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these data suggest that HOXA4 is a potential diagnostic and prognostic marker in lung cancer, and its overexpression could inhibit lung cancer progression in part by promoting GSK3beta transcription.
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HOXA4 may play a role in regulating human growth by epigenetic mechanisms.
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HOXA4/HOXB3 gene expression-based risk score may be useful for prognostic risk stratification and warrants prospective validation in HGSOC patients.
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Overexpression of HOXA4 and HOXA9 contributes to self-renewal and overpopulation of stem cells in colorectal cancers.
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HOXA4 increases short-term repopulation to higher levels than HOXB4, which may involve Notch signaling to induce self-renewal of primitive hematopoietic cells
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The NK AML patients with NPM1 mutations exhibited elevated HOXA4 methylation and expression levels of HOXA5 and MEIS1 compared with the NPM1 wildtype patients.
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promoter hypermethylation of HOXA4 gene could be an epigenetic mechanism mediating IM resistance in CML patients.
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HOXA4 showed nuclear & perinuclear staining in endothelial & smooth muscle cells in aorta. Spatial variation in expression in human aortas persisted into adulthood. Downregulation of HOXA4 expression was associated with abdominal aortic aneurysm.
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Studies suggest that HOXA4, HOXA5 and HOXB4 provide the spatial information needed to restrict the response to signals from the notochord, and not up regulated in pancreatic cancer.
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Results confirm that HOXA4 inhibits cell motility, show that it suppresses cell spreading and filopodia formation while enhancing cell-cell adhesion, and suggest a role for beta1 integrin in mediating these changes.
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upregulated significantly in acute myeloid leukemia patients with a white blood cell count higher than 30 x 10(9)/L cells.
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aberrant DNA methylation may have a major role in the control of HOXA4 gene expression in chronic lymphocytic leukemia
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analysis of the role of deregulated PcG genes in acute myeloid leukemia, and the downstream PcG targets HOXA4, HOXA9 and MEIS1
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combination of low HOXA4 and low MEIS1 gene expression is a favourable predictor for outcome in all AML patients and that the expression levels are governed by the methylation state of these genes.