Publications by authors named "G Nagaraju"

Dysbiosis in the gut microbiota plays a significant role in GI cancer development by influencing immune function and disrupting metabolic functions. Dysbiosis can drive carcinogenesis through pathways like immune dysregulation and the release of carcinogenic metabolites, and altered metabolism, genetic instability, and pro-inflammatory signalling, contributing to GI cancer initiation and progression. infection and genotoxins released from dysbiosis, lifestyle and dietary habits are other factors that contribute to GI cancer development.

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Pancreatic ductal adenocarcinoma (PDAC) has a minimal (<15%) 5-year existence, in part due to resistance to chemoradiotherapy. Previous research reveals the impact of paricalcitol (P) and hydroxychloroquine (H) on altering the lysosomal fusion, decreasing stromal burden, and triggering PDAC to chemotherapies. This investigation aims to elucidate the molecular properties of the H and P combination and their potential in sensitizing PDAC to gemcitabine (G).

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RAS is a common driver of cancer that was considered undruggable for decades. Recent advances have enabled the development of RAS inhibitors, but the efficacy of these inhibitors remains limited by resistance. Here, we developed a pan-RAS inhibitor, ADT-007, that binds nucleotide-free RAS to block GTP activation of effector interactions and MAPK/AKT signaling, resulting in mitotic arrest and apoptosis.

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Breast cancer (BC) is a complex disease exhibiting significant heterogeneity and encompassing various molecular subtypes. Among these, triple-negative breast cancer (TNBC) stands out as one of the most challenging types, characterized by its aggressive nature and poor prognosis. This review embarks on a comprehensive exploration of the immune landscape of BC, with a primary focus on the functional and structural characterization of immunoglobulin-binding protein (BiP) and its pivotal role in regulating the unfolded response (UPR) pathway of proteins.

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Article Synopsis
  • ADT-1004 is a new oral prodrug that effectively inhibits tumor growth and RAS activation in pancreatic ductal adenocarcinoma (PDAC) models without causing significant toxicity.
  • It works by blocking ERK phosphorylation in tumor cells, showing effectiveness against various KRAS mutations and increasing immune cell presence in the tumor microenvironment.
  • ADT-1004’s broad antitumor activity and selectivity for KRAS mutant tumors make it a promising candidate for clinical trials in treating PDAC, potentially outperforming existing KRAS inhibitors.
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