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High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation
Background: Overexpression of dedicator of cytokinesis 1 (DOCK1) has been confirmed as an unfavorable prognostic marker in acute myeloid leukemia (AML). Purpose: This study is to explore the clinical implications of DOCK1 on AML patients underwent allogeneic hematopoietic stem cell transplantation (...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489661/ https://www.ncbi.nlm.nih.gov/pubmed/31114350 http://dx.doi.org/10.2147/CMAR.S192845 |
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author | Zhang, Gaoqi Zhang, Jilei Yang, Xinrui Zhang, Xinpei Yang, Siyuan Wang, Jing Hu, Kai Shi, Jinlong Ke, Xiaoyan Fu, Lin |
author_facet | Zhang, Gaoqi Zhang, Jilei Yang, Xinrui Zhang, Xinpei Yang, Siyuan Wang, Jing Hu, Kai Shi, Jinlong Ke, Xiaoyan Fu, Lin |
author_sort | Zhang, Gaoqi |
collection | PubMed |
description | Background: Overexpression of dedicator of cytokinesis 1 (DOCK1) has been confirmed as an unfavorable prognostic marker in acute myeloid leukemia (AML). Purpose: This study is to explore the clinical implications of DOCK1 on AML patients underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT). Patients and methods: We analyzed 71 de novo AML patients treated with allo-HSCT and divided them into two groups (DOCK1(high) vs DOCK1(low)) by the median expression level of DOCK1. Results: High DOCK1 expression was associated with older age (P=0.019), wild-type CEBPA (P=0.002), IDH1/2 mutations (P=0.010) and RUNX1 mutation (P=0.005). Univariate analyses showed that DOCK1(high) and RUNX1 mutation were associated with shorter OS (P<0.001, P=0.024). Multivariate analysis confirmed the negative effect of high DOCK1 level on overall survival (P=0.010). Conclusion: Our results demonstrate that in AML patients who received allo-HSCT, high DOCK1 expression might have a persistent negative prognostic impact post-transplant. |
format | Online Article Text |
id | pubmed-6489661 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-64896612019-05-21 High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation Zhang, Gaoqi Zhang, Jilei Yang, Xinrui Zhang, Xinpei Yang, Siyuan Wang, Jing Hu, Kai Shi, Jinlong Ke, Xiaoyan Fu, Lin Cancer Manag Res Original Research Background: Overexpression of dedicator of cytokinesis 1 (DOCK1) has been confirmed as an unfavorable prognostic marker in acute myeloid leukemia (AML). Purpose: This study is to explore the clinical implications of DOCK1 on AML patients underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT). Patients and methods: We analyzed 71 de novo AML patients treated with allo-HSCT and divided them into two groups (DOCK1(high) vs DOCK1(low)) by the median expression level of DOCK1. Results: High DOCK1 expression was associated with older age (P=0.019), wild-type CEBPA (P=0.002), IDH1/2 mutations (P=0.010) and RUNX1 mutation (P=0.005). Univariate analyses showed that DOCK1(high) and RUNX1 mutation were associated with shorter OS (P<0.001, P=0.024). Multivariate analysis confirmed the negative effect of high DOCK1 level on overall survival (P=0.010). Conclusion: Our results demonstrate that in AML patients who received allo-HSCT, high DOCK1 expression might have a persistent negative prognostic impact post-transplant. Dove 2019-04-11 /pmc/articles/PMC6489661/ /pubmed/31114350 http://dx.doi.org/10.2147/CMAR.S192845 Text en © 2019 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhang, Gaoqi Zhang, Jilei Yang, Xinrui Zhang, Xinpei Yang, Siyuan Wang, Jing Hu, Kai Shi, Jinlong Ke, Xiaoyan Fu, Lin High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title | High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title_full | High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title_fullStr | High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title_full_unstemmed | High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title_short | High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
title_sort | high expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489661/ https://www.ncbi.nlm.nih.gov/pubmed/31114350 http://dx.doi.org/10.2147/CMAR.S192845 |
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