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Dalvi, N.

Publications and source records attributed to Dalvi, N..

2 recordsLinked to original sources

Comprehensive drug efficacy data for mucinous ovarian carcinoma using a novel and extensive biobank of patient-derived organoid models

Mucinous Ovarian Carcinoma (MOC) is a rare ovarian cancer histological subtype with distinct pathology, genomics and clinical outcomes compared to other epithelial ovarian cancers. Accordingly, there is little evidence to guide clinical care, particularly in the use of systemic therapies, and the field has lacked informative and diverse pre-clinical models. We developed MOC-specific methods for generating tumour organoids with a success rate of 70% for long-term cultured lines (n=19). Organoid lines were developed from localised, advanced and recurrent tumours, including from biopsy tissue, and represent diverse genomic features not previously captured by existing cell lines. The organoid lines were highly similar to the tumours of origin for genomic and immunohistochemical markers. Screening using a panel of 11 chemotherapy agents highlighted resistance to standard-of-care agents such as carboplatin. Gastrointestinal cancer chemotherapy agents and their combination regimens lacked activity. Paclitaxel was often highly potent at low doses but failed to kill all cells. However, less frequently used drugs such as gemcitabine, topotecan and doxorubicin inhibited many of the lines more effectively than paclitaxel. Available, but non-standard of care, chemotherapy agents should be considered for clinical management of MOC. This is the largest (by [~]10 fold) cohort of fully characterised patient-derived MOC organoid lines described and the first with extensive drug screening data affording an opportunity for drug discovery and screening for personalised treatment.

cancer biology↗

Repurposing statin and L-glutamine: replenishing β-cells in hyperlipidemic T2D mouse model

While cases of obesity-induced type 2 diabetes (T2D) are on the upswing, current therapies help only manage the symptoms. Of late, L-glutamine has been implicated in the amelioration of T2D by virtue of its glucagon like peptide-1 (GLP-1) secretagogue property. Alongside, there are mixed reports on adiponectin (insulin sensitizer) potentiating property of statins. We aimed to investigate the effect of pitavastatin (P) and L-glutamine (LG) combination on glycemic control and pancreatic {beta}-cell regeneration in a high-fat diet (HFD)+Streptozotocin (STZ) induced T2D mouse model. C57BL6/J mice treated with HFD+STZ were randomly assigned into four groups: Diabetic control, L-glutamine, Pitavastatin and P+LG. Control group was fed with the chow diet. Significant amelioration in insulin resistance along with plasma glucose, lipid profile, adiponectin levels, and mitochondrial complexes I, II, III activities were observed in P+LG group as compared to HFD+STZ treated group. Phosphoenolpyruvate carboxykinase, glucose 6-phophatase, glycogen phosphorylase, and GLUT2 transcript levels were reduced with increased glycogen synthase transcript levels in liver. Further, the protein levels of Insulin receptor 1-{beta}, pAkt/Akt, and AdipoR1 were restored in the skeletal muscle and a significant increase in islet number as a result of {beta}-cell regeneration and reduced {beta}-cell death were also observed in the combination drug treated group. Thus, L-glutamine and pitavastatin in combination can induce {beta}-cell regeneration and regulate glucose homeostasis to bring about amelioration of HFD+STZ induced T2D.

biochemistry↗