A multigene expression panel for the molecular diagnosis of Barrett's esophagus and Barrett's adenocarcinoma of the esophagus

Brabender, Jan; Marjoram, Paul; Salonga, Dennis; Metzger, Ralf; Schneider, Paul M.; Park, Ji Min; Schneider, Sylke; Hölscher, A. H.; Yin, Jing; Meltzer, Stephen J.; Danenberg, Kathleen D.; Danenberg, Peter V.; Lord, Reginald V.

doi:10.1038/sj.onc.1207663

Cited by 61 publications

(48 citation statements)

References 22 publications

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“…Very little work has been performed in Barrett's associated adenocarcinoma to determine the availability of RA and whether its signalling is intact. Altered expression of retinoic acid receptors (RAR) a and g as well as all three RXR has been described (Lord et al, 2001;Brabender et al, 2004); however, the molecular mechanism and functional consequences of these alterations have not been investigated. Here we focused on the CYP26A1 enzyme; however, it is also possible that reduced RA levels are due to aberrant expression of cellular retinalbinding protein or lecithin:retinal acyltransferase.…”

Section: Discussionmentioning

confidence: 99%

A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett's associated adenocarcinoma

Hong

Lao-Sirieix

et al. 2007

Oncogene

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Section: Discussionmentioning

confidence: 99%

A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett's associated adenocarcinoma

Hong

Lao-Sirieix

et al. 2007

Oncogene

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“…4 We confirm the previously reported reduced expression for the genes PAI-2 (plasminogen activator inhibitor type-2), 37,38 GSTP1 (glutathione S-transferase pi), 39 RB1 (retinoblastoma) 40 and PITX1 (pituitary homeobox 1). 9,24 Of note, PAI-2 expression was more than 100 times lower in EAC than normal esophagus. PAI-2 inhibits both tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA).…”

Section: Discussionmentioning

confidence: 99%

“…Based on studies showing the discriminatory power of tetraspanin 1 (TSPAN1) expression, which is upregulated in BE when compared to normal squamous esophagus (NE) and then downregulated in EAC when compared to BE ( Table 1), [9][10][11] we investigated the previously unreported tetraspanin members TSPAN8, 24 and 29. The expression pattern for TSPAN8 all have fold change greater than 2 or -2 and p value <0.001 after using the Benjamini hochberg method for controlling the false detection rate (FDR) at alpha 0.01.…”

Section: Discussionmentioning

confidence: 99%

Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues.

Botelho¹,

Schneiders²,

Lord³

et al. 2010

Cancer Biology & Therapy

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“…Gene expression profiling studies have been used in the examination of cancer progression, diagnosis, drug target discovery, and gene therapy evaluation (Brabender et al, 2004;Chang et al, 2004;Tamoto et al, 2004). Our previous cDNA microarray-based expression profiling studies global genetic signatures in esophageal cancer Xu et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

Wang

Zhan

Yin³

et al. 2006

Oncogene

111

106

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To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

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A multigene expression panel for the molecular diagnosis of Barrett's esophagus and Barrett's adenocarcinoma of the esophagus

Cited by 61 publications

References 22 publications

A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett's associated adenocarcinoma

A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett's associated adenocarcinoma

Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues.

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

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