Publications by authors named "Alessandra Di Grande"
Article Synopsis
- BCL-2 is a key target for treating early T-cell progenitor acute lymphoblastic leukemia (ETP-ALL), but resistance to therapies like ABT-199 is a major issue.
- In vivo studies show that LOUCY cells treated with ABT-199 led to residual disease predominantly in the spleen, suggesting this organ’s microenvironment plays a crucial role in resistance.
- The research indicates that cells from the spleen exhibit reduced BCL-2 dependence and altered differentiation, which may contribute to their survival despite BCL-2 inhibition, highlighting the need for further exploration of the splenic environment in leukemia treatment.
Article Synopsis
- Triple-negative breast cancer (TNBC) lacks targeted therapies, and about 70% of patients experience treatment resistance often due to abnormal mitochondrial apoptosis signaling.
- Researchers conducted a phenotypic small-molecule screen and discovered a compound called BAS-2 that operates similarly to histone deacetylase inhibitors (HDAC).
- BAS-2 was found to selectively inhibit HDAC6, leading to the identification of its new role in regulating glycolytic metabolism in TNBC cells through advanced mass spectrometry techniques.
BET Inhibition as a Rational Therapeutic Strategy for Invasive Lobular Breast Cancer.
Clin Cancer Res
December 2019
Purpose: Invasive lobular carcinoma (ILC) is a subtype of breast cancer accounting for 10% of breast tumors. The majority of patients are treated with endocrine therapy; however, endocrine resistance is common in estrogen receptor-positive breast cancer and new therapeutic strategies are needed. Bromodomain and extraterminal inhibitors (BETi) are effective in diverse types of breast cancer but they have not yet been assessed in ILC.
View Article and Find Full Text PDFRecent studies suggest that mild hypoxia-induced neonatal seizures can trigger an acute neuroinflammatory response leading to long-lasting changes in brain excitability along with associated cognitive and behavioral deficits. The cellular elements and signaling pathways underlying neuroinflammation in this setting remain incompletely understood but could yield novel therapeutic targets. Here we show that brief global hypoxia-induced neonatal seizures in mice result in transient cytokine production, a selective expansion of microglia and long-lasting changes to the neuronal structure of pyramidal neurons in the hippocampus.
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