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Crossing Paths in Human Renal Cell Carcinoma (hRCC)

Historically, cell-signaling pathways have been studied as the compilation of isolated elements into a unique cascade that transmits extracellular stimuli to the tumor cell nucleus. Today, growing evidence supports the fact that intracellular drivers of tumor progression do not flow in a single line...

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Autores principales: Gallego, Guadalupe Aparicio, Villaamil, Vanessa Medina, Grande, Enrique, Caínzos, Isabel Santamarina, Antón Aparicio, Luís M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497295/
https://www.ncbi.nlm.nih.gov/pubmed/23202921
http://dx.doi.org/10.3390/ijms131012710
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author Gallego, Guadalupe Aparicio
Villaamil, Vanessa Medina
Grande, Enrique
Caínzos, Isabel Santamarina
Antón Aparicio, Luís M.
author_facet Gallego, Guadalupe Aparicio
Villaamil, Vanessa Medina
Grande, Enrique
Caínzos, Isabel Santamarina
Antón Aparicio, Luís M.
author_sort Gallego, Guadalupe Aparicio
collection PubMed
description Historically, cell-signaling pathways have been studied as the compilation of isolated elements into a unique cascade that transmits extracellular stimuli to the tumor cell nucleus. Today, growing evidence supports the fact that intracellular drivers of tumor progression do not flow in a single linear pathway, but disseminate into multiple intracellular pathways. An improved understanding of the complexity of cancer depends on the elucidation of the underlying regulatory networks at the cellular and intercellular levels and in their temporal dimension. The high complexity of the intracellular cascades causes the complete inhibition of the growth of one tumor cell to be very unlikely, except in cases in which the so-called “oncogene addiction” is known to be a clear trigger for tumor catastrophe, such as in the case of gastrointestinal stromal tumors or chronic myeloid leukemia. In other words, the separation and isolation of the driver from the passengers is required to improve accuracy in cancer treatment. This review will summarize the signaling pathway crossroads that govern renal cell carcinoma proliferation and the emerging understanding of how these pathways facilitate tumor escape. We outline the available evidence supporting the putative links between different signaling pathways and how they may influence tumor proliferation, differentiation, apoptosis, angiogenesis, metabolism and invasiveness. The conclusion is that tumor cells may generate their own crossroads/crosstalk among signaling pathways, thereby reducing their dependence on stimulation of their physiologic pathways.
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spelling pubmed-34972952012-11-29 Crossing Paths in Human Renal Cell Carcinoma (hRCC) Gallego, Guadalupe Aparicio Villaamil, Vanessa Medina Grande, Enrique Caínzos, Isabel Santamarina Antón Aparicio, Luís M. Int J Mol Sci Review Historically, cell-signaling pathways have been studied as the compilation of isolated elements into a unique cascade that transmits extracellular stimuli to the tumor cell nucleus. Today, growing evidence supports the fact that intracellular drivers of tumor progression do not flow in a single linear pathway, but disseminate into multiple intracellular pathways. An improved understanding of the complexity of cancer depends on the elucidation of the underlying regulatory networks at the cellular and intercellular levels and in their temporal dimension. The high complexity of the intracellular cascades causes the complete inhibition of the growth of one tumor cell to be very unlikely, except in cases in which the so-called “oncogene addiction” is known to be a clear trigger for tumor catastrophe, such as in the case of gastrointestinal stromal tumors or chronic myeloid leukemia. In other words, the separation and isolation of the driver from the passengers is required to improve accuracy in cancer treatment. This review will summarize the signaling pathway crossroads that govern renal cell carcinoma proliferation and the emerging understanding of how these pathways facilitate tumor escape. We outline the available evidence supporting the putative links between different signaling pathways and how they may influence tumor proliferation, differentiation, apoptosis, angiogenesis, metabolism and invasiveness. The conclusion is that tumor cells may generate their own crossroads/crosstalk among signaling pathways, thereby reducing their dependence on stimulation of their physiologic pathways. Molecular Diversity Preservation International (MDPI) 2012-10-05 /pmc/articles/PMC3497295/ /pubmed/23202921 http://dx.doi.org/10.3390/ijms131012710 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0).
spellingShingle Review
Gallego, Guadalupe Aparicio
Villaamil, Vanessa Medina
Grande, Enrique
Caínzos, Isabel Santamarina
Antón Aparicio, Luís M.
Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title_full Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title_fullStr Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title_full_unstemmed Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title_short Crossing Paths in Human Renal Cell Carcinoma (hRCC)
title_sort crossing paths in human renal cell carcinoma (hrcc)
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497295/
https://www.ncbi.nlm.nih.gov/pubmed/23202921
http://dx.doi.org/10.3390/ijms131012710
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