Recurrent Genomic Alterations With Impact on Survival in Colorectal Cancer Identified by Genome-Wide Array Comparative Genomic Hybridization

Kim, Mi–Young; Yim, Seon‐Hee; Kwon, Miseon; Kim, Tae–Min; Shin, Sun; Kang, Hyun Mi; Lee, Charles; Chung, Yeun‐Jun

doi:10.1053/j.gastro.2006.10.021

Cited by 60 publications

(53 citation statements)

References 41 publications

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“…CAMTA1 is homozygously deleted in a subset of gliomas (9) and is the only gene mapping to the 1p36 smallest region of overlapping heterozygous deletion in this entity (10). In colorectal cancer, genome-wide copy number analysis revealed that loss of a 2 Mb region encompassing CAMTA1 has the strongest impact on survival among all identified genomic alterations (11). Further, as in neuroblastoma, low expression of CAMTA1 is an independent predictor of poor outcome in colorectal cancer (11).…”

Section: Introductionmentioning

confidence: 99%

CAMTA1, a 1p36 Tumor Suppressor Candidate, Inhibits Growth and Activates Differentiation Programs in Neuroblastoma Cells

et al. 2011

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A distal portion of human chromosome 1p is often deleted in neuroblastomas and other cancers and it is generally assumed that this region harbors one or more tumor suppressor genes. In neuroblastoma, a 261 kb region at 1p36.3 that encompasses the smallest region of consistent deletion pinpoints the locus for calmodulin binding transcription activator 1 (CAMTA1). Low CAMTA1 expression is an independent predictor of poor outcome in multivariate survival analysis, but its potential functionality in neuroblastoma has not been explored. In this study, we used inducible cell models to analyze the impact of CAMTA1 on neuroblastoma biology. In neuroblastoma cells that expressed little endogenous CAMTA1, its ectopic expression slowed cell proliferation, increasing the relative proportion of cells in G 1 /G 0 phases of the cell cycle, inhibited anchorage-independent colony formation, and suppressed the growth of tumor xenografts. CAMTA1 also induced neurite-like processes and markers of neuronal differentiation in neuroblastoma cells. Further, retinoic acid and other differentiationinducing stimuli upregulated CAMTA1 expression in neuroblastoma cells. Transciptome analysis revealed 683 genes regulated on CAMTA1 induction and gene ontology analysis identified genes consistent with CAMTA1-induced phenotypes, with a significant enrichment for genes involved in neuronal function and differentiation. Our findings define properties of CAMTA1 in growth suppression and neuronal differentiation that support its assignment as a 1p36 tumor suppressor gene in neuroblastoma. Cancer Res; 71(8); 3142-51. Ó2011 AACR.

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Section: Introductionmentioning

confidence: 99%

CAMTA1, a 1p36 Tumor Suppressor Candidate, Inhibits Growth and Activates Differentiation Programs in Neuroblastoma Cells

et al. 2011

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“…25% of colorectal cancer cases, 37 and a variety of hematological malignancies including AML, 38 chronic myelogenous leukemia 39 and non-Hodgkin's lymphoma. 40 In neuroblastoma and colorectal cancer, reduced expression levels of the CAMTA1 gene correlated with adverse outcome, suggesting that CAMTA1 could act as the 1p36-specifc tumor suppressor gene in these malignancies.…”

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confidence: 99%

“…40 In neuroblastoma and colorectal cancer, reduced expression levels of the CAMTA1 gene correlated with adverse outcome, suggesting that CAMTA1 could act as the 1p36-specifc tumor suppressor gene in these malignancies. 36,37 Another interesting target gene in this genomic region is the CHD5 gene, which has been shown to be a tumor suppressor that controls proliferation and apoptosis via the p19Arf/p53 pathway. 41 Other potential target genes within this genomic region are HES2 and HES3, both of which are highly similar to HES1 that is a basic helix-loop-helix transcriptional repressor and known NOTCH1 target gene.…”

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confidence: 99%

Cooperative genetic defects in TLX3 rearranged pediatric T-ALL

et al. 2008

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes. About 20% of pediatric T-ALL cases are characterized by TLX3 expression due to a cryptic translocation t(5;14)(q35;q32). Although a number of collaborating genetic events have been identified in TLX3 rearranged T-ALL patients (NOTCH1 mutations, p15/p16 deletions, NUP214-ABL1 amplifications), further elucidation of additional genetic lesions could provide a better understanding of the pathogenesis of this specific T-ALL subtype. In this study, we used array-CGH to screen TLX3 rearranged T-ALL patients for new chromosomal imbalances. Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del (19)(p13.2). From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases. In addition, 19 other genetic lesions were detected once in TLX3 rearranged T-ALL cases, including a cryptic WT1 deletion and a deletion covering the FBXW7 gene, an U3-ubiquitin ligase that mediates the degradation of NOTCH1, MYC, JUN and CyclinE. This study provides a genome-wide overview of copy number changes in TLX3 rearranged T-ALL and offers great new challenges for the identification of new target genes that may play a role in the pathogenesis of T-ALL.

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“…The methodologies used in those studies might have caused the discrepancy between their results. In addition, we recommend that the microdissected cells extracted from CRC tumors should be applied for array CGH analysis to avoid bias in the quantity and quality (5,6). It is possible that the reported discrepancies between the amplified genetic regions and the transcriptional levels are not only characteristic of the genes themselves, but also due to technical errors.…”

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confidence: 99%

Overexpression of SUGT1 in human colorectal cancer and its clinicopathological significance

et al. 2010

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Abstract. As recent technological innovations make it possible to clarify the concordant relationship between genomic alterations and aberrant gene expression during the progression of colorectal cancer (CRC), we aimed at identifying new overexpressing genes with genomic amplification on the responsible loci in CRC. The candidate gene was found using cDNA microarray and array-based comparative genomic hybridization (CGH) analysis after laser microdissection (LMD) in 132 Japanese CRC. We focused on SUGT1, which is associated with the assembling of kinetochore proteins at the metaphase of the cell cycle, with significant association between genetic alterations and expression. SUGT1 mRNA expression was evaluated in 98 CRC cases to determine the clinicopathological significance of SUGT1 expression. The mean level of SUGT1 mRNA expression in tumor tissue specimens was significantly higher than in non-tumor tissue. The high SUGT1 expression group was characterized by a significantly elevated frequency of recurrence and a significantly poorer prognosis than the low expression group. There was a significant association between poor prognosis of CRC cases and the overexpression of SUGT1 with genomic amplification of the loci concordantly. The amplification of SUGT1 might give rise to promote the transcription of the gene directly subsequent to the progression of CRC cases with worsening prognosis.

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Recurrent Genomic Alterations With Impact on Survival in Colorectal Cancer Identified by Genome-Wide Array Comparative Genomic Hybridization

Cited by 60 publications

References 41 publications

CAMTA1, a 1p36 Tumor Suppressor Candidate, Inhibits Growth and Activates Differentiation Programs in Neuroblastoma Cells

CAMTA1, a 1p36 Tumor Suppressor Candidate, Inhibits Growth and Activates Differentiation Programs in Neuroblastoma Cells

Cooperative genetic defects in TLX3 rearranged pediatric T-ALL

Overexpression of SUGT1 in human colorectal cancer and its clinicopathological significance

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