Publications by authors named "Avani Mangoli"
Article Synopsis
- Researchers are investigating how stimulating the innate immune system could help treat gliomas, especially focusing on the interaction between ATRX mutations and IDH mutations.
- ATRX-deficient glioma models show increased sensitivity to dsRNA treatments, leading to reduced tumor lethality and higher T-cell infiltration, but IDH1 mutations negatively affect immune gene expression.
- IDH1 doesn't prevent the sensitivity to dsRNA, but it does diminish the immune response, suggesting that targeting innate immunity could be a promising therapeutic strategy for astrocytomas.
Diffuse midline gliomas (DMGs) are lethal brain tumors characterized by p53-inactivating mutations and oncohistone H3.3K27M mutations that rewire the cellular response to genotoxic stress, which presents therapeutic opportunities. We used RCAS/tv-a retroviruses and Cre recombinase to inactivate p53 and induce K27M in the native allele in a lineage- and spatially-directed manner, yielding primary mouse DMGs.
View Article and Find Full Text PDFStimulating the innate immune system has been explored as a therapeutic option for the treatment of gliomas. Inactivating mutations in , defining molecular alterations in -mutant astrocytomas, have been implicated in dysfunctional immune signaling. However, little is known about the interplay between ATRX loss and mutation on innate immunity.
View Article and Find Full Text PDFBackground: Maintaining dose-dense, interval-compressed chemotherapy improves survival in patients with Ewing sarcoma but is limited by myelosuppression. Romiplostim is a thrombopoietin receptor agonist that may be useful in the treatment of chemotherapy-induced thrombocytopenia (CIT).
Methods: Patients aged between 3 and 33 years with Ewing sarcoma from 2010 to 2020 were reviewed.