Comparison of MLL Fusion Genes Expression among the Cytogenetics Abnormalities of Acute Myeloid Leukemia and Their Clinical Effects

Dogan, Senol; Kurtovic-Kozaric, Amina

doi:10.4172/2155-6180.1000312

Cited by 5 publications

(5 citation statements)

References 21 publications

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“…The main MLL type rearrangements are (4;11), t(6;11), t(9;11), t (11;19) which are clustered within a 9-kb BamHI genomic region and 5-kb region and diagnosis, overall survival rate and therapy methods are arranged depending on the type rearrangements. For example, while t(6;11)(q27;q23) and t(10;11)(p12;q23) are correlated with a poor prognosis, t(9;11)(p22;q23) type survival rate is significantly longer than others [13,14].…”

Section: Mll Re-arrangementsmentioning

confidence: 99%

Untitled

2017

BPOJ

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MLL is one of the most aggressive leukemias which mostly targets pediatric patients. Genetic rearrangement of the 11q23 location is the main reason for this type of acute leukemia. MLL gene and its fusion proteins have produced a core complex which leads to abnormal hematopoesis. Although many clinical and lab studies have been done to show the prominent role of MLL in leukemogenesis since its discovery in 1992, large-scale genomic data seems to be the most effective way to analyse the hematologic malignancies extensively. Gene expression, methylation, mutation, RNA-seq, and SNP arrays have updated the understanding of the transformation oncohematologic disorder mechanism. As a result of the genomic data analysis, new biomarkers may have been detected as therapy target genes and used for personalized medicine. The genomics-bioinformatics studies and novel technical advances provide some precious knowledge to discover novel therapeutic strategies and better treatment outcomes in the future.

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Section: Mll Re-arrangementsmentioning

confidence: 99%

Untitled

2017

BPOJ

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“…Computer aided statistical analysis of cancer genomes for establishing the potential correlation among gene expression in cancer is getting frequent in current research and development [14,15]. Therefore, it is of interest to report stable and flexible gene expression patterns in cancer cells [16]. Hence, we describe a statistics model to identify stable and flexible genes among six different cancer types (colon, breast, lung, ovarian, brain and renal) as shown in Figure 1.…”

Section: Introductionmentioning

confidence: 99%

Detection and analysis of stable and flexible genes towards a genome signature framework in cancer

2019

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Comparison and detection of stable cancer genes across cancer types is of interest. The gene expression data of 6 different cancer types (colon, breast, lung, ovarian, brain and renal) and a control group from The Cancer Genome Atlas (TCGA) database were used in this study. The comparison of gene expression data together with the calculation standard deviations of such data was completed using a statistical model for the detection of stable genes. Genes having similar expression (referred as flexible genes) pattern to the control group in four out of six cancer types are PATE, NEUROD4 and TRAFD1. Moreover, 13 genes showed low difference compared to the control group with low standard deviation across cancer types (referred as stable genes). Among them, genes GDF2, KCNT1 and RNF151 showed consistent low expression while ODF4, OR5I1, MYOG and OR2B11 showed consistent high expression. Thus, the detection and analysis of stable and flexible cancer genes help towards the design and development of a framework (outline) for specific genome signature (biomarker) in cancer.

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“…Novel methylation in the promoter region and histone protein change the epigenetics of MLL type leukemia and involve with abnormal gene expression signature [13,14]. MLL gene with partner fusion proteins binds DOT1L, which is a key gene to understand the methylation status of leukemia, methylates H3 at lysine 79 and initiates the chromatin modification during transcriptional elongation [15,16]. It is necessary to show the genomic difference and responsible genes of MLL than AML.…”

Section: Introductionmentioning

confidence: 99%

New Possible Targetable Genes for Future Treatment of Mixed Lineage Leukemia

Dogan¹

2017

J Biom Biostat

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Aim of study: Leukemia has different subtypes, which present unique clinical and molecular characteristics. MLL (Mixed Lineage Leukemia) is one of the new different subtypes than AML and ALL. Materials and Methods:Genomic characterization is the main key understanding the differences of MLL by analysis of differential gene expression, methylation patterns and mutational spectra that were compared and analyzed between MLL and AML types (n=197).Results: According to the genomic characterization of MLL, differentially expressed 114 genes were selected and 37 of them targeted genes having more than 2 fold expression change, including HOXA9, CFH, DDX4, MSH4, MSMB, TWIST1, ZSWIM2, POU6F2. To measure the aberrant methylation is the second genomic characterization of this research because the rearrangements of MLL gene leading to aberrant methylation. The methylation data were compared between cancer and control, so high methylated genes have been detected between MLL and AML types. The methylation loci were categorized into two groups: ≥ 10 fold difference and ≥ 5 and ≤ 10 fold difference. Some of the genes high methylated more than one location such as; RAET1E, HSD17B2, RNASE11, DGK1, POU6F2, NAGS, PIK3C2G, GADL1, and KRT13. In addition to that, analysis of somatic mutation gives us that CFH has the highest point mutation 9,92%. Conclusion:Overall, the MLL genomic characterization shows that it is different than AML and exhibits a unique molecular and biological phenotype and point to new possible targetable genes for future treatment of MLL leukemia are two important values.

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Comparison of MLL Fusion Genes Expression among the Cytogenetics Abnormalities of Acute Myeloid Leukemia and Their Clinical Effects

Cited by 5 publications

References 21 publications

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Detection and analysis of stable and flexible genes towards a genome signature framework in cancer

New Possible Targetable Genes for Future Treatment of Mixed Lineage Leukemia

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