Publications by authors named "Lidio Conte"

Background: The dynamic epigenome and proteins specialized in the interpretation of epigenetic marks critically contribute to leukemic pathogenesis but also offer alternative therapeutic avenues. Targeting newly discovered chromatin readers involved in leukemogenesis may thus provide new anticancer strategies. Accumulating evidence suggests that the PRC1 complex member CBX2 is overexpressed in solid tumors and promotes cancer cell survival.

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Article Synopsis
  • Mutations in the NPM1 gene are linked to acute myeloid leukemia (AML) and are associated with better treatment responses, but their mechanisms are not fully understood.* -
  • The oncogenic NPM1c mutant disrupts mitochondrial function and the formation of promyelocytic leukemia nuclear bodies, which regulate mitochondrial health and cellular aging.* -
  • Actinomycin D (ActD) enhances the effectiveness of treatments by targeting mitochondria, increasing reactive oxygen species, and restoring PML nuclear body formation, particularly when combined with venetoclax for improved AML treatment outcomes.*
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The ubiquitin proteasome system (UPS) is the main cellular degradation machinery designed for controlling turnover of critical proteins involved in cancer pathogenesis, including hematological malignancies. UPS plays a functional role in regulating turnover of key proteins involved in cell cycle arrest, apoptosis and terminal differentiation. When deregulated, it leads to several disorders, including cancer.

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Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer cells, which are unable to differentiate. Although genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives.

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Polycomb group (PcG) proteins regulate transcription, playing a key role in stemness and differentiation. Deregulation of PcG members is known to be involved in cancer pathogenesis. Emerging evidence suggests that CBX2, a member of the PcG protein family, is overexpressed in several human tumors, correlating with lower overall survival.

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