Francesca Chiarini

ORCID: 0000-0002-4568-3189
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About
Contact & Profiles
Research Areas
  • Acute Lymphoblastic Leukemia research
  • PI3K/AKT/mTOR signaling in cancer
  • Chronic Lymphocytic Leukemia Research
  • Biochemical and Molecular Research
  • Acute Myeloid Leukemia Research
  • Chronic Myeloid Leukemia Treatments
  • Cell death mechanisms and regulation
  • Protein Degradation and Inhibitors
  • T-cell and Retrovirus Studies
  • Synthesis and Characterization of Heterocyclic Compounds
  • Epigenetics and DNA Methylation
  • Histone Deacetylase Inhibitors Research
  • Nuclear Structure and Function
  • Cancer therapeutics and mechanisms
  • Cancer-related gene regulation
  • Protein Kinase Regulation and GTPase Signaling
  • Synthesis and biological activity
  • Hemoglobinopathies and Related Disorders
  • Ubiquitin and proteasome pathways
  • Autophagy in Disease and Therapy
  • Wnt/β-catenin signaling in development and cancer
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Mesenchymal stem cell research
  • Research on Leishmaniasis Studies
  • Polyamine Metabolism and Applications

University of Modena and Reggio Emilia
2023-2025

Istituto di Genetica Molecolare
2018-2022

Istituto Ortopedico Rizzoli
2007-2022

National Research Council
2012-2021

Istituto di Scienze Marine del Consiglio Nazionale delle Ricerche
2020-2021

Bologna Research Area
2013-2020

Institute of Molecular Genetics
2014

University of Bologna
2007-2013

Weatherford College
2013

Consorzio Roma Ricerche
2013

Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance. These observations lend compelling weight to the application PI3K/Akt/mTOR inhibitors in therapy T-ALL. Here, we analyzed therapeutic potential novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable...

10.1158/0008-5472.can-10-1814 article EN Cancer Research 2010-09-29

Recent investigations have documented that constitutively activated phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature T-cell acute lymphoblastic leukemia (T-ALL), where it strongly influences growth and survival. These findings lend compelling weight for the application PI3K/Akt/mTOR inhibitors in T-ALL. However, our knowledge T-ALL limited not clear whether could be an effective innovative therapeutic strategies. Here, we analyzed...

10.1158/0008-5472.can-08-4884 article EN Cancer Research 2009-04-08

Lipid signaling pathways are involved in cell growth, differentiation, and apoptosis, could have a role the progression of myelodysplastic syndromes (MDS) into acute myeloid leukemia (AML). Indeed, recent studies showed that phosphoinositide-phospholipase (PI-PL)Cbeta1 mono-allelic deletion correlates with higher risk AML evolution. Also, single patient treated azacitidine, DNA methyltransferase inhibitor currently used MDS, displayed direct correlation between PI-PLCbeta1 gene expression...

10.1073/pnas.0907109106 article EN Proceedings of the National Academy of Sciences 2009-09-11

Abstract To potentiate the response of acute myelogenous leukemia (AML) cells to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) cytotoxicity, we have examined efficacy a combination with perifosine, novel phosphatidylinositol-3-kinase (PI3K)/Akt signaling inhibitor. The rationale for using such is that perifosine was recently described increase TRAIL-R2 receptor expression and decrease cellular FLICE-inhibitory protein (cFLIP) in human lung cancer cell lines. Perifosine...

10.1158/0008-5472.can-08-2815 article EN Cancer Research 2008-11-14
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