A5018026415- Lung Cancer Treatments and Mutations
- Lymphoma Diagnosis and Treatment
- CAR-T cell therapy research
- Chronic Lymphocytic Leukemia Research
- Melanoma and MAPK Pathways
- Lung Cancer Research Studies
- Cancer therapeutics and mechanisms
- Protein Tyrosine Phosphatases
- PI3K/AKT/mTOR signaling in cancer
- RNA modifications and cancer
- Ubiquitin and proteasome pathways
- Cancer Genomics and Diagnostics
- Protein Kinase Regulation and GTPase Signaling
- HER2/EGFR in Cancer Research
- Cancer Mechanisms and Therapy
- Cancer Immunotherapy and Biomarkers
- RNA Research and Splicing
- Cytokine Signaling Pathways and Interactions
- Neuroblastoma Research and Treatments
- Cancer Research and Treatments
- Colorectal Cancer Treatments and Studies
- Cancer-related Molecular Pathways
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Cancer-related gene regulation
University of Turin
2011-2025
Dana-Farber Cancer Institute
2016-2024
Weatherford College
2024
Disco (Germany)
2024
Harvard University
2016-2022
Karolinska Institutet
2022
Spanish National Cancer Research Centre
2012-2017
Boston Children's Hospital
2016
Johns Hopkins Medicine
2012
Johns Hopkins University
2012
Generation of genetically engineered mouse models (GEMMs) for chromosomal translocations in the endogenous loci by a knockin strategy is lengthy and costly. The CRISPR/Cas9 system provides an innovative flexible approach genome engineering genomic vitro vivo. Here, we report use specific translocation adult mice We designed lentiviral vectors to induce cleavage murine Eml4 Alk order generate Eml4-Alk gene rearrangement recurrently found non-small-cell lung cancers (NSCLCs). Intratracheal or...
Abstract RAS oncogenes (collectively NRAS , HRAS and especially KRAS ) are among the most frequently mutated genes in cancer, with common driver mutations occurring at codons 12, 13 61 1 . Small molecule inhibitors of KRAS(G12C) oncoprotein have demonstrated clinical efficacy patients multiple cancer types led to regulatory approvals for treatment non-small cell lung 2,3 Nevertheless, G12C account only around 15% -mutated cancers 4,5 there no approved majority tumours containing other...
Abstract Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are commonly used to treat non-small cell lung cancers with EGFR mutations, but drug resistance often emerges. Intratumor heterogeneity is a known cause of targeted therapy and considered major in treatment failure. This study identifies clones EGFR-mutant tumors expressing low levels both wild-type mutant protein. These EGFR-low cells intrinsically more tolerant inhibitors, invasive, exhibit an...
Abstract Purpose: BRAF mutations are divided into functional classes distinguished by signaling mechanism and kinase activity: V600-mutant kinase-activating monomers (class I), dimers II), kinase-inactivating heterodimers III). The relationship between class disease characteristics in BRAF-mutant non–small cell lung cancer (NSCLC) has not been fully explored. Experimental Design: We performed a retrospective analysis of NSCLCs treated at 2 institutions from 2005 to 2017 determine...
Selective KRAS
Transformed cells in lymphomas usually maintain the phenotype of postulated normal lymphocyte from which they arise. By contrast, anaplastic large cell lymphoma (ALCL) is a T-cell with aberrant because defective expression receptor and other T-cell-specific molecules for still undetermined mechanisms. The majority ALCL carries translocation t(2;5) that encodes oncogenic tyrosine kinase NPM-ALK, fundamental survival, proliferation, migration transformed T cells. Here, we show loss cases...
Abstract Anaplastic large cell lymphomas (ALCL) are mainly characterized by the reciprocal translocation t(2;5)(p23;q35) that involves anaplastic lymphoma kinase (ALK) gene and generates fusion protein NPM-ALK with intrinsic tyrosine activity. triggers several signaling cascades, leading to increased growth, resistance apoptosis, changes in morphology migration of transformed cells. To search for new interacting molecules, we developed a mass spectrometry–based proteomic approach HEK293...
Abstract Purpose: Despite the challenge to directly target mutant KRAS due its high GTP affinity, some agents are under development against downstream signaling pathways, such as MEK inhibitors. However, it remains controversial whether inhibitors can boost current chemotherapy in KRAS-mutant lung tumors clinic. Considering genomic heterogeneity among patients with cancer, is valuable test potential therapeutics mutation–driven mouse models. Experimental Design: We first compared pERK1/2...
Abstract Purpose: Activating missense mutations of KRAS are the most frequent oncogenic driver events in lung adenocarcinoma (LUAD). However, isoforms highly heterogeneous, and data on potential isoform-dependent therapeutic vulnerabilities still lacking. Experimental Design: We developed an isogenic cell-based platform to compare properties specific actionability KRAS-mutant isoforms. In parallel, we analyzed clinicopathologic genomic from 3,560 patients with non–small cell cancer (NSCLC)...