Common markers of proliferation

Whitfield, Michael L.; George, Lacy K.; Grant, Gavin D.; Perou, Charles M.

doi:10.1038/nrc1802

Cited by 558 publications

(488 citation statements)

References 62 publications

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“…We have identified clusters containing genes known to be associated with BE, ADC, and SCC analogous to clusters described by others. For example, the SPARC and proliferation clusters, described by Su et al 32 and Whitfield et al, 39 and a cluster containing trefoil factor 1 by Fox et al 49 was consistent with our digestion cluster in BE and ADC.…”

Section: Cluster Analysis Of Genessupporting

confidence: 69%

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Gene expression profiling of esophageal cancer: Comparative analysis of Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma

Greenawalt¹,

Duong²,

Smyth³

et al. 2007

Intl Journal of Cancer

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Esophageal cancer is a particularly aggressive tumor with poor prognosis, however, our current knowledge of the genes and pathways involved in tumorigenesis of the esophagus are limited. To obtain insight into the molecular processes underlying tumorigenesis of the esophagus, we have used cDNA microarrays to compare the gene expression profiles of 128 tissue samples representing the major histological subtypes of esophageal cancer (squamous cell carcinoma and adenocarcinoma (ADC)) as well as Barrett's esophagus (BE), the precursor lesion to ADC, and normal esophageal epithelium. Linear discriminant analysis and unsupervised hierarchical clustering show the separation of samples into 4 distinct groups consistent with their histological subtype. Differentially expressed genes were identified between each of the tissue types. Comparison of gene ontologies and gene expression profiles identified gene profiles specific to esophageal cancer, as well as BE. “Esophageal cancer clusters,” representing proliferation, immune response, and extracellular matrix genes were identified, as well as digestion, hydrolase, and transcription factor clusters specific to the columnar phenotype observed during BE and esophageal ADC. These clusters provide valuable insight into the molecular and functional differences between normal esophageal epithelium, BE, and the 2 histologically distinct forms of esophageal cancers. Our thorough, unbiased analysis provides a rich source of data for further studies into the molecular basis of tumorigenesis of the esophagus, as well as identification of potential biomarkers for early detection of progression. © 2007 Wiley‐Liss, Inc.

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Section: Cluster Analysis Of Genessupporting

confidence: 69%

“…39 This cluster contains genes responsible for cytokinesis and cell cycle checkpoints, specifically genes involved in the M phase of the mitotic cell cycle including BUB1, STK6, CENPA, CENPE, TOP2A, CHEK1, and CDC2.…”

Section: Cluster Analysis Of Genesmentioning

confidence: 99%

Gene expression profiling of esophageal cancer: Comparative analysis of Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma

Greenawalt¹,

Duong²,

Smyth³

et al. 2007

Intl Journal of Cancer

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“…Recently, gene array techniques have revealed the Ki-67 gene's role in several 'proliferation signatures', showing that a set of genes with increased expression patterns is correlated with tumour cell proliferation rates, as assessed by the Ki-67 labelling index (Perou et al, 1999;Whitfield et al, 2006). Moreover, Ki-67 is one of the 21 prospectively selected genes of the Oncotype DX TM assay used to predict the risk of recurrence in a node-negative, tamoxifentreated BC population enrolled in the National Surgical Adjuvant , as well to predict the magnitude of chemotherapy benefit in women with node-negative, estrogen receptor (ER)-positive BC enrolled in the NSABP B20 trial (Paik et al, 2004(Paik et al, , 2006.…”

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confidence: 99%

Ki-67 as prognostic marker in early breast cancer: a meta-analysis of published studies involving 12 155 patients

et al. 2007

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The Ki-67 antigen is used to evaluate the proliferative activity of breast cancer (BC); however, Ki-67's role as a prognostic marker in BC is still undefined. In order to better define the prognostic value of Ki-67/MIB-1, we performed a meta-analysis of studies that evaluated the impact of Ki-67/MIB-1 on disease-free survival (DFS) and/or on overall survival (OS) in early BC. Sixty-eight studies were identified and 46 studies including 12 155 patients were evaluable for our meta-analysis; 38 studies were evaluable for the aggregation of results for DFS, and 35 studies for OS. Patients were considered to present positive tumours for the expression of Ki-67/MIB-1 according to the cut-off points defined by the authors. Ki-67/MIB-1 positivity is associated with higher probability of relapse in all patients (HR ¼ 1.93 (95% confidence interval (CI): 1.74 -2.14); Po0.001), in node-negative patients (HR ¼ 2.31 (95% CI: 1.83 -2.92); Po0.001) and in node-positive patients (HR ¼ 1.59 (95% CI: 1.35 -1.87); Po0.001). Furthermore, Ki-67/MIB-1 positivity is associated with worse survival in all patients (HR ¼ 1.95 (95% CI: 1.70 -2.24; Po0.001)), node-negative patients (HR ¼ 2.54 (95% CI: 1.65 -3.91); Po0.001) and node-positive patients (HR ¼ 2.33 (95% CI: 1.83 -2.95); Po0.001). Our meta-analysis suggests that Ki-67/ MIB-1 positivity confers a higher risk of relapse and a worse survival in patients with early BC.

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“…The similarity in expression profile for Brip1 and E2F1 supports our findings of Brip1 being a direct E2F target gene and suggests co-regulated expression of Brip1 and E2F1 in breast cancer tissues. Co-regulation of E2F1 and Ki67 has been shown before (Zhang et al, 2000;Saiz et al, 2002) and microarray studies have shown the existence of a cluster of 'proliferation genes' of which the expression is induced in aggressive types of breast cancer and to which both E2F itself and a number of E2F target genes belong (Perou et al, 2000;Sorlie 2004;Whitfield et al, 2006). Brip1 is therefore not unlikely to belong to this kind of proliferation signature.…”

Section: Discussionmentioning

confidence: 72%

Expression of the BRCA1-interacting protein Brip1/BACH1/FANCJ is driven by E2F and correlates with human breast cancer malignancy

et al. 2008

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Mutations in the BRCA1-interacting DEAH helicase Brip1 confer an increased risk of breast cancer. In the present study we aimed to unravel the transcriptional control of Brip1 and to determine its expression levels in a set of 101 primary invasive breast carcinomas. Transcription of Brip1 was found to be cell growth-related and controlled by the E2F/retinoblastoma (Rb) pathway through a conserved E2F-responsive site. Repression of Brip1 expression by the cell growth-inhibiting compound 1a,25-dihydroxyvitamin D 3 depended on this same E2F-responsive site. In spite of its role as a tumor suppressor, both quantitative reverse transcriptase-PCR analyses and immunohistochemical stainings showed significantly elevated Brip1 expression levels in grade 3 tumors as compared to grade 1 or 2 carcinomas. Furthermore, increased Brip1 transcript levels were found in tumors with an estrogen receptor-negative, progesterone receptornegative or HER-2-positive status. In conclusion, these data show that Brip1 is a genuine target gene for the E2F/ Rb pathway and that elevated expression levels of Brip1 are detected in primary invasive breast carcinomas with unfavorable characteristics.

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Common markers of proliferation

Cited by 558 publications

References 62 publications

Gene expression profiling of esophageal cancer: Comparative analysis of Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma

Gene expression profiling of esophageal cancer: Comparative analysis of Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma

Ki-67 as prognostic marker in early breast cancer: a meta-analysis of published studies involving 12 155 patients

Expression of the BRCA1-interacting protein Brip1/BACH1/FANCJ is driven by E2F and correlates with human breast cancer malignancy

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