neuronal injury in phenylketonuria patients, gene expression profiles were studied in cell culture of embryonic rat cortical neurons induced by phenylalanine. Randomly chosen cortical cultures for 3 d were treated by 0.9 mmol/L phenylalanine for 12 h. Control group of the same batch was treated with the same volume of medium. Total RNA was extracted and hybridized with the Affymetrix gene chip U34 according to the protocol provided by the Affymetrix Company. Real-time PCR was used to further confirm the result. We found that the hybridization signals of 167 genes were increased among the total 1323 probes plotted on the chip. The 167 increased genes could be functionally categorized into signal transduction, neuron related, cytoskeleton, metabolism, ion channels, transcription factors, cytokines, and apoptosis related. Signals of 7 probes were decreased, which accounted to 0.5% of the total number. A series of genes that were not reported before were up-regulated by phenylalanine, including Ca(2+)/calmodulin-dependent protein kinase, Brain type II (CaMK II), Ras, P38 MAP kinase, L-voltage dependent calcium channel, some genes related to vesicle formation and transmitter release, some glutamate receptor subunits and glutamate transporters. According to the gene expression profile, it is likely that multi-processes are involved in the neuronal injury induced by high phenylalanine, such as the activation of the NMDR-Ca(2+)- CaMK II - Ras- P38 axis, the abnormality in neurotransmitter release. Our study also suggests that the excitatory neurotransmitter glutamate may play a role in the neural pathology of phenylketonuria.

Animals↗

PubMed2001

Ulcerative colitis and Crohn's disease: distinctive gene expression profiles and novel susceptibility candidate genes.

To elucidate the biological dysregulation underlying two forms of inflammatory bowel disease (IBD), ulcerative colitis (UC) and Crohn's disease (CD), we examined global gene expression profiles of inflamed colonic tissue using DNA microarrays. Our results identified several genes with altered expression not previously linked to IBD. In addition to the expected upregulation of various cytokine and chemokine genes, novel immune function-related genes such as IGHG3, IGLL2 and CD74, inflammation-related lipocalins HNL and NGAL, and proliferation-related GRO genes were over-expressed in UC. Certain cancer-related genes such as DD96, DRAL and MXI1 were differentially expressed only in UC. Other genes over-expressed in both UC and CD included the REG gene family and the calcium-binding S100 protein genes S100A9 and S100P. The natural antimicrobial defensin DEFA5 and DEFA6 genes were particularly over-expressed in CD. Overall, significant differences in the expression profiles of 170 genes identified UC and CD as distinct molecular entities. The genomic map locations of the dysregulated genes may identify novel candidates for UC and CD genetic susceptibility.

Adult↗

PubMed2004

Gene expression profiling of inflamed human endothelial cells and influence of activated protein C.

BACKGROUND: During systemic inflammation, activation of vascular endothelium by proinflammatory cytokines leads to hypotension, microvascular thrombosis, and organ damage. Recent data suggest a link between coagulation and inflammation through the activated protein C (APC) pathway. We studied gene expression profiles in human coronary artery endothelial cells (HCAECs) exposed to proinflammatory stimuli and the influence of APC on expression of candidate genes regulated by these stimuli. METHODS AND RESULTS: HCAECs were stimulated with interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha. In gene expression profiling, 400 of 8400 genes were regulated >2-fold. Verification of selected candidate genes was achieved by measuring expression of mRNA species by real-time polymerase chain reaction, cytokine secretion by ELISA, and metabolites of tetrahydrobiopterin (BH4) biosynthesis by high-performance liquid chromatography. BH4 synthesis, interleukin-6, interleukin-8, monocyte chemotactic protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) were downregulated by APC at the transcriptional and protein level. Endothelial nitric oxide synthase, endothelial adhesion molecule, and vascular cell adhesion molecule-1 were not affected by APC. Activities of transcription factors c-Fos, FosB, and c-Rel were inhibited by APC in inflamed HCAECs. CONCLUSIONS: Our study revealed a novel antiinflammatory mechanism of APC-dependent gene regulation in HCAECs since c-Fos-dependent induction of MCP-1 and ICAM-1 was suppressed. APC downregulates expression and activity of genes related to inflammation, most pronounced under intermediate or mild inflammatory conditions.

Biopterins↗

PubMed2004

Loss of heterozygosity and its correlation with expression profiles in subclasses of invasive breast cancers.

Gene expression array profiles identify subclasses of breast cancers with different clinical outcomes and different molecular features. The present study attempted to correlate genomic alterations (loss of heterozygosity; LOH) with subclasses of breast cancers having distinct gene expression signatures. Hierarchical clustering of expression array data from 89 invasive breast cancers identified four major expression subclasses. Thirty-four of these cases representative of the four subclasses were microdissected and allelotyped using genome-wide single nucleotide polymorphism detection arrays (Affymetrix, Inc.). LOH was determined by comparing tumor and normal single nucleotide polymorphism allelotypes. A newly developed statistical tool was used to determine the chromosomal regions of frequent LOH. We found that breast cancers were highly heterogeneous, with the proportion of LOH ranging widely from 0.3% to >60% of heterozygous markers. The most common sites of LOH were on 17p, 17q, 16q, 11q, and 14q, sites reported in previous LOH studies. Signature LOH events were discovered in certain expression subclasses. Unique regions of LOH on 5q and 4p marked a subclass of breast cancers with "basal-like" expression profiles, distinct from other subclasses. LOH on 1p and 16q occurred preferentially in a subclass of estrogen receptor-positive breast cancers. Finding unique LOH patterns in different groups of breast cancer, in part defined by expression signatures, adds confidence to newer schemes of molecular classification. Furthermore, exclusive association between biological subclasses and restricted LOH events provides rationale to search for targeted genes.

Breast Neoplasms↗

PubMed2001

Chemokine receptor expression profile of eosinophils at inflamed tissue sites: Decreased CCR3 and increased CXCR4 expression by lung eosinophils.

BACKGROUND: To date, most studies dealing with eosinophil chemokine receptors have used eosinophils isolated from peripheral blood. During the movement of eosinophils from the peripheral blood to inflamed tissue sites, microenvironmental signals might alter their expression of chemokine receptors. However, little is known about the profile of expression of chemokine receptors by eosinophils at inflamed tissue sites in human beings. OBJECTIVE: The purpose of this study was to determine whether eosinophils that have migrated into inflamed tissues exhibit a profile of chemokine receptor expression that is qualitatively and/or quantitatively different from that of eosinophils in peripheral locations. METHODS: We studied simultaneously the expression and function of chemokine receptors in eosinophils in both bronchoalveolar lavage fluid (BALF) and peripheral blood specimens of 7 patients with eosinophilic lung diseases. RESULTS: De novo expression of CCR2, CCR4, and CCR5 was not detected at either the protein or the mRNA level. However, surface expression of CCR3 was decreased and CXCR4 was conversely increased with statistical significance in BALF eosinophils. Moreover, the changes in CCR3 and CXCR4 expression were reflected in the altered migratory response to their ligands. On the other hand, the levels of CXCR1, CXCR2, CXCR3, and CCR1 were virtually unchanged in BALF eosinophils, and these receptors did not have functional significance. CONCLUSION: Eosinophils at inflamed tissue sites exhibited an expression profile qualitatively similar to that in peripheral locations, except for decreased CCR3 and increased CXCR4 expression. Our results suggest that CCR3 is primarily and CXCR4 is cooperatively involved in eosinophil accumulation at inflamed tissue sites.

Adult↗

PubMed2003

Myoepithelial mRNA expression profiling reveals a common tumor-suppressor phenotype.

A series of myoepithelial cell lines and xenografts derived from benign human myoepithelial tumors of diverse sources (salivary gland, breast, and lung) exhibit common mRNA expression profiles indicative of a tumor-suppressor phenotype. Previously established myoepithelial cell lines and xenografts (HMS-#; HMS-#X) were compared to nonmyoepithelial breast carcinoma cells (MDA-MB-231 and MDA-MB-468, and inflammatory breast carcinoma samples, IBCr, and IBCw), a normal mammary epithelial cell line (HMEC) and individual cases of human breast cancer (zcBT#T), and matched normal human breast tissues (zcBT#N) (overall samples = 22). The global gene expression profile (22,000 genes) of these individual samples was examined using Affymetrix Microarray Gene Chips and subsequently analyzed with both Affymetrix and DChip algorithms. The myoepithelial cell lines/xenografts were distinct and very different from the nonmyoepithelial breast carcinoma cells and the normal breast and breast tumor biopsies. Two hundred and seven specifically selected genes represented a subset of genes that distinguished (P < 0.05) all the myoepithelial cell lines/xenografts from all the other samples and which themselves exhibited hierarchical clustering. Further analysis of these genes revealed increased expression in genes belonging to the classes of extracellular matrix proteins, angiogenic inhibitors, and proteinase inhibitors and decreased expression belonging to the classes of angiogenic factors and proteinases. Developmental genes were also differentially expressed (either over or underexpressed). These studies confirm our previous impression that human myoepithelial cells express a distinct tumor-suppressor phenotype.

Breast Neoplasms↗

PubMed2003

Expression profiling and bioinformatic analyses of a novel stress-regulated multispanning transmembrane protein family from cereals and Arabidopsis.

Cold acclimation is a multigenic trait that allows hardy plants to develop efficient tolerance mechanisms needed for winter survival. To determine the genetic nature of these mechanisms, several cold-responsive genes of unknown function were identified from cold-acclimated wheat (Triticum aestivum). To identify the putative functions and structural features of these new genes, integrated genomic approaches of data mining, expression profiling, and bioinformatic predictions were used. The analyses revealed that one of these genes is a member of a small family that encodes two distinct groups of multispanning transmembrane proteins. The cold-regulated (COR)413-plasma membrane and COR413-thylakoid membrane groups are potentially targeted to the plasma membrane and thylakoid membrane, respectively. Further sequence analysis of the two groups from different plant species revealed the presence of a highly conserved phosphorylation site and a glycosylphosphatidylinositol-anchoring site at the C-terminal end. No homologous sequences were found in other organisms suggesting that this family is specific to the plant kingdom. Intraspecies and interspecies comparative gene expression profiling shows that the expression of this gene family is correlated with the development of freezing tolerance in cereals and Arabidopsis. In addition, several members of the family are regulated by water stress, light, and abscisic acid. Structure predictions and comparative genome analyses allow us to propose that the cor413 genes encode putative G-protein-coupled receptors.

Acclimatization↗

PubMed2003

Interrogating mouse mammary cancer models: insights from gene expression profiling.

Numerous mouse models for mammary cancer have been developed and characterized based upon their biological, molecular, and histopathological features. In an effort to dissect the molecular anatomy of such models and compare their gene expression profiles to those of human breast cancer, six models representing various oncogenic pathways have been investigated using cDNA microarray technology. Results of these analyses are presented and discussed in the context of technological challenges presented by analyzing data on such a large scale. Further expression profiling coupled with emerging proteomic technologies will more completely define and distinguish mouse models of mammary cancer from each other and provide a comprehensive basis for comparing such models with the human disease they are intended to represent.

Animals↗

PubMed2006

Differentiation of spontaneous and induced mammary adenocarcinomas of the rat by gene expression profiling.

The differentiation of spontaneous and induced adenocarcinomas is of interest in the setting of carcinogenicity studies. In the experiment reported here, a differentiation of morphologically similar spontaneous and induced mammary adenocarcinomas of the rat is achieved by gene expression profiling. By choosing one marker gene based on the gene expression profile for each tumour type, we were able to distinguish the tumours by real-time quantitative polymerase chain reaction (RT-QPCR) as well.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2006

Comparative analysis of gene expression profiles in intact and damaged regions of human osteoarthritic cartilage.

OBJECTIVE: To analyze the differences in gene expression profiles of chondrocytes in intact and damaged regions of cartilage from the same knee joint of patients with osteoarthritis (OA) of the knee. METHODS: We compared messenger RNA expression profiles in regions of intact and damaged cartilage (classified according to the Mankin scale) obtained from patients with knee OA. Five pairs of intact and damaged regions of OA cartilage were evaluated by oligonucleotide array analysis using a double in vitro transcription amplification technique. The microarray data were confirmed by real-time quantitative polymerase chain reaction (PCR) amplification and were compared with previously published data. RESULTS: About 1,500 transcripts, which corresponded to 8% of the expressed transcripts, showed > or = 2-fold differences in expression between the cartilage tissue pairs. Approximately 10% of these transcripts (n = 151) were commonly expressed in the 5 patient samples. Accordingly, 114 genes (35 genes expressed in intact > damaged; 79 genes expressed in intact < damaged) were selected. The expression of some genes related to the wound-healing process, including cell proliferation and interstitial collagen synthesis, was higher in damaged regions than in intact regions, similar to the findings for genes that inhibit matrix degradation. Comparisons of the real-time quantitative PCR data with the previously reported data support the validity of our microarray data. CONCLUSION: Differences between intact and damaged regions of OA cartilage exhibited a similar pattern among the 5 patients examined, indicating the presence of common mechanisms that contribute to cartilage destruction. Elucidation of this mechanism is important for the development of effective treatments for OA.

Cartilage, Articular↗

PubMed2006

Sequential gene expression profiling in lung transplant recipients with chronic rejection.

STUDY OBJECTIVES: Chronic allograft rejection is the leading cause of morbidity and mortality for long-term survivors of lung transplantation. Previous studies have implicated only isolated genes in the development of chronic rejection and have not examined multiple pathways in an individual concurrently. Using microarray technology, we identified and compared gene expression profiling in lung transplant recipients with and without chronic rejection, and follow sequential expression of genes differentially expressed between the two groups. DESIGN: Prospective, cohort study. SETTING: Single lung transplant center. PATIENTS OR PARTICIPANTS: Eleven transplant recipients with chronic rejection were matched with 9 control transplant recipients. INTERVENTIONS: All recipients underwent surveillance bronchoscopies at predetermined times to rule out infection and/or acute rejection. Gene expression profiling was obtained from hybridizing BAL fluid cell RNA to a 96-gene microarray. MEASUREMENTS AND RESULTS: Fifteen genes were found to be significantly differentially expressed between the two patient groups, and they are involved in inflammatory, fibrotic, and apoptotic pathways. Temporal expression of the significant genes demonstrated a change in their levels at the onset of chronic rejection, with normalization to prerejection levels as rejection continued. CONCLUSIONS: We conclude that microarray technology is valuable in studying the mechanism of chronic lung rejection, and the expression of genes in multiple pathways is elevated in patients with chronic lung rejection.

Adult↗

PubMed2004

Gene expression profiling of leiomyoma and myometrial smooth muscle cells in response to transforming growth factor-beta.

Altered expression of the TGF-beta system is recognized to play a central role in various fibrotic disorders, including leiomyoma. In this study we performed microarray analysis to characterize the gene expression profile of leiomyoma and matched myometrial smooth muscle cells (LSMC and MSMC, respectively) in response to the time-dependent action of TGF-beta and, after pretreatment with TGF-beta type II receptor (TGF-beta RII) antisense oligomer-blocking/reducing TGF-beta autocrine/paracrine actions. Unsupervised and supervised assessments of the gene expression values with a false discovery rate selected at P < or = 0.001 identified 310 genes as differentially expressed and regulated in LSMC and MSMC in a cell- and time-dependent manner by TGF-beta. Pretreatment with TGF-beta RII antisense resulted in changes in the expression of many of the 310 genes regulated by TGF-beta, with 54 genes displaying a response to TGF-beta treatment. Comparative analysis of the gene expression profile in TGF-beta RII antisense- and GnRH analog-treated cells indicated that these treatments target the expression of 222 genes in a cell-specific manner. Gene ontology assigned these genes functions as cell cycle regulators, transcription factors, signal transducers, tissue turnover, and apoptosis. We validated the expression and TGF-beta time-dependent regulation of IL-11, TGF-beta-induced factor, TGF-beta-inducible early gene response, early growth response 3, CITED2 (cAMP response element binding protein-binding protein/p300-interacting transactivator with ED-rich tail), Nur77, Runx1, Runx2, p27, p57, growth arrest-specific 1, and G protein-coupled receptor kinase 5 in LSMC and MSMC using real-time PCR. Together, the results provide the first comprehensive assessment of the LSMC and MSMC molecular environment targeted by autocrine/paracrine action of TGF-beta, highlighting potential involvement of specific genes whose products may influence the outcome of leiomyoma growth and fibrotic characteristics by regulating inflammatory response, cell growth, apoptosis, and tissue remodeling.

Apoptosis↗

PubMed2002

Gene expression profile of renal proximal tubules regulated by proteinuria.

BACKGROUND: Proximal tubules activated by reabsorption of protein are thought to play significant roles in the progression of kidney diseases. Thus, identification of genes related to proteinuria should provide insights into the pathological process of tubulointerstitial fibrosis. METHOD: Gene expression profiles were constructed by means of direct sequencing procedures to identify genes induced in the mouse kidney proximal tubules (PT) exposed to proteinuria. RESULTS: By comparing the gene expression of control PT to that of disease model PT, the abundantly expressed genes in control PT were down-regulated presumably because of potentially toxic effects of proteinuria. From the more than 1000 up-regulated genes, an immunity related gene, thymic shared antigen-1 (TSA-1), and a novel gene, GS188, were selected for further characterization. The increased expression of TSA-1, a member of the Ly-6 family, and of GS188 in response to proteinuria was confirmed by Northern analysis, immunohistochemistry, in situ hybridization and laser microdissection along with real-time PCR analysis. Full length cloning of GS188 identified it as a family member of LR8 that was reported to express predominantly in fibroblasts. CONCLUSIONS: The gene expression profiles showed that the expression patterns in PT were changed dramatically by proteinuria. The profiles include novel genes that should be further characterized to aid the understanding of the pathophysiology of progressive kidney diseases.

Amino Acid Sequence↗

PubMed2006

Gene expression profiling during cellular differentiation in the embryonic pituitary gland using cDNA microarrays.

The anterior pituitary is comprised of five major hormone-secreting cell types that differentiate during embryonic development in a temporally distinct manner. Microarrays containing 5,128 unique cDNAs expressed in the chicken neuroendocrine system were produced and used to identify genes with potential involvement in the onset of thyroid-stimulating hormone beta-subunit (TSHbeta), growth hormone (GH), and prolactin (PRL) mRNA during embryonic development. We identified 352 cDNAs that were differentially expressed (P < or = 0.05) on embryonic day 10 (e10), e12, e14, or e17, the period of thyrotroph, somatotroph, and lactotroph differentiation. Self-organizing maps were used to identify genes that may function to initiate hormone gene transcription. Consistent with cellular ontogeny, TSHbeta mRNA increased steadily between e10 and e17, GH mRNA increased between e12 and e17, and PRL mRNA did not increase until e17. Expression of 141 genes increased in a manner similar to TSHbeta mRNA, and 64 genes decreased between e10 and e17. Although genes with these expression profiles are likely involved in development of the pituitary gland as a whole, some of these could be specifically associated with thyrotroph differentiation. Similarly, the expression profiles of 69 and 61 genes indicate a potential involvement in the induction of GH and PRL mRNA, respectively. Quantitative real-time RT-PCR was used to confirm microarray results for 31 genes. This is the first study to evaluate changes in anterior pituitary gene expression during embryonic development of any species using microarrays, and numerous transcription factors and signaling molecules not previously implicated in pituitary development were identified.

Animals↗

PubMed2005

Gene expression profiles differ markedly in mouse strains that are (or are not) susceptible to hyperthyroidism induced using thyrotropin receptor-expressing adenovirus.

BALB/c mice are susceptible and C57BL/6 mice are resistant to Graves' hyperthyroidism induced by immunization with adenovirus encoding the thyrotropin receptor (TSHR) A-subunit. Both strains develop comparable levels of TSHR antibodies, but potent TSH blocking antibody activity in C57BL/6 mice likely blocks development of hyperthyroidism. We used microarrays to compare gene expression in spleens of mice immunized with A-subunit adenovirus (TSHR-Ad) or control adenovirus (Con-Ad). To preclude the effects of variable thyroxine (T(4)) levels, mice were studied when euthyroid as follows: BALB/c mice immunized three times with TSHR-Ad or Con-Ad and C57BL/6 mice immunized three times with TSHR-Ad or Con-Ad. Among the 14,000 expressed probe sets, there were no statistically significant differences in gene expression in BALB/c mice immunized with TSHR-Ad versus Con-Ad. In contrast, expression of 57 transcripts (representing 40 genes) changed in response to TSHR-Ad in C57BL/6 mice. Diverse genes were identified, including proteins involved in immune responses, inflammation, and cell cycling as well as heat-shock proteins and proteases. Down-regulation of chitinase 3- and-4 gene expression likely reflects cytokines produced by T-helper 2 (Th2) type cells. Indeed, the immunoglobulin (IgG) subclass for TSHR antibodies reflects a deviation away from Th2 cytokines and toward Th1 in C57BL/6 mice. In conclusion, TSHR-Ad immunization altered gene expression profiles in C57BL/6, but not in BALB/c, mice. This response primarily involved reduced gene expression. In C57BL/6 mice, decreased expression of genes such as cathelicidin, calgranulins, and lipocalin following TSHR A-subunit adenovirus immunization suggests the importance of innate immunity in this response.

Adenoviridae↗

PubMed2005

Gene expression profiles in peripheral blood mononuclear cells of SARS patients.

AIM: To investigate the role of inflammatory and anti-viral genes in the pathogenesis of SARS. METHODS: cDNA microarrays were used to screen the gene expression profiles of peripheral blood mononuclear cells (PBMCs) in two SARS patients (one in the acute severe phase and the other in the convalescent phase) and a healthy donor. In addition, real-time qualitative PCR was also performed to verify the reproducibility of the microarray results. The data were further analyzed. RESULTS: Many inflammatory and anti-viral genes were differentially expressed in SARS patients. Compared to the healthy control or the convalescent case, plenty of pro-inflammatory cytokines such as IL-1, TNF-alpha, IL-8, and MAPK signaling pathway were significantly upregulated in the acute severe case. However, anti-inflammatory agents such as IL-4 receptor, IL-13 receptor, IL-1Ra, and TNF-alpha-induced proteins 3 and 6 also increased dramatically in the acute severe case. On the contrary, a lot of IFN-stimulated genes like PKR, GBP-1 and 2, CXCL-10 and 11, and JAK/STAT signal pathway were downregulated in the acute severe case compared to the convalescent case. CONCLUSION: Gene expression in SARS patients mirrors a host state of inflammation and anti-viral immunity at the transcription level, and understanding of gene expression profiles may make contribution to further studies of the SARS pathogenesis.

Adult↗

PubMed2002

Functional genomic comparison of lineage-related human bladder cancer cell lines with differing tumorigenic and metastatic potentials by spectral karyotyping, comparative genomic hybridization, and a novel method of positional expression profiling.

We have recently characterized T24T, an invasive and metastatic variant of the T24 human bladder cell line, resulting in a model for bladder cancer progression. To gain additional insight into the repertoire of genetic changes that may be responsible for the invasive and metastatic phenotype, we used spectral karyotyping (SKY) in combination with comparative genomic hybridization (CGH) in these cells. To assess the functional significance of the genetic differences found between the two cell lines, we have developed a positional expression profiling (PEP) method for comparing gene expression data obtained from oligonucleotide microarrays based upon chromosomal position. Using SKY and CGH, we were able to define the genetic changes in the cell lines, and in addition, resolve the identity of all marker chromosomes from our initial karyotyping and G-band analysis. PEP analysis revealed important similarities and differences when compared with the cytogenetic data, allowing insights of how genomic structural changes affect gene expression on a regional scale. The shape of the expression profiles for chromosomes 8, 12, and X correlated well with the numerical imbalances revealed by CGH and SKY, whereas regions like 10q, gained in T24T compared with T24, was not associated with changes in gene expression. Furthermore, we have shown that 12p, a region of agreement between CGH and PEP harbors RhoGDI2, a candidate gene, the expression of which inversely correlates with bladder tumor progression, demonstrating the usefulness of this multimodal approach in identifying promising genetic changes that may be responsible for the invasive phenotype.

Chromosome Aberrations↗