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This is a report of established invasive Aspergillus rhinosinusitis in a patient diagnosed with COVID-19 and afflicted by AML, which was initially considered to be rhinocerebral mucormycosis. [ABSTRACT FROM AUTHOR]

Background: Acute myeloid leukemia (AML) may originate from the combination of genetic susceptibility factors and environmental exposure. The aim of this study was to investigate the association of GSTM1 and GSTT1 null genotypes and CYP1A1*2A allele with susceptibility to AML in an Iranian population. Method: In this case-control study, 200 patients with AML and 200 normal individuals as controls were included. GSTM1 and GSTT1 null genotypes were amplified using multiplex PCR and CYP1A1*2A polymorphisms were genotyped by PCR-RFLP. Result: The frequency of GSTM1 null genotype was significantly higher in the control group compared to the case group. The frequency of GSST1 null genotype was significantly lower in the controls. No association was observed between the studied CYP1A1*2A variant and the risk of acute myeloid leukemia. The combination of GSTT1 null genotype and CYP1A1 *2A AA and AC alleles further increased the risk of AML. Conclusion: GSTT1 null genotype can increase the risk of AML, particularly when combined with CYP1A1*2A allele. GSTM1 null genotype can also play a protective role and reduce the risk of AML. However, further studies are required on a larger number of patients. [ABSTRACT FROM AUTHOR]

Background: Recently, in an effort to fully characterize the underlying genetic causes of the acute myeloid leukemia (AML), attention has been devoted to the newest aspect of gene expression regulations which inferred to the regulatory long none coding RNAs. Objectives: ANRIL is one of the disease associated IncRNAs which is transcribed from a critical genomic region that has an important role in the expression regulation of its neighbor genes CDKN2A and CDKN2B encoding 3 major tumor suppressor genes p14ARF, p15INK4b and p16INK4a. Methods: Since the identified variants in the CDKN2A and CDKN2B genes or ANRIL locus are reported to be associated with tumorigenesis in different cancers, we investigate 4 single nucleotide polymorphisms (SNP) of ANRIL in Iranian AML patients in comparison to control individuals Results: The results showed significant association neither for allelic and genotypic frequencies nor for haplotype blocks with AML patients versus control subjects. Conclusions: With regard to the indicated roles of ANRIL in epigenetic gene expression regulation, exploring its AML-associated genetic defects or its aberrant expression in patients is still a growing area of research and further investigations may illustrate its potential to serve as a diagnostic biomarker or a therapeutic target for AML. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a complex hematological neoplasm with poor prognosis. At present, overwhelming evidence indicates that different genetic abnormalities are relevant to the pathogenesis of AML. Nevertheless, its exact molecular mechanism is still unknown. Recently, it was reported that lncRNAs play crucial roles in tumorigenesis. But, their role in the molecular pathogenesis of AML has not been extensively explored. GAS5, one of the earliest known lncRNAs, has an essential role in the formation and progression of multiple human cancers. It was recently demonstrated that GAS5 acts as a riborepressor of the Glucocorticoid receptor) GR) and abnormal levels of GAS5 may alter response of hematopoietic cells to glucocorticoids. GAS5 can have interaction with the GR that encoded by NR3C1 gene and inhibit its transcriptional activity. To test whether the genetic variants can be associated with AML risk, we genotyped rs55829688 (T > C) polymorphism in GAS5 and three NR3C1 SNPs namely rs6195, rs41423247 and rs6189/rs6190 in a population of 100 Iranian AML patients and 100 healthy subjects. The analysis of the data showed the frequency of alleles and genotypes of rs55829688 and rs6189/rs6190 polymorphisms did not differ between patients and healthy subjects. But, rs41423247 and rs6195 demonstrated a significant correlation with AML risk. The rs6195 was associated with higher AML susceptibility in the co-dominant (OR = 4.58, 95% CI = 2.11-9.981, P < .0001), dominant (OR = 4.55, 95% CI = 2.155-9.613, P < .0001), and over-dominant (OR = 4.43, 95% CI = 2.042-9.621, P < .0001) models. Also, the rs41423247 polymorphism was associated with higher risk of AML in co-dominant (OR = 2.07, 95% CI = 1.171-4.242, P = .012) and dominant (OR = 2.47, 95% CI = 1.192-5.142, P = .010) models. Furthermore, haplotype analysis (rs41423247, rs6189.rs6190, rs6195, and rs55829688 respectively) demonstrated that GGAT, CGGT, and GGGT haplotypes were associated with higher risk of AML in the studied population (p-values = .007, 0.042 and 0.044, respectively). The present study reveals a possible role for NR3C1 in the pathogenesis of AML., (Copyright © 2020 Elsevier Inc. All rights reserved.)