Publications by authors named "M R Pitari"
Article Synopsis
- - The miR-17-92 cluster is linked to cancer growth and serves as a target for treatment in MYC-driven cancers; researchers developed LNA gapmeR antisense oligonucleotides (ASOs) to stop the production of these oncogenic miRNAs.
- - The key ASO, MIR17PTi, successfully inhibited the growth of multiple cancer cell lines and triggered cell death in multiple myeloma (MM) by disrupting critical regulatory loops involving MYC and miR-17-92.
- - In animal studies, MIR17PTi showed strong anti-tumor effects and favorable safety, paving the way for potential early-phase clinical trials against MM and other cancers associated with MYC overexpression
Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs.
View Article and Find Full Text PDFEpigenetic abnormalities are common in hematologic malignancies, including multiple myeloma, and their effects can be efficiently counteracted by a class of tumor suppressor miRNAs, named epi-miRNAs. Given the oncogenic role of histone deacetylases (HDAC) in multiple myeloma, we investigated whether their activity could be antagonized by miR-29b, a well-established epi-miRNA. We demonstrated here that miR-29b specifically targets HDAC4 and highlighted that both molecules are involved in a functional loop.
View Article and Find Full Text PDFPurpose: The onset of drug resistance is a major cause of treatment failure in multiple myeloma. Although increasing evidence is defining the role of miRNAs in mediating drug resistance, their potential activity as drug-sensitizing agents has not yet been investigated in multiple myeloma.
Experimental Design: Here we studied the potential utility of miR-221/222 inhibition in sensitizing refractory multiple myeloma cells to melphalan.