Reverse phase protein microarrays which capture disease progression show activation of pro-survival pathways at the cancer invasion front

Paweletz, Cloud P.; Charboneau, Lu; Bichsel, Verena E.; Simone, Nicole L.; Chen, Tina; Gillespie, John W.; Emmert‐Buck, Michael R.; Roth, Mark J.; Petricoin, Emanuel F.; Liotta, Lance A.

doi:10.1038/sj.onc.1204265

Cited by 897 publications

(763 citation statements)

References 35 publications

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“…As an adjunct to focused mechanistic studies, which are usually performed in vitro, our understanding of the occurring biological processes could be increased by global in vivo gene expression studies. Several interesting studies in this direction have been reported, [4][5][6][7][8] but to our knowledge studies with a clear focus on the gene expression patterns of the host tissue excluding the tumorous epithelial compartment have not yet been published.…”

mentioning

confidence: 99%

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Bandapalli

Geheeb

Kobelt

et al. 2005

Intl Journal of Cancer

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Host cell reactions are a crucial determinant for tumor invasion. We analyzed on a genomewide scale gene expression differences between microdissected tissues taken from unaffected liver tissue of a human colorectal tumor (LS174) growing in the livers of nude mice and tissue from the host part of the invasive front. Due to the low degree of interspecies cross‐hybridization of 15% as determined on Affymetrix microarrays, our xenograft model allowed for the distinction of genes of murine versus human origin even if the respective tissues could not be isolated separately. Using the gene ontology (GO) classification, we were able to determine patterns of up‐ and downregulated genes in the liver part of the invasive front. We observed a pronounced overrepresentation, e.g., of the GO terms “extracellular matrix,” “cell communication,” “response to biotic stimulus,” “structural molecule activity” and “cell growth,” indicating a very pronounced host cell response to tumor invasion. On the single gene level, hepatic stellate cell (HSC) activation markers were overrepresented in the liver part of the invasion front. Immunohistochemistry and qPCR confirmed an activation of HSC as well as an increased number of HSC in the invasive front as compared to the noninvaded liver tissue. In summary, our data demonstrate the feasibility of an interspecies differential gene expression approach on a genomewide scale. © 2005 Wiley‐Liss, Inc.

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mentioning

confidence: 99%

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Bandapalli

Geheeb

Kobelt

et al. 2005

Intl Journal of Cancer

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“…On the other hand, phospho-inactivation of GSK3b has been shown to boost the production of Bcl-2 by enhancing the activity of CREB-ATF-1 in the context of t-Darpp-mediated PI3K-Akt activation (Belkhiri et al 2008) (t-Darpp: truncated isoform of dopamine and cyclic-AMP-regualted phosphoprotein of Mr 32,000). Other studies confirm this phenomenon by providing quantitative evidence that phosphorylation of Akt and subsequent inactivation of its substrate GSK3b are capable of suppressing apoptosis in invasive prostate cancer (Paweletz et al 2001). All these lines of evidence unveiled the complexity of GSK3b influences on cell apoptosis and cancer progression.…”

Section: Gsk3b-mediated Control Of Apoptosis and Its Implications In Ecmentioning

confidence: 77%

The Role of Glycogen Synthase Kinase 3-β in Immunity and Cell Cycle: Implications in Esophageal Cancer

Gao

Brown

Wang

et al. 2013

Arch. Immunol. Ther. Exp.

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Esophageal cancer (EC) is one of the most aggressive gastrointestinal malignancies, possessing an insidious onset and a poor prognosis. Numerous transcription factors and inflammatory mediators have been reported to play a pivotal role in the initiation and progression of this cancer. However, the specifics of the signaling network responsible for said factors, especially which elements are the critical regulators, are still being elucidated. Glycogen synthesis kinases 3 (GSK3)b was originally regarded as a kinase regulating glucose metabolism. Accumulating evidence demonstrated that it also played an essential role in a variety of cellular processes including proliferation, differentiation, inflammation, motility, and survival by regulating various transcription factors such as c-Jun, AP-1, b-catenin, CREB, and NF-jB. Aberrant regulation of GSK3b has been shown to promote cell growth in some cancers, while suppressing it in others, and thus may play an important role in the development of EC. This review will discuss our current understanding of GSK3b signaling, and its control of the expression and activation of various transcription factors that mediate the inflammatory response. We will also explore some of the known mediators of EC progression, and based on current literature, elucidate the potential roles and implications of GSK3 in this disease.

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“…Eine genaue Quantifizierung und Bestimmung des Aktivierungsstatus von Rezeptoren (z. B. HER-Rezeptoren) und nachgeschalteter Signalwegsmoleküle ist in der IHC jedoch äußerst schwierig [6]. So könnten aktivierte Rezeptoren, Rezeptorkomplexe oder deregulierte Signalwegsmoleküle erklären, warum nur ein Teil der Patientinnen auf solche Therapien ansprechen.…”

Section: Proteinquantifizierungunclassified

Analyse von Signalwegen in formalinfixierten Brustkrebsgeweben

et al. 2010

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Reverse phase protein microarrays which capture disease progression show activation of pro-survival pathways at the cancer invasion front

Cited by 897 publications

References 35 publications

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

The Role of Glycogen Synthase Kinase 3-β in Immunity and Cell Cycle: Implications in Esophageal Cancer

Analyse von Signalwegen in formalinfixierten Brustkrebsgeweben

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