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Significance of ATM Gene Polymorphisms in Chronic Myeloid Leukemia - a Case Control Study from India
Gorre, Manjula,Mohandas, Prajitha Edathara,Kagita, Sailaja,Cingeetham, Anuradha,Vuree, Sugunakar,Jarjapu, Sarika,Nanchari, Santhoshirani,Meka, Phanni Bhushann,Annamaneni, Sandhya,Dunna, Nageswara Rao Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.2
Background: Development of chronic myeloid leukemia (CML) involves formation of double strand breaks (DSBs) which are initially sensed by the ataxia telangiectasia mutated (ATM) signal kinase to induce a DNA damage response (DDR). Mutations or single nucleotide polymorphisms in ATM gene are known to influence the signaling capacity resulting in susceptibility to certain genetic diseases such as cancers. Materials and Methods: In the present study, we have analyzed -5144A>T (rs228589) and C4138T (rs3092856) polymorphisms of theATM gene through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 925 subjects (476 CML cases and 449 controls). Results: The A allele of -5144A>T polymorphism and T allele of C4138T polymorphism which were known to be influencing ATM signaling capacity are significantly associated with enhanced risk for CML independently and also in combination (evident from the haplotype and diplotype analyses). Significant elevation in the frequencies of both the risk alleles among high risk groups under European Treatment and Outcome Study (EUTOS) score suggests the possible role of these polymorphisms in predicting the prognosis of CML patients. Conclusions: This study provides the first evidence of association of functional ATM gene polymorphisms with the increased risk of CML development as well as progression.
jatoth deepak naik,Pradeep Gorre,Naga Ganesh Akuri,Sandeep Kumar,Ala’aDdin Al-Shidaifat,송한정 한국바이오칩학회 2022 BioChip Journal Vol.16 No.3
A complex analysis of spike monitoring in neuro-prosthetic diagnosis demands a high-speed sub-nanoscale transistors with an advanced device technologies. This work reports the high performance of Graphene field-effect transistor (GFET) based front-end amplifier (FEA) design for the neuro-prosthetic application. The 9 nm Graphene FET device is optimized by characterization of transconductance and drain current towards high sensitivity and small factor. The proposed GFET-based FEA with pseudo-resistor technique demonstrates very high-input impedance in Tera-ohms that nullify the input leakage current. Here, gain-bandwidth product and noise optimization of GFET FEA enhances the overall gain with negligible noise. The proposed design operates at low voltage, further reduces the power consumption, and achieves less chip area in sub-nano size so it could be more suitable for implantable devices. The GFET-based FEA architecture achieves an action potential spike of 1.4 μV while the local field potentials spike of 1.8 mV. The proposed architecture is implemented in Advanced Design System using the design kit of the GFET process. Power consumption of 3.14 μW is observed with a supply voltage of 0.9 V. The simulated and experimental results of the proposed design achieve an input impedance of 2 TΩ with excellent noise performance over a wideband of 13.85 MHz. The proposed work demonstrates better neural activity sensing when compared to the state-of-the-artwork, which could be highly beneficial for future neuroscientists.
Role of the MDM2 Promoter Polymorphism (-309T>G) in Acute Myeloid Leukemia Development
Cingeetham, Anuradha,Vuree, Sugunakar,Jiwatani, Sangeeta,Kagita, Sailaja,Dunna, Nageswara Rao,Meka, Phanni Bhushann,Gorre, Manjula,Annamaneni, Sandhya,Digumarti, Raghunadharao,Sinha, Sudha,Satti, Vish Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.7
Background: The human homologue of the mouse double minute 2 (MDM2) gene is a negative regulator of Tp53. MDM2-309T>G a functional promoter polymorphism was found to be associated with overexpression thereby attenuation of Tp53 stress response and increased cancer susceptibility. We have planned to evaluate the possible role of MDM2-309T>G polymorphism with risk and response to chemotherapy in AML. Materials and Methods: A total of 223 de novo AML cases and 304 age and sex matched healthy controls were genotyped for the MDM2-309T>G polymorphism through the tetra-primer amplification refractory mutation system (ARMS)-PCR method. In order to assess the functional relationship of -309T>G SNP with MDM2 expression level, we quantified MDM2 mRNA in 30 primary AML blood samples through quantitative RT-PCR. Both the (-309T>G) genotypes and the MDM2 expression were correlated with disease free survival (DFS) rates among patients who have achieved complete remission (CR) after first induction chemotherapy. Results: MDM2-309T>G polymorphism was significantly associated with AML development (p<0.0001). The presence of either GG genotype or G allele at MDM2-309 confered 1.79 (95% CI: 1.12-2.86; p<0.001) and 1.46 fold (95%CI: 1.14-1.86; p= 0.003) increased AML risk. Survival analysis revealed that CR+ve cases with GG genotype had significantly increased DFS rates (16months, p=0.05) compared to CR+ve TT (11 months) and TG (9 months) genotype groups. Further, MDM2 expression was also found to be significantly elevated in GG genotype patients (p=0.0039) and among CR+ve cases (p=0.0036). Conclusions: The MDM2-309T>G polymorphism might be involved in AML development and also serve as a good prognostic indicator.
Meka, Phanni bhushann,Jarjapu, Sarika,Nanchari, Santhoshi Rani,Vishwakarma, Sandeep Kumar,Edathara, Prajitha Mohandas,Gorre, Manjula,Cingeetham, Anuradha,Vuree, Sugunakar,Annamaneni, Sandhya,Dunna, Na Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.12
LCN2 (Lipocalin 2) is a 25 KD secreted acute phase protein, reported to be a novel regulator of angiogenesis in breast cancer. Up regulation of LCN2 had been observed in multiple cancers including breast cancer, pancreatic cancer and ovarian cancer. However, the role of LCN2 promoter methylation in the formation of microvessels is poorly understood. The aim of this study was to analyze the association of LCN 2 promoter methylation with microvessel formation and tumor cell proliferation in breast cancer patients. The LCN2 promoter methylation status was studied in 64 breast cancer tumors by methylation specific PCR (MSP). Evaluation of microvessel density (MVD) and Ki67 cell proliferation index was achieved by immunohistochemical staining using CD34 and MIB-1 antibodies, respectively. LCN2 promoter unmethylation status was observed in 43 (67.2%) of breast cancer patients whereas LCN2 methylation status was seen in 21 (32.8%). Further, LCN2 promoter unmethylation status was associated with aggressive tumor phenotype and elevated mean MVD in breast cancer patients.