Publications by authors named "Murali Ishwarya"
Although BCL2 mutations are reported as later occurring events leading to venetoclax resistance, many other mechanisms of progression have been reported though remain poorly understood. Here, we analyze longitudinal tumor samples from 11 patients with disease progression while receiving venetoclax to characterize the clonal evolution of resistance. All patients tested showed increased in vitro resistance to venetoclax at the posttreatment time point.
View Article and Find Full Text PDFPurpose: PI3K inhibitors (PI3Ki) are approved for relapsed chronic lymphocytic leukemia (CLL). Although patients may show an initial response to these therapies, development of treatment intolerance or resistance remain clinical challenges. To overcome these, prediction of individual treatment responses based on actionable biomarkers is needed.
View Article and Find Full Text PDFArticle Synopsis
- Inhibitors targeting the B-cell receptor signaling pathway, specifically BTK and PI3Kδ, have significantly improved chronic lymphocytic leukemia (CLL) treatments, but resistance mechanisms are not fully understood.
- A study involving 28 CLL patients found that 60% of nonresponders had mutations in MAP2K1, BRAF, and KRAS genes, which contribute to resistance against PI3Kδ inhibitors.
- The research indicates that activating MAPK/ERK pathways leads to resistance, suggesting that combining PI3Kδ inhibitors with ERK inhibitors could enhance treatment effectiveness for patients with these mutations.
The damage to liver mitochondria is universally observed in both humans and animal models after excessive alcohol consumption. Acute alcohol treatment has been shown to stimulate calcium (Ca) release from internal stores in hepatocytes. The resultant increase in cytosolic Ca is expected to be accumulated by neighboring mitochondria, which could potentially lead to mitochondrial Ca overload and injury.
View Article and Find Full Text PDFThis study reports the probable impact of the coupled mutations observed in our clinical isolate of HCMV UL54 polymerase, through structural bioinformatics approaches. The reported variant was found to be resistant to Ganciclovir (GCV) as per the clinical records. The presence of Glutamine deletion at 639 (Glu639) and a mis sense mutation of Serine 655 Leucine (Ser655Leu) in UL54 were identified by DNA sequencing and were predicted to lie in the DNA polymerase type-II domain.
View Article and Find Full Text PDFBackground: The present study was undertaken to determine the rate of occurrence of Human cytomegalovirus (HCMV) among kidney transplant recipients and donors by application of direct detection methods and to understand HCMV infection/disease development among transplanted patients as a prospective study.
Results: Peripheral blood samples collected from 76 kidney donors and 76 recipients from September 2007 to August 2009 were subjected to pp65 antigenemia and Quantitative real-time PCR (qRT-PCR) assays. Data were analyzed under Group A, B and C.