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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN Imprimir: 0893-9675
ISSN On-line: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v13.i1.20
pages 39-74

Aberrant Receptor Signaling and Trafficking as Mechanisms in Oncogenesis

Kaisa Haglund
Centre for Cancer Biomedicine, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway
Tor Erik Rusten
Centre for Cancer Biomedicine, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway
Harald Stenmark
Rikshospitalet-Radiumhospitalet Comprehensive Cancer Centre, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway

RESUMO

Intracellular signaling pathways activated through cell surface receptors are essential for cell proliferation, differentiation, survival, and migration. Dysregulation of such signaling through mutations, chromosome rearrangements, aberrant gene expression, or epigenetic changes is a key factor in oncogenesis. Prominent examples of receptor signaling pathways that are dysregulated in cancers include those initiated by receptor tyrosine kinases, WNT, TGFβ, and Notch receptors. In this review we will discuss these signaling pathways and how their dysfunction may contribute to oncogenesis. We will also highlight the important role of endocytic membrane trafficking in receptor signaling and tumor suppression.


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