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Yi-Chang Liu

Researcher at Kaohsiung Medical University

Publications -  99
Citations -  1289

Yi-Chang Liu is an academic researcher from Kaohsiung Medical University. The author has contributed to research in topics: Hematopoietic stem cell transplantation & Myeloid leukemia. The author has an hindex of 16, co-authored 88 publications receiving 1051 citations. Previous affiliations of Yi-Chang Liu include Fooyin University.

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MALAT1 long non-coding RNA is overexpressed in multiple myeloma and may serve as a marker to predict disease progression.

TL;DR: MALAT1 was overexpressed in patients with myeloma and may play a role in its pathogenesis and in addition, MALAT1 may serve as a molecular predictor of early progression.
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Downregulation of circadian clock genes in chronic myeloid leukemia: alternative methylation pattern of hPER3.

TL;DR: The results suggest that the downregulated hPER3 expression in CML is correlated with the inactivation of hPER2 by methylation, and the methylated CpG frequencies differed significantly in patients at blastic crisis and at chronic phase.
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Altered Expression of Circadian Clock Genes in Human Chronic Myeloid Leukemia

TL;DR: Comparisons were made between the expression profiles of 9 circadian clock genes from peripheral blood mononuclear cells (PBMCs) and polymorphonuclear Cells (PMNs) and patients with chronic myeloid leukemia to indicate a possible association of the disrupted daily patterns of circadian clock gene expression with the pathogenesis of CML.
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Deregulated expression of circadian clock genes in gastric cancer.

TL;DR: The results suggest deregulated expressions of circadian clock genes exist in GC and circadian rhythm disturbance may be associated with the development of GC.
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Induction of Cellular Senescence by Doxorubicin Is Associated with Upregulated miR-375 and Induction of Autophagy in K562 Cells

TL;DR: This study has demonstrated that in the absence of p53 and p16, the induction of senescence by DOX was associated with upregulation of miR-375 and autophagy initiation, and the anti-proliferative function of mi R-375 is possibly exerted, at least in part, by targeting 14-3-3zeta and SP1 genes.