ArticleMedical oncology (Northwood, London, England)2014
Intact expression status of RASSF1A in acute myeloid leukemia.
Article in Medical oncology (Northwood, London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Lack of Altered BECN1 Gene Expression in Iranian Patients with Acute Myeloid LeukemiaAsian Pacific journal of cancer prevention : APJCP · 2016Article
- Valproic acid may exerts its cytotoxic effect through rassf1a expression induction in acute myeloid leukemia.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- RASSF1A Site-Specific Methylation Hotspots in Cancer and Correlation with RASSF1C and MOAP-1.Cancers · 2016Article
- PML/RARα-Regulated miR-181a/b Cluster Targets the Tumor Suppressor RASSF1A in Acute Promyelocytic Leukemia.Cancer research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a typical tumor suppressor gene, transcriptional silencing of ras-association domain family 1, isoform A (RASSF1A) is caused by biallelic methylation or the condition that one allele is methylated and then the other allele lost by allelic loss, as second hit. RASSF1A is inactivated epigenetically and thus down-regulated in many solid tumors. In summary, for the first time, we analyzed the expression status of RASSF1A in a cohort of 56 de novo acute myeloid leukemia (AML) patients using quantitative real-time polymerase chain reaction. Results of our study indicate that patients with AML exhibited no differences in the RASSF1A gene expression comparing to normal controls. In conclusion, expression status of RASSF1A remained intact in our target samples, indicating that RASSF1A expression variation does not participate in the pathogenesis and the progression of AML.
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Registered trials
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