The Detection of Extremely High and Low Expressed Genes by EGEF Algorithm in Invasive Breast Cancer

Dogan, Senol; Kurtovic-Kozaric, Amina

doi:10.4172/2155-6180.1000286

Cited by 8 publications

(7 citation statements)

References 23 publications

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“…The main idea of the method is to compare the target genes between dead and alive patients. t-test has been applied to the gene expression values to find the statistically significant P-value between dead and alive dataset [14][15].…”

Section: Methodsmentioning

confidence: 99%

Analysis of Gaucher Disease Responsible Genes in Colorectal Adenocarcinoma

Karataş¹,

Turan²

2016

J Biom Biostat

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Gaucher disease is a hereditary genetic abnormality which defects the pathway of sphingolipid catabolism. The mutation of GBA gene which encodes lysosomal β-glucosidase enzyme is the main characteristics of the disease also is observed in different cancer types. To find the relation between the disease and colon adenocarcinoma, the responsible gene expression of Gaucher disease was analyzed. The gene expression of colon adenocarcinoma was compared between death and alive patients and analyzed statistically to profile the differences between Gaucher disease genes expression changes. GBA, GBA2, GBA3, SCARB2 and PSAP have the maximum genetic alteration which is observed in colon adenocarcinoma.

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Section: Methodsmentioning

confidence: 99%

Analysis of Gaucher Disease Responsible Genes in Colorectal Adenocarcinoma

Karataş¹,

Turan²

2016

J Biom Biostat

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“…GCase is encoded by the housekeeping gene glucosylceramidase beta acid 1 (GBA1, OMIM*606463) with cytogenetic location 1q21 [11]. More than 460 mutations are reported to disrupt the GBA1 gene [12,13], thereby abolishing its catalytic activity [14] and decreasing enzyme stability [15]. The improper breakdown of highly hydrophobic GC results in its accumulation in the lysosomes of macrophages, leading to dysfunctions in spleen, liver, and bone marrow [16,17].…”

Section: Introductionmentioning

confidence: 99%

Enzyme Kinetics and Inhibition Parameters of Human Leukocyte Glucosylceramidase

Karataş

Dogan

Spahiu³

et al. 2020

Preprint

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Glucosylceramidase (GCase) is a lysosomal enzyme that catalyzes the cleavage of β-glucosidic linkage of glucocerebroside (GC) into glucose and ceramide; thereby, plays an essential function in the degradation of complex lipids and the turnover of cellular membranes.The growing list of 460 mutations in the gene coding for it—glucosylceramidase beta acid 1 (GBA1)—is reported to abolish its catalytic activity and decrease its enzyme stability, associating it with severe health conditions such as Gaucher disease (GD), Parkinson Disease and Dementia with Lewy bodies.Although the three-dimensional structure of wild type glucosylceramidase is elucidated, little is known about its features in human cells. Moreover, alternative sources of GCase that prove to be effective in the treatment of diseases with enzyme treatment therapies, impose the need for simple and cost-effective procedures to study the enzyme behaviour. This work, for the first time, shows a well established, yet simple, cost- and time-efficient protocol for the study of GCase enzyme in human leukocytes by the artificial substrate PNPG. Characterization of the enzyme in human leukocytes for activation parameters (optimal pH, Km, and Vmax) and enzyme inhibition, was done. The results indicate that the optimum pH of GCase enzyme with PNPG is 5.1. The Km and Vmax values were 12.6mM and 333 U/mg, respectively. Gluconolactone successfully inhibits GCase in a competitive manner, with a Ki value of 0.023 mM and IC 50 of 0.047 mM. Glucose inhibition was uncompetitive with a Ki of 1.94 mM and IC50 of 55.3 mM. This is the first report for the inhibitory effect of glucose, δ-gluconolactone on leukocyte GCase activity.

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“…For example, gene expression profile demonstrates a novel profile that is different than AML and ALL patients [12]. 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].…”

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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The Detection of Extremely High and Low Expressed Genes by EGEF Algorithm in Invasive Breast Cancer

Cited by 8 publications

References 23 publications

Analysis of Gaucher Disease Responsible Genes in Colorectal Adenocarcinoma

Analysis of Gaucher Disease Responsible Genes in Colorectal Adenocarcinoma

Enzyme Kinetics and Inhibition Parameters of Human Leukocyte Glucosylceramidase

New Possible Targetable Genes for Future Treatment of Mixed Lineage Leukemia

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