Comprehensive genome-wide comparison of DNA and RNA level scan using microarray technology for identification of candidate cancer-related genes in the HL-60 cell line

Ülger, Celal; Toruner, Gokce; Alkan, M.; Mohammed, Mansoor; Damani, Shamsha; Kang, Jason; Galante, Anthony; Aviv, Hana; Soteropoulos, Patricia; Tolias, Peter; Schwalb, Marvin N.; Dermody, James

doi:10.1016/s0165-4608(03)00155-9

Cited by 41 publications

(32 citation statements)

References 21 publications

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“…22 However, many of our findings had not yet been reported, including amplifications involving the oncogene JAK2 in UT-7 and NB-4. Furthermore, in NB-4, we also found two distinct novel amplifications on chromosome 19 (amp(19)(p13) B6 Mb; amp(19)(q13) B7.5 Mb; Figure 2).…”

Section: Characterization Of Myeloid Cell Lines By Arraycomparative Gmentioning

confidence: 62%

Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations

et al. 2006

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To model and investigate different facets of leukemia pathogenesis, a widely accepted approach is to use immortalized leukemia cell lines. Although these provide powerful tools to our knowledge, few studies have addressed the question whether hematopoietic cell lines represent accurate and reliable model systems. To improve the molecular characterization of these model systems, we analyzed 17 myeloid leukemia cell lines using DNA microarray technology. By array-based comparative genomic hybridization, we identified recurrent genomic DNA gains and losses, as well as high-level amplifications. Parallel analysis of gene expression helped delineate potential candidate genes, and unsupervised analysis of gene expression data revealed cell lines to cluster in part based on underlying cytogenetic abnormalities. Comparison with clinical leukemia specimens showed that key signatures were retained, as myeloid cell lines with characteristic cytogenetic aberrations co-clustered with leukemia samples carrying the respective abnormality. Signatures were also quite robust, as expression data from cell lines correlated highly with published data. Thus, our analyses demonstrate myeloid cell lines to exhibit conserved and stable signatures reflecting the underlying primary cytogenetic aberrations. Our refined molecular characterization of myeloid cell lines supports the utility of cell lines as faithful and powerful model systems and provides additional insights into the molecular mechanisms of leukemogenesis.

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Section: Characterization Of Myeloid Cell Lines By Arraycomparative Gmentioning

confidence: 62%

Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations

et al. 2006

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“…In addition, loss of α-catenin occurs in cell lines derived from myeloid leukemia, leukocyte, colon, prostate [33][34][35][36] and other cancers, as well as primary human cancers (Table 1). Although many cancer cell lines have mutations in α-catenin, similar mutations have not been identified in primary human cancers.…”

Section: Molecular and Functional Characterization Of α-Catenin In Nomentioning

confidence: 99%

Bench to bedside and back again: Molecular mechanisms of α-catenin function and roles in tumorigenesis

Benjamin

Nelson

2008

Seminars in Cancer Biology

107

115

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The cadherin/catenin complex, comprised of E-cadherin, β-catenin and α-catenin, is essential for initiating cell-cell adhesion, establishing cellular polarity and maintaining tissue organization. Disruption or loss of the cadherin/catenin complex is common in cancer. As the primary cell-cell adhesion protein in epithelial cells, E-cadherin has long been studied in cancer progression. Similarly, additional roles for β-catenin in the Wnt signaling pathway has led to many studies of the role of β-catenin in cancer. Alpha-catenin, in contrast, has received less attention. However, recent data demonstrate novel functions for α-catenin in regulating the actin cytoskeleton and cell-cell adhesion, which when perturbed could contribute to cancer progression. In this review, we use cancer data to evaluate molecular models of α-catenin function, from the canonical role of α-catenin in cell-cell adhesion to non-canonical roles identified following conditional α-catenin deletion. This analysis identifies α-catenin as a prognostic factor in cancer progression.

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“…HFF cells were infected with Toledo BAC and Toledo ⌬15kb viruses at an MOI of 3 for 3 days, and total RNA was isolated with TRIZOL reagent (Gibco BRL). The cDNAs were synthesized and labeled with Cy3 and Cy5 fluorescent dyes as described previously (39). The HCMV oligonucleotide microarray was executed as described in reference 11.…”

Section: Cells and Virusesmentioning

confidence: 99%

Human Cytomegalovirus Genes in the 15-Kilobase Region Are Required for Viral Replication in Implanted Human Tissues in SCID Mice

Wang¹,

Taylor

Leisenfelder

et al. 2005

J Virol

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Since animal models for studying human cytomegalovirus (HCMV) replication in vivo and pathogenesis are not available, severe combined immunodeficiency mice into which human tissues were implanted (SCID-hu mice) provide an alternative and valuable model for such studies. The HCMV clinical isolates, including those of the Toledo strain, replicate to high titers in human tissue implanted into SCID mice; however, the attenuated AD169 strain has completely lost this ability. The major difference between Toledo and AD169 is a 15-kb segment, encoding 19 open reading frames, which is present in all virulent strains but deleted from attenuated strains. This fact suggests that crucial genes required for HCMV replication in vivo are localized to this region. In this study, the importance of this 15-kb segment for HCMV replication in vivo was determined. First, Toledo BAC virus (produced from a Toledo bacterial artificial chromosome) and AD169 virus were tested for growth in SCID-hu mice. Toledo BAC , like Toledo, grew to high titers in implanted human thymus and liver tissues, while AD169 did not. This outcome showed that the Toledo genome propagated in bacteria (Toledo BAC ) retained its virulence. The 15-kb segment was then deleted from Toledo BAC , and the resulting virus, Toledo ⌬15kb , was tested for growth in both human foreskin fibroblast (HFF) cells and SCID-hu mice. Toledo ⌬15kb had a minor growth defect in HFF but completely failed to replicate in human thymus and liver implants. This failure to grow was rescued when the 15-kb region was inserted back into the Toledo ⌬15kb genome. These results directly demonstrated that the genes located in the 15-kb segment are crucial for HCMV replication in vivo.

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Comprehensive genome-wide comparison of DNA and RNA level scan using microarray technology for identification of candidate cancer-related genes in the HL-60 cell line

Cited by 41 publications

References 21 publications

Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations

Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations

Bench to bedside and back again: Molecular mechanisms of α-catenin function and roles in tumorigenesis

Human Cytomegalovirus Genes in the 15-Kilobase Region Are Required for Viral Replication in Implanted Human Tissues in SCID Mice

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