TAMing resistance to multi-targeted kinase inhibitors through Axl and Met inhibition

D. J. Pinato; S. Chowdhury; J. Stebbing

doi:10.1038/onc.2015.374

TAMing resistance to multi-targeted kinase inhibitors through Axl and Met inhibition

D. J. Pinato
, S. Chowdhury
, J. Stebbing

Research output: Contribution to journal › Review article › peer-review

Abstract

TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met are implicated in several hallmarks of cancer progression including sustained angiogenesis, enhanced motility, tissue invasion and acquisition of metastatic potential through the upregulation of epithelial-to-mesenchymal transition. Increasing evidence has confirmed Axl and Met as emerging central drivers of adaptive resistance to targeted therapies across a wide variety of cancers. In this issue of Oncogene, Zhou et al. describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic resistant RCC.

Original language	English
Pages (from-to)	2684-2686
Number of pages	3
Journal	Oncogene
Volume	35
Issue number	21
DOIs	https://doi.org/10.1038/onc.2015.374
Publication status	Published - 1 May 2016
Externally published	Yes

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10.1038/onc.2015.374

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title = "TAMing resistance to multi-targeted kinase inhibitors through Axl and Met inhibition",

abstract = "TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met are implicated in several hallmarks of cancer progression including sustained angiogenesis, enhanced motility, tissue invasion and acquisition of metastatic potential through the upregulation of epithelial-to-mesenchymal transition. Increasing evidence has confirmed Axl and Met as emerging central drivers of adaptive resistance to targeted therapies across a wide variety of cancers. In this issue of Oncogene, Zhou et al. describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic resistant RCC.",

author = "Pinato, \{D. J.\} and S. Chowdhury and J. Stebbing",

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doi = "10.1038/onc.2015.374",

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AU - Pinato, D. J.

AU - Chowdhury, S.

AU - Stebbing, J.

PY - 2016/5/1

Y1 - 2016/5/1

N2 - TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met are implicated in several hallmarks of cancer progression including sustained angiogenesis, enhanced motility, tissue invasion and acquisition of metastatic potential through the upregulation of epithelial-to-mesenchymal transition. Increasing evidence has confirmed Axl and Met as emerging central drivers of adaptive resistance to targeted therapies across a wide variety of cancers. In this issue of Oncogene, Zhou et al. describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic resistant RCC.

AB - TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met are implicated in several hallmarks of cancer progression including sustained angiogenesis, enhanced motility, tissue invasion and acquisition of metastatic potential through the upregulation of epithelial-to-mesenchymal transition. Increasing evidence has confirmed Axl and Met as emerging central drivers of adaptive resistance to targeted therapies across a wide variety of cancers. In this issue of Oncogene, Zhou et al. describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic resistant RCC.

UR - https://www.scopus.com/pages/publications/84971233859

U2 - 10.1038/onc.2015.374

DO - 10.1038/onc.2015.374

M3 - Review article

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VL - 35

SP - 2684

EP - 2686

JO - Oncogene

JF - Oncogene

IS - 21

ER -

TAMing resistance to multi-targeted kinase inhibitors through Axl and Met inhibition

Abstract

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