Enzo Médico

University of Turin

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Document Type

Co-Authors

Claudio Isella

Candiolo Cancer Institute

222

Livio Trusolino

Candiolo Cancer Institute

147

Andrea Bertotti

Candiolo Cancer Institute

146

Alberto Bardelli

University of Turin

108

Paolo M. Comoglio

IFOM

Federica Di Nicolantonio

Candiolo Cancer Institute

Salvatore Siena

Azienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda

Alberto Pisacane

Candiolo Cancer Institute

Andrea Sartore‐Bianchi

University of Milan

Francesco Sassi

Candiolo Cancer Institute

Cooperative Institutions

University of Turin

465

Istituti di Ricovero e Cura a Carattere Scientifico

352

Candiolo Cancer Institute

310

University of Milan

102

Harvard University

Azienda Ospedaliera Citta' della Salute e della Scienza di Torino

Azienda Ospedaliero Universitaria San Giovanni Battista

Fondazione Piemontese per la Ricerca sul Cancro Onlus

Fondazione IRCCS Istituto Nazionale dei Tumori

The University of Texas MD Anderson Cancer Center

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IGF2 is an actionable target that identifies a distinct subpopulation of colorectal cancer patients with marginal response to anti-EGFR therapies

Science Translational Medicine (2015)

Eugenia R. Zanella Francesco Galimi Francesco Sassi Giorgia Migliardi Francesca Cottino

Among patients with colorectal cancer who benefit from therapy targeted to the epidermal growth factor receptor (EGFR), stable disease (SD) occurs more frequently than massive regressions. Exploring the mechanisms of this incomplete sensitivity to devise more efficacious treatments will likely improve patients' outcomes. We tested therapies tailored around hypothesis-generating molecular features in patient-derived xenografts ("xenopatients"), which originated from 125 independent samples that did not harbor established resistance-conferring mutations. Samples from xenopatients that responded to cetuximab, an anti-EGFR agent, with disease stabilization displayed high levels of EGFR family ligands and receptors, indicating high EGFR pathway activity. Five of 21 SD models (23.8%) characterized by particularly high expression of EGFR and EGFR family members regressed after intensified EGFR blockade by cetuximab and a small-molecule inhibitor. In addition, a subset of cases in which enhanced EGFR inhibition was unproductive (6 of 16, 37.5%) exhibited marked overexpression of insulin-like growth factor 2 (IGF2). Enrichment of IGF2 overexpressors among cases with SD was demonstrated in the entire xenopatient collection and was confirmed in patients by mining clinical gene expression data sets. In functional studies, IGF2 overproduction attenuated the efficacy of cetuximab. Conversely, interception of IGF2-dependent signaling in IGF2-overexpressing xenopatients potentiated the effects of cetuximab. The clinical implementation of IGF inhibitors awaits reliable predictors of response, but the results of this study suggest rational combination therapies for colorectal cancer and provide evidence for IGF2 as a biomarker of reduced tumor sensitivity to anti-EGFR therapy and a determinant of response to combined IGF2/EGFR targeting.

10.1126/scitranslmed.3010445

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Citations (107)

Cardiac concentric hypertrophy promoted by activated Met receptor is mitigated in vivo by inhibition of Erk1,2 signalling with Pimasertib

Journal of Molecular and Cellular Cardiology (2016)

Valentina Sala Simona Gallo Stefano Gatti Enzo Médico Elisa Vigna

Pressure overload

10.1016/j.yjmcc.2016.02.017

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Citations (17)

Additional file 7 of Multi-label transcriptional classification of colorectal cancer reflects tumor cell population heterogeneity

Figshare (2023)

Silvia Cascianelli Chiara Barbera Alexandra Ambra Ulla Elena Grassi Barbara Lupo

Additional file 7: Table S7. Summary of the number of samples assigned to secondary classes with peculiar molecular features as MSI status, BRAF/KRAS mutation and EMT, WNT and paneth scoring. For dichotomous variables, hypergeometric p-value has been computed to assign statistical significance at the ratio Observed over the Expected. For continuous variable, Student's T-test was performed. NC, not assigned to reference class, i.e. not assigned to that class.

10.6084/m9.figshare.22827021

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Supplementary Tables S1-S5 from A Molecularly Annotated Model of Patient-Derived Colon Cancer Stem–Like Cells to Assess Genetic and Nongenetic Mechanisms of Resistance to Anti-EGFR Therapy

Paolo Luraghi Viola Bigatto Elia Cipriano Gigliola Reato Francesca Orzan

Supplementary Table-S1: Somatic mutations in xenospheres Supplementary Table-S2: Pearson's correlation values between xenospheres' and xenopatients' gene expression profiles. Supplementary Table-S3: genes affected by copy number variations, as detected by WES in xenopsheres. Supplementary Table-S4: genes affected by somatic mutations, as detected by WES in xenopsheres. Supplementary Table-S5: total number of shared and private somatic mutations and copy number variations in matched xenospheres and xenopatients.

Table (database)

10.1158/1078-0432.22464227

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Supplementary Figures 1-9 from The MET Oncogene Is a Functional Marker of a Glioblastoma Stem Cell Subtype

Francesca De Bacco Elena Casanova Enzo Médico Serena Pellegatta Francesca Orzan

PDF file - 2.3MB, Figure S1: Histopathology of primary glioblastomas and genetic lesions of neurospheres. Figure S2: Genome-wide expression profiling and unsupervised hierarchical clustering of neurospheres (classical, mesenchymal and proneural centroids). Figure S3: Expression of MET, EGFR, and a panel of self-renewal markers in neurospheres. Figure S4: Genome-wide expression profiling and unsupervised hierarchical clustering of neurospheres (multiple signatures). Figure S5: Proliferative response, activation of tyrosine kinase receptors, and differentiation pattern in Met-neg-NS and Met-pos-NS. Figure S6: Methigh and Metneg sorting parameters. Figure S7: The Methigh subpopulation of Met-pos-NS retains clonogenic and tumorigenic cells. Figure S8: H&E and Met immunohistochemical staining of histological sections from tumors formed by BT302 neurosphere and its sorted subpopulations. Figure S9: HGF sustains the stem-like and invasive phenotype of Met-pos-NS.

Neurosphere

Clonogenic assay

10.1158/0008-5472.22393746

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Stimulation of the neurotrophin receptor TrkB on astrocytes drives nitric oxide production and neurodegeneration

The Journal of Cell Biology (2012)

Emanuela Colombo Chiara Cordiglieri Giorgia Melli Jia Newcombe Markus Krumbholz

10.1083/jcb1966oia8

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Citations (7)

Supplementary Table S3 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits

Simona Corso Claudio Isella Sara E. Bellomo Maria Apicella Stefania Durando

GC PDXs are annotated for: CNV of HER2, EGFR, FGFR2, MET, KRAS ({greater than or equal to}8 gene copies); COSMIC Mutations/Frameshifts (Allelic frequency >0.3)

10.1158/0008-5472.22422258

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Supplementary Table S7 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations

Francesco Galimi Davide Torti Francesco Sassi Claudio Isella Davide Corà

Supplementary Table S7 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations

10.1158/1078-0432.22441291

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Supplementary Table 4 from Precision Oncology and Systemic Targeted Therapy in Pseudomyxoma Peritonei

Jordi Martínez‐Quintanilla Débora Cabot Doménico Sabia Oriol Arqués Jordi Vergés

Supplementary Table 4. Correlation of PMP markers in patient samples and their corresponding organoid model.

Pseudomyxoma Peritonei

Table (database)

Precision oncology

10.1158/1078-0432.27013736

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Figure 3 from Precision Oncology and Systemic Targeted Therapy in Pseudomyxoma Peritonei

Jordi Martínez‐Quintanilla Débora Cabot Doménico Sabia Oriol Arqués Jordi Vergés

Treatment with BRAF inhibitor is enough to block RAS/ERK signaling pathway and reduce cell viability in PMP models. BRAFWT (T70) or BRAFV600E (CTAX34) colorectal cancer PDXO and BRAFV600E PMP PDXO (PMP5.1) or PDO (PMP5.2) derived from two different peritoneal metastasis from PMP patient 5 treated with vehicle, mitomycin C 150 ng/mL, cetuximab 100 μg/mL, encorafenib 1 μmol/L, doublet (encorafenib + cetuximab). A and B, Cell viability (A) and caspase 3/7 activation (B) were measured after 5 days or 48 hours on treatment, respectively. Mean ± SD of triplicates is shown. Significant differences were assessed using one-way ANOVA and Dunnett’s multiple comparisons tests compared to control (*, P value < 0.05; **, P value < 0.01; ***, P value < 0.001; ****, P value < 0.0001). C and D, Western blot analysis of phospho-ERK, phospho-EGFR, ERK, and EGFR was performed after 30 minutes or 24 hours on treatment. Quantification of phospho-EGFR/EGFR (C) and phospho-ERK/ERK (D) ration in all the samples. r.u, relative units. PMP, Pseudomyxoma peritonei; CRC, Colorectal cancer; PDO, Patient-derived organoid; PDXO, Patient-derived xenografts organoid.

Pseudomyxoma Peritonei

Systemic therapy

Targeted Therapy

Precision oncology

10.1158/1078-0432.27013787

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