The oncogenic fusion protein CBFB-SMMHC downregulates CD48 to evade NK cell recognition

Shira Kahlon; Dorin Shreibman; Tamar Unger; Dina Ben-Yehuda; Shlomo Elias

doi:10.1038/s41408-018-0082-7

The oncogenic fusion protein CBFB-SMMHC downregulates CD48 to evade NK cell recognition

Shira Kahlon, Dorin Shreibman, Tamar Unger, Dina Ben-Yehuda, Shlomo Elias

Life Sciences Core Facilities

Weizmann Institute of Science

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

Abstract

Chromosomal translocations are often found in acute leukemia and frequently result in the generation of fusion proteins with oncogenic properties. We recently studied the immune evasion properties of PML-RARA and AML1-ETO, two common oncogenic fusion proteins in acute myeloid leukemia (AML). We found that both of these fusion proteins downregulate the expression of CD48, a ligand of the NK cell-activating receptor 2B4, thus leading to impaired NK cell cytotoxicity. However, it remained unclear whether other leukemic fusion proteins can manipulate NK cell ligands. To explore this issue, here we tested the effects of several leukemic fusion proteins on the expression of NK cell ligands.

Original language	English
Article number	48
Number of pages	4
Journal	Blood Cancer Journal
Volume	8
Issue number	5
DOIs	https://doi.org/10.1038/s41408-018-0082-7
State	Published - 1 May 2018

All Science Journal Classification (ASJC) codes

Hematology
Oncology

UN SDGs

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

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10.1038/s41408-018-0082-7

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title = "The oncogenic fusion protein CBFB-SMMHC downregulates CD48 to evade NK cell recognition",

abstract = "Chromosomal translocations are often found in acute leukemia and frequently result in the generation of fusion proteins with oncogenic properties. We recently studied the immune evasion properties of PML-RARA and AML1-ETO, two common oncogenic fusion proteins in acute myeloid leukemia (AML). We found that both of these fusion proteins downregulate the expression of CD48, a ligand of the NK cell-activating receptor 2B4, thus leading to impaired NK cell cytotoxicity. However, it remained unclear whether other leukemic fusion proteins can manipulate NK cell ligands. To explore this issue, here we tested the effects of several leukemic fusion proteins on the expression of NK cell ligands.",

author = "Shira Kahlon and Dorin Shreibman and Tamar Unger and Dina Ben-Yehuda and Shlomo Elias",

note = "Funding Information: The study was supported by the Israel Science Foundation (grant 502/15), the Kass Medical Research Award, and the Israeli Society of Hematology and Transfusion Medicine (to S.E.). We thank Dr. Svetelana Krichevsky and Ms. Orly Yehuda Weinstein from Hadassah Medical Center for their help in collecting the human patient samples.",

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AU - Ben-Yehuda, Dina

AU - Elias, Shlomo

N1 - Funding Information: The study was supported by the Israel Science Foundation (grant 502/15), the Kass Medical Research Award, and the Israeli Society of Hematology and Transfusion Medicine (to S.E.). We thank Dr. Svetelana Krichevsky and Ms. Orly Yehuda Weinstein from Hadassah Medical Center for their help in collecting the human patient samples.

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N2 - Chromosomal translocations are often found in acute leukemia and frequently result in the generation of fusion proteins with oncogenic properties. We recently studied the immune evasion properties of PML-RARA and AML1-ETO, two common oncogenic fusion proteins in acute myeloid leukemia (AML). We found that both of these fusion proteins downregulate the expression of CD48, a ligand of the NK cell-activating receptor 2B4, thus leading to impaired NK cell cytotoxicity. However, it remained unclear whether other leukemic fusion proteins can manipulate NK cell ligands. To explore this issue, here we tested the effects of several leukemic fusion proteins on the expression of NK cell ligands.

AB - Chromosomal translocations are often found in acute leukemia and frequently result in the generation of fusion proteins with oncogenic properties. We recently studied the immune evasion properties of PML-RARA and AML1-ETO, two common oncogenic fusion proteins in acute myeloid leukemia (AML). We found that both of these fusion proteins downregulate the expression of CD48, a ligand of the NK cell-activating receptor 2B4, thus leading to impaired NK cell cytotoxicity. However, it remained unclear whether other leukemic fusion proteins can manipulate NK cell ligands. To explore this issue, here we tested the effects of several leukemic fusion proteins on the expression of NK cell ligands.

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The oncogenic fusion protein CBFB-SMMHC downregulates CD48 to evade NK cell recognition

Abstract

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