scholarly journals Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia

2018 ◽  
Author(s):  
Xiao‑Hui Zhang ◽  
Lin Yang ◽  
Xiao‑Jun Liu ◽  
Ying Zhan ◽  
Yu‑Xia Pan ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Myeloid Leukemia ◽  
Suppressor Gene ◽  
Acute Myeloid

scholarly journals DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication

Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 2013-2016 ◽  
Author(s):  
Susan P. Whitman ◽  
Björn Hackanson ◽  
Sandya Liyanarachchi ◽  
Shujun Liu ◽  
Laura J. Rush ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Myeloid Leukemia ◽  
Tandem Duplication ◽  
Suppressor Gene ◽  
Dna Hypermethylation ◽  
Partial Tandem Duplication ◽  
Acute Myeloid

Abstract Posttranslationally modified histones and DNA hypermethylation frequently interplay to deregulate gene expression in cancer. We report that acute myeloid leukemia (AML) with an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-PTD), exhibits increased global DNA methylation versus AML with MLL-wildtype (MLL-WT; P = .02). Among the differentially methylated genes, the SLC5A8 tumor suppressor gene (TSG) was more frequently hypermethylated (P = .003). In MLL-PTD+ cell lines having SLC5A8 promoter hypermethylation, incubation with decitabine activated SLC5A8 expression. Ectopic SLC5A8 expression enhanced histones H3 and H4 acetylation in response to the histone deacetylase inhibitor, valproate, consistent with the encoded protein—SMCT1—short-chain fatty acid transport function. In addition, enhanced cell death was observed in SMCT1-expressing MLL-PTD+ AML cells treated with valproate. Within the majority of MLL-PTD AML is a mechanism in which DNA hypermethylation silences a TSG that, together with MLL-PTD, can contribute further to aberrant chromatin remodeling and altered gene expression.

scholarly journals Polymerase chain reaction-based diagnosis of del (5q) in acute myeloid leukemia and myelodysplastic syndrome identifies a minimal deletion interval

Blood ◽  
1996 ◽  
Vol 88 (7) ◽  
pp. 2665-2670 ◽  
Author(s):  
SK Horrigan ◽  
CA Westbrook ◽  
AH Kim ◽  
M Banerjee ◽  
W Stock ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Myeloid Leukemia ◽  
Suppressor Gene ◽  
Malignant Cells ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Acute Myeloid

Loss of all or part of the long arm of human chromosome 5 is a recurrent abnormality in patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), especially after chemotherapy for a prior malignancy. It is one of the worst prognostic indicators in AML, associated with chemotherapy resistance and short survival. These deletions center at band 5q31, which has thus been proposed as the location of a tumor suppressor gene; this site is to be distinguished from that observed in 5q- syndrome, centering at 5q32. To define the molecular extent and the clinical prevalence of 5q31 deletions, we collected a series of AML and MDS cases of mixed karyotype, taking care to exclude MDS cases with 5q- syndrome. The samples were analyzed for loss of heterozygosity (LOH) using a panel polymerase chain reaction (PCR)-based microsatellite markers from 5q, comparing malignant cells with normal tissue derived from lymphoblastoid cell lines or buccal mucosa scrapings. Losses were detected in seven of 29 matched samples, including four of 17 with MDS, and three of 12 with AML; six of these seven also had a cytogenetically-visible del(5q) or -5. The one case without a cytogenetic deletion showed molecular loss of three contiguous markers, with retention of flanking markers interleukin-9 (IL-9) and D5S414, and thus contained a small deletion that is below cytogenetic resolution. PCR failed to detect 5q loss in two cases with large cytogenetic deletions, but both had been treated and contained low percentages of malignant cells in the samples. This study thus led to the identification of a case with a minimal deletion for the 5q31 tumor suppressor gene, specified by IL-9-D5S414, that is approximately 1 Mb (2 cM) in extent. Additionally, we demonstrate that PCR-based allelotyping is a reliable method for the detection of chromosomal deletion in myeloid malignancy, providing the specimens contain a high proportion of malignant cells. These studies will help to identify the tumor-suppressor gene at 5q31, and will help to develop molecular methods for diagnosis and monitoring of these disorders.

scholarly journals HIF-1α can act as a tumor suppressor gene in murine acute myeloid leukemia

Blood ◽  
2014 ◽  
Vol 124 (24) ◽  
pp. 3597-3607 ◽  
Author(s):  
Talia Velasco-Hernandez ◽  
Axel Hyrenius-Wittsten ◽  
Matilda Rehn ◽  
David Bryder ◽  
Jörg Cammenga
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Myeloid Leukemia ◽  
Suppressor Gene ◽  
Key Points ◽  
Disease Initiation ◽  
Acute Myeloid

Key Points Disease initiation and maintenance in murine AML models occurs via HIF-1α independent mechanisms. HIF-1α deficiency in mice accelerates leukemogenesis induced by certain oncogenes.

scholarly journals Aberrant DNA hypermethylation of the ITIH5 tumor suppressor gene in acute myeloid leukemia

2011 ◽  
Vol 2 (2) ◽  
pp. 419-423 ◽  
Author(s):  
Christoph Oing ◽  
Edgar Jost ◽  
Edgar Dahl ◽  
Stefan Wilop ◽  
Tim H. Brümmendorf ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Myeloid Leukemia ◽  
Suppressor Gene ◽  
Dna Hypermethylation ◽  
Acute Myeloid
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