Checks and balances: Interplay of RTKs and PTPs in cancer progression

Sarita K. Sastry; Lisa A. Elferink

doi:10.1016/j.bcp.2011.06.016

Checks and balances: Interplay of RTKs and PTPs in cancer progression

Sarita K. Sastry, Lisa A. Elferink

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Research output: Contribution to journal › Comment/debate › peer-review

27 Scopus citations

Abstract

In recent years, targeted therapies for receptor tyrosine kinases (RTKs) have shown initial promise in the clinical setting for the treatment of several tumors driven by these oncogenic signaling pathways. Unfortunately, clinical relapse due to acquired resistance to these molecular therapeutics is common. An improved understanding of how tumors bypass the inhibitory effects of RTK-targeted therapies has revealed a rich myriad of possible mechanisms for acquired resistance. Protein tyrosine phosphatases (PTPs) can function as oncogenes or tumor suppressors to either enhance or suppress RTK signaling. Recent studies suggest that the loss or gain of function of PTP's can significantly impinge on RTK signaling during tumor progression. Here we review the interplay between RTKs and PTPs as an emerging mechanism for acquired resistance to RTK-targeted therapies, that may aid in the design of improved therapies to prevent and overcome resistance in treatments for cancer patients.

Original language	English (US)
Pages (from-to)	435-440
Number of pages	6
Journal	Biochemical Pharmacology
Volume	82
Issue number	5
DOIs	https://doi.org/10.1016/j.bcp.2011.06.016
State	Published - Sep 1 2011

Keywords

Acquired resistance
Cancer
Phosphatase
Receptor tyrosine kinase

ASJC Scopus subject areas

Pharmacology
Biochemistry

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10.1016/j.bcp.2011.06.016

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title = "Checks and balances: Interplay of RTKs and PTPs in cancer progression",

abstract = "In recent years, targeted therapies for receptor tyrosine kinases (RTKs) have shown initial promise in the clinical setting for the treatment of several tumors driven by these oncogenic signaling pathways. Unfortunately, clinical relapse due to acquired resistance to these molecular therapeutics is common. An improved understanding of how tumors bypass the inhibitory effects of RTK-targeted therapies has revealed a rich myriad of possible mechanisms for acquired resistance. Protein tyrosine phosphatases (PTPs) can function as oncogenes or tumor suppressors to either enhance or suppress RTK signaling. Recent studies suggest that the loss or gain of function of PTP's can significantly impinge on RTK signaling during tumor progression. Here we review the interplay between RTKs and PTPs as an emerging mechanism for acquired resistance to RTK-targeted therapies, that may aid in the design of improved therapies to prevent and overcome resistance in treatments for cancer patients.",

keywords = "Acquired resistance, Cancer, Phosphatase, Receptor tyrosine kinase",

author = "Sastry, {Sarita K.} and Elferink, {Lisa A.}",

note = "Funding Information: The authors regret that due to space limitations, they were unable to cite a number of outstanding papers relevant to this article. The authors gratefully acknowledge Mr. John Helms (UTMB Cancer Center) for expert assistance with graphic arts. This work was supported by grants from the National Institutes of Health to L.A.E. ( CA-119075 ) and S.K.S. ( CA-118405 ).",

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doi = "10.1016/j.bcp.2011.06.016",

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T2 - Interplay of RTKs and PTPs in cancer progression

AU - Sastry, Sarita K.

AU - Elferink, Lisa A.

N1 - Funding Information: The authors regret that due to space limitations, they were unable to cite a number of outstanding papers relevant to this article. The authors gratefully acknowledge Mr. John Helms (UTMB Cancer Center) for expert assistance with graphic arts. This work was supported by grants from the National Institutes of Health to L.A.E. ( CA-119075 ) and S.K.S. ( CA-118405 ).

PY - 2011/9/1

Y1 - 2011/9/1

N2 - In recent years, targeted therapies for receptor tyrosine kinases (RTKs) have shown initial promise in the clinical setting for the treatment of several tumors driven by these oncogenic signaling pathways. Unfortunately, clinical relapse due to acquired resistance to these molecular therapeutics is common. An improved understanding of how tumors bypass the inhibitory effects of RTK-targeted therapies has revealed a rich myriad of possible mechanisms for acquired resistance. Protein tyrosine phosphatases (PTPs) can function as oncogenes or tumor suppressors to either enhance or suppress RTK signaling. Recent studies suggest that the loss or gain of function of PTP's can significantly impinge on RTK signaling during tumor progression. Here we review the interplay between RTKs and PTPs as an emerging mechanism for acquired resistance to RTK-targeted therapies, that may aid in the design of improved therapies to prevent and overcome resistance in treatments for cancer patients.

AB - In recent years, targeted therapies for receptor tyrosine kinases (RTKs) have shown initial promise in the clinical setting for the treatment of several tumors driven by these oncogenic signaling pathways. Unfortunately, clinical relapse due to acquired resistance to these molecular therapeutics is common. An improved understanding of how tumors bypass the inhibitory effects of RTK-targeted therapies has revealed a rich myriad of possible mechanisms for acquired resistance. Protein tyrosine phosphatases (PTPs) can function as oncogenes or tumor suppressors to either enhance or suppress RTK signaling. Recent studies suggest that the loss or gain of function of PTP's can significantly impinge on RTK signaling during tumor progression. Here we review the interplay between RTKs and PTPs as an emerging mechanism for acquired resistance to RTK-targeted therapies, that may aid in the design of improved therapies to prevent and overcome resistance in treatments for cancer patients.

KW - Acquired resistance

KW - Cancer

KW - Phosphatase

KW - Receptor tyrosine kinase

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JO - Biochemical Pharmacology

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Checks and balances: Interplay of RTKs and PTPs in cancer progression

Abstract

Keywords

ASJC Scopus subject areas

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