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Kairisto, V.

Publications and source records attributed to Kairisto, V..

2 recordsLinked to original sources

Variant calling tool evaluation for variable size indel calling from next generation whole genome and targeted sequencing data

Insertions and deletions (indels) in human genomes are associated with a wide range of phenotypes, including various clinical disorders. High-throughput, next generation sequencing (NGS) technologies enable detection of short genetic variants, such as single nucleotide variants (SNVs) and indels. However, the variant calling accuracy for indels remains considerably lower than for SNVs. Here we present a comparative study of the performance of variant calling tools on indel calling, evaluated with a wide repertoire of NGS datasets. While there is no single optimal tool to suit all circumstances, our results demonstrate that the choice of variant calling tool greatly impacts the precision and recall of indel calling. Furthermore, to reliably detect indels, it is essential to choose NGS technologies that offer a long read length and high coverage, coupled with specific variant calling tools. Author summaryThe development of next generation sequencing (NGS) technologies and computational algorithms enabled large scale, simultaneous detection of wide range of genetic variants, such as single nucleotide variants as well as insertions and deletions (indels), which may confer potential clinical significance. Recently, many studies have been conducted to evaluate variant calling tools on indel calling. However, the optimal indel size range for different variant calling tools remain unclear. A good benchmarking dataset for indel calling evaluation should contain biologically representative high-confident indels with a wide size range and preferably come from various sequencing settings. In this article, we created a semi-simulated whole genome sequencing dataset where the sequencing data was computationally generated. The indels in the semi-simulated genome were incorporated from a real human sample to represent biologically realistic indels and to avoid inclusion of variants due to potential technical sequencing errors. Furthermore, we used three real-world NGS datasets generated by whole genome or targeted sequencing to further evaluate our candidate tools. Our results demonstrated that variant calling tools varies greatly in calling different sizes of indels. Deletion calling and insertion calling also showed differences among the tools. The sequencing settings in coverage and read length also had a great impact on indel calling. Our results suggest that the accurate indel calling was dependent on the combination of a variant calling tool, indel size range and sequencing settings.

bioinformatics

ARPP19 promotes MYC expression and associates with patient relapse in acute myeloid leukemia

Despite of extensive genetic analysis of acute myeloid leukemia (AML), we still do not understand comprehensively mechanism that promote disease relapse from standard chemotherapy. Based on recent indications for non-genomic inhibition of tumor suppressor protein phosphatase 2A (PP2A) in AML, we examined mRNA expression of PP2A inhibitor proteins in AML patient samples. Notably, out of examined PP2A inhibitor proteins, overexpression of ARPP19 mRNA was found independent of current AML risk classification. Functionally, ARPP19 promoted AML cell viability and expression of oncoproteins MYC, CDK1, and another PP2A inhibitor CIP2A. Clinically, ARPP19 mRNA expression was significantly lower at diagnosis (p=0.035) in patients whose disease did not relapse after standard chemotherapy. ARPP19 was an independent predictor for relapse both in univariable (p=0.007) and in multivariable analyses (p=0.0001); and gave additive information to EVI1 expression and risk group status (additive effect, p=0.005). Low ARPP19 expression also associated with better patient outcome in TCGA LAML cohort (p=0.019). In addition, in matched patient samples from diagnosis, remission and relapse phases, ARPP19 expression associated with disease activity (p=0.034).\n\nTogether, these data identify ARPP19 as a novel oncogenic PP2A inhibitor protein in AML, and demonstrate its risk group independent role in predicting AML patient relapse tendency.

cancer biology