Monica Ceccon

Monza, Italy

Last Updated: 09/26/2026

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Found 18 publications

Correction: Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.

Correction: Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.

Journal: Oncogene

Published: May 02, 2025

Identification of non-ATP-competitive α-carboline inhibitors of the anaplastic lymphoma kinase.

Identification of non-ATP-competitive α-carboline inhibitors of the anaplastic lymphoma kinase.

Journal: European journal of medicinal chemistry

Published: April 15, 2022

Synergistic Drug Combinations Prevent Resistance in ALK+ Anaplastic Large Cell Lymphoma.

Synergistic Drug Combinations Prevent Resistance in ALK+ Anaplastic Large Cell Lymphoma.

Journal: Cancers

Published: July 13, 2021

Whole Exome Sequencing reveals NOTCH1 mutations in anaplastic large cell lymphoma and points to Notch both as a key pathway and a potential therapeutic target.

Whole Exome Sequencing reveals NOTCH1 mutations in anaplastic large cell lymphoma and points to Notch both as a key pathway and a potential therapeutic target.

Journal: Haematologica

Published: September 19, 2019

Mitochondrial Hyperactivation and Enhanced ROS Production are Involved in Toxicity Induced by Oncogenic Kinases Over-Signaling.

Mitochondrial Hyperactivation and Enhanced ROS Production are Involved in Toxicity Induced by Oncogenic Kinases Over-Signaling.

Journal: Cancers

Published: November 06, 2018

Lorlatinib Treatment Elicits Multiple On- and Off-Target Mechanisms of Resistance in ALK-Driven Cancer.

Lorlatinib Treatment Elicits Multiple On- and Off-Target Mechanisms of Resistance in ALK-Driven Cancer.

Journal: Cancer research

Published: June 15, 2018

Synergistic activity of ALK and mTOR inhibitors for the treatment of NPM-ALK positive lymphoma.

Synergistic activity of ALK and mTOR inhibitors for the treatment of NPM-ALK positive lymphoma.

Journal: Oncotarget

Published: March 22, 2016

Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.

Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.

Journal: Oncogene

Published: July 08, 2015

In vitro and in vivo identification of ABCB1 as an efflux transporter of bosutinib.

In vitro and in vivo identification of ABCB1 as an efflux transporter of bosutinib.

Journal: Journal of hematology & oncology

Published: April 03, 2015

Activity of second-generation ALK inhibitors against crizotinib-resistant mutants in an NPM-ALK model compared to EML4-ALK.

Activity of second-generation ALK inhibitors against crizotinib-resistant mutants in an NPM-ALK model compared to EML4-ALK.

Journal: Cancer medicine

Published: November 04, 2014

NPM/ALK mutants resistant to ASP3026 display variable sensitivity to alternative ALK inhibitors but succumb to the novel compound PF-06463922.

NPM/ALK mutants resistant to ASP3026 display variable sensitivity to alternative ALK inhibitors but succumb to the novel compound PF-06463922.

Journal: Oncotarget

Published: September 19, 2014

Reversal of microRNA-150 silencing disadvantages crizotinib-resistant NPM-ALK(+) cell growth.

Reversal of microRNA-150 silencing disadvantages crizotinib-resistant NPM-ALK(+) cell growth.

Journal: The Journal of clinical investigation

Published: August 11, 2014

Showing 1-12 of 18

Last Updated: 09/26/2026