Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia

Cancer: Mismatched molecules unleash leukemia cell proliferation A chromosomal rearrangement commonly observed in certain leukemias selectively inactivates a gene that otherwise thwarts cancerous growth. Between 7 and 12% of acute myeloid leukemia cases exhibit a dramatic alteration in chromosomal s...

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Main Authors: Lei Zhou, Lin Fu, Na Lv, Jing Liu, Yan Li, Xiaosu Chen, Qingyu Xu, Guofeng Chen, Baoxu Pang, Lili Wang, Yonghui Li, Xiaodong Zhang, Li Yu
Format: Article
Language:English
Published: Nature Publishing Group 2018-04-01
Series:Experimental and Molecular Medicine
Online Access:https://doi.org/10.1038/s12276-018-0067-4
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author Lei Zhou
Lin Fu
Na Lv
Jing Liu
Yan Li
Xiaosu Chen
Qingyu Xu
Guofeng Chen
Baoxu Pang
Lili Wang
Yonghui Li
Xiaodong Zhang
Li Yu
author_facet Lei Zhou
Lin Fu
Na Lv
Jing Liu
Yan Li
Xiaosu Chen
Qingyu Xu
Guofeng Chen
Baoxu Pang
Lili Wang
Yonghui Li
Xiaodong Zhang
Li Yu
author_sort Lei Zhou
collection DOAJ
description Cancer: Mismatched molecules unleash leukemia cell proliferation A chromosomal rearrangement commonly observed in certain leukemias selectively inactivates a gene that otherwise thwarts cancerous growth. Between 7 and 12% of acute myeloid leukemia cases exhibit a dramatic alteration in chromosomal structure that results in the production of an abnormal fusion protein. Researchers led by Li Yu at the General Hospital of Shenzen University in China have learned that this protein promotes disease progression by switching off an important tumor suppressor. Yu and colleagues showed that it binds a genomic sequence that regulates the gene encoding a second protein called BASP1, dramatically reducing its production. This gene silencing facilitates tumor growth. Chemicals that reactivated BASP1 production slowed proliferation and initiated ‘self-destruct’ mechanisms in leukemia cells. These findings suggest that BASP1-oriented therapies could offer a fruitful avenue of treatment for some patients.
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spelling doaj.art-ddf406b030b44c1695a30a0b819794232022-12-21T23:34:41ZengNature Publishing GroupExperimental and Molecular Medicine2092-64132018-04-015041810.1038/s12276-018-0067-4Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemiaLei Zhou0Lin Fu1Na Lv2Jing Liu3Yan Li4Xiaosu Chen5Qingyu Xu6Guofeng Chen7Baoxu Pang8Lili Wang9Yonghui Li10Xiaodong Zhang11Li Yu12Department of Hematology, Chinese PLA General HospitalDepartment of Hematology and Lymphoma Research Center, Peking University, Third HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Chemical Immunology, Leiden University Medical CenterDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, Chinese PLA General HospitalDepartment of Hematology, No. 202 Hospital of PLADepartment of Hematology, Chinese PLA General HospitalCancer: Mismatched molecules unleash leukemia cell proliferation A chromosomal rearrangement commonly observed in certain leukemias selectively inactivates a gene that otherwise thwarts cancerous growth. Between 7 and 12% of acute myeloid leukemia cases exhibit a dramatic alteration in chromosomal structure that results in the production of an abnormal fusion protein. Researchers led by Li Yu at the General Hospital of Shenzen University in China have learned that this protein promotes disease progression by switching off an important tumor suppressor. Yu and colleagues showed that it binds a genomic sequence that regulates the gene encoding a second protein called BASP1, dramatically reducing its production. This gene silencing facilitates tumor growth. Chemicals that reactivated BASP1 production slowed proliferation and initiated ‘self-destruct’ mechanisms in leukemia cells. These findings suggest that BASP1-oriented therapies could offer a fruitful avenue of treatment for some patients.https://doi.org/10.1038/s12276-018-0067-4
spellingShingle Lei Zhou
Lin Fu
Na Lv
Jing Liu
Yan Li
Xiaosu Chen
Qingyu Xu
Guofeng Chen
Baoxu Pang
Lili Wang
Yonghui Li
Xiaodong Zhang
Li Yu
Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
Experimental and Molecular Medicine
title Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
title_full Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
title_fullStr Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
title_full_unstemmed Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
title_short Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
title_sort methylation associated silencing of basp1 contributes to leukemogenesis in t 8 21 acute myeloid leukemia
url https://doi.org/10.1038/s12276-018-0067-4
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