Sphingosine Kinase 2 Supports the Development of BCR/ABL-Independent Acute Lymphoblastic Leukemia in Mice

Vicki Xie; Daochen Tong; Craig Wallington-Beddoe; Ken Bradstock; Linda Bendall

doi:10.1186/s40364-018-0120-4

Sphingosine Kinase 2 Supports the Development of BCR/ABL-Independent Acute Lymphoblastic Leukemia in Mice

Vicki Xie, Daochen Tong, Craig Wallington-Beddoe, Ken Bradstock, Linda Bendall

College of Medicine and Public Health

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

Background: Sphingosine kinase (SphK) 2 has been implicated in the development of a range of cancers and inhibitors of this enzyme are currently in clinical trial. We have previously demonstrated a role for SphK2 in the development of acute lymphoblastic leukemia (ALL). Methods: In this and our previous study we use mouse models: in the previous study the disease was driven by the proto-oncogene BCR/ABL1, while in this study cancer risk was elevated by deletion of the tumor suppressor ARF. Results: Mice lacking ARF and SphK2 had a significantly reduced incidence of ALL compared mice with wild type SphK2. Conclusions: These results show that the role of SphK2 in ALL development is not limited to BCR/ABL1 driven disease extending the potential use of inhibitors of this enzyme to ALL patients whose disease have driver mutations other than BCR/ABL1.

Original language	English
Article number	6
Number of pages	7
Journal	Biomarker Research
Volume	6
Issue number	1
DOIs	https://doi.org/10.1186/s40364-018-0120-4
Publication status	Published - 5 Feb 2018

Keywords

Acute lymphoblastic leukemia
Mouse models
Sphingosine kinase 2

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/s40364-018-0120-4

Cite this

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title = "Sphingosine Kinase 2 Supports the Development of BCR/ABL-Independent Acute Lymphoblastic Leukemia in Mice",

abstract = "Background: Sphingosine kinase (SphK) 2 has been implicated in the development of a range of cancers and inhibitors of this enzyme are currently in clinical trial. We have previously demonstrated a role for SphK2 in the development of acute lymphoblastic leukemia (ALL). Methods: In this and our previous study we use mouse models: in the previous study the disease was driven by the proto-oncogene BCR/ABL1, while in this study cancer risk was elevated by deletion of the tumor suppressor ARF. Results: Mice lacking ARF and SphK2 had a significantly reduced incidence of ALL compared mice with wild type SphK2. Conclusions: These results show that the role of SphK2 in ALL development is not limited to BCR/ABL1 driven disease extending the potential use of inhibitors of this enzyme to ALL patients whose disease have driver mutations other than BCR/ABL1.",

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AU - Tong, Daochen

AU - Wallington-Beddoe, Craig

AU - Bradstock, Ken

AU - Bendall, Linda

PY - 2018/2/5

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N2 - Background: Sphingosine kinase (SphK) 2 has been implicated in the development of a range of cancers and inhibitors of this enzyme are currently in clinical trial. We have previously demonstrated a role for SphK2 in the development of acute lymphoblastic leukemia (ALL). Methods: In this and our previous study we use mouse models: in the previous study the disease was driven by the proto-oncogene BCR/ABL1, while in this study cancer risk was elevated by deletion of the tumor suppressor ARF. Results: Mice lacking ARF and SphK2 had a significantly reduced incidence of ALL compared mice with wild type SphK2. Conclusions: These results show that the role of SphK2 in ALL development is not limited to BCR/ABL1 driven disease extending the potential use of inhibitors of this enzyme to ALL patients whose disease have driver mutations other than BCR/ABL1.

AB - Background: Sphingosine kinase (SphK) 2 has been implicated in the development of a range of cancers and inhibitors of this enzyme are currently in clinical trial. We have previously demonstrated a role for SphK2 in the development of acute lymphoblastic leukemia (ALL). Methods: In this and our previous study we use mouse models: in the previous study the disease was driven by the proto-oncogene BCR/ABL1, while in this study cancer risk was elevated by deletion of the tumor suppressor ARF. Results: Mice lacking ARF and SphK2 had a significantly reduced incidence of ALL compared mice with wild type SphK2. Conclusions: These results show that the role of SphK2 in ALL development is not limited to BCR/ABL1 driven disease extending the potential use of inhibitors of this enzyme to ALL patients whose disease have driver mutations other than BCR/ABL1.

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KW - Mouse models

KW - Sphingosine kinase 2

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Sphingosine Kinase 2 Supports the Development of BCR/ABL-Independent Acute Lymphoblastic Leukemia in Mice

Abstract

Keywords

UN SDGs

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