Maurizio Scaltriti

Inhibitors of HSP90 block p95-HER2 signaling in Trastuzumab-resistant tumors and suppress their growth.

Clinical benefit of lapatinib-based therapy in patients with human epidermal growth factor receptor 2-positive breast tumors coexpressing the truncated p95HER2 receptor.

AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity.

Cyclin E amplification/overexpression is a mechanism of trastuzumab resistance in HER2+ breast cancer patients.

mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling.

RSK3/4 mediate resistance to PI3K pathway inhibitors in breast cancer.

mTORC1 inhibition is required for sensitivity to PI3K p110α inhibitors in PIK3CA-mutant breast cancer.

Targeting the MUC1-C oncoprotein downregulates HER2 activation and abrogates trastuzumab resistance in breast cancer cells.

Clinical response to a lapatinib-based therapy for a Li-Fraumeni syndrome patient with a novel HER2V659E mutation.

Potential biomarkers of long-term benefit from single-agent trastuzumab or lapatinib in HER2-positive metastatic breast cancer.

Evaluation and clinical analyses of downstream targets of the Akt inhibitor GDC-0068.

Antagonism of EGFR and HER3 enhances the response to inhibitors of the PI3K-Akt pathway in triple-negative breast cancer.

Effect of p95HER2/611CTF on the response to trastuzumab and chemotherapy.

Convergent loss of PTEN leads to clinical resistance to a PI(3)Kα inhibitor.

Therapeutic antibodies in breast cancer.

High HER2 expression correlates with response to the combination of lapatinib and trastuzumab.

AXL mediates resistance to PI3Kα inhibition by activating the EGFR/PKC/mTOR axis in head and neck and esophageal squamous cell carcinomas.

PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor-positive breast cancer.

Quantification of HER family receptors in breast cancer.

MEK plus PI3K/mTORC1/2 Therapeutic Efficacy Is Impacted by TP53 Mutation in Preclinical Models of Colorectal Cancer.

High HER2 protein levels correlate with increased survival in breast cancer patients treated with anti-HER2 therapy.

Taselisib (GDC-0032), a Potent β-Sparing Small Molecule Inhibitor of PI3K, Radiosensitizes Head and Neck Squamous Carcinomas Containing Activating PIK3CA Alterations.

AKT signaling in ERBB2-amplified breast cancer.

Molecular Pathways: AXL, a Membrane Receptor Mediator of Resistance to Therapy.

Pten loss promotes MAPK pathway dependency in HER2/neu breast carcinomas.

Somatic PIK3CA mutations as a driver of sporadic venous malformations.

Differential Receptor Tyrosine Kinase PET Imaging for Therapeutic Guidance.

Rationale-based therapeutic combinations with PI3K inhibitors in cancer treatment.

P-selectin is a nanotherapeutic delivery target in the tumor microenvironment.

PDK1-SGK1 Signaling Sustains AKT-Independent mTORC1 Activation and Confers Resistance to PI3Kα Inhibition.

Stratification and therapeutic potential of PML in metastatic breast cancer.

Systematic Functional Characterization of Resistance to PI3K Inhibition in Breast Cancer.

The emerging role of serum/glucocorticoid-regulated kinases in cancer.

PIM1 kinase regulates cell death, tumor growth and chemotherapy response in triple-negative breast cancer.

CDK12 Inhibition Reverses De Novo and Acquired PARP Inhibitor Resistance in BRCA Wild-Type and Mutated Models of Triple-Negative Breast Cancer.

Tumour-specific PI3K inhibition via nanoparticle-targeted delivery in head and neck squamous cell carcinoma.

PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D.

Overcoming resistance to HER2-targeted therapy with a novel HER2/CD3 bispecific antibody.

A Next-Generation TRK Kinase Inhibitor Overcomes Acquired Resistance to Prior TRK Kinase Inhibition in Patients with TRK Fusion-Positive Solid Tumors.

Somatic chromosomal engineering identifies BCAN-NTRK1 as a potent glioma driver and therapeutic target.

Genotyping tumour DNA in cerebrospinal fluid and plasma of a HER2-positive breast cancer patient with brain metastases.

Genetic Predictors of Response to Systemic Therapy in Esophagogastric Cancer.

The prognostic value of PI3K mutational status in breast cancer: A meta-analysis.

HER kinase inhibition in patients with HER2- and HER3-mutant cancers.

Coamplification of protects -amplified breast cancers from targeted therapy.

A network modeling approach to elucidate drug resistance mechanisms and predict combinatorial drug treatments in breast cancer.

Oncogenic TRK fusions are amenable to inhibition in hematologic malignancies.

Ado-Trastuzumab Emtansine for Patients With HER2-Mutant Lung Cancers: Results From a Phase II Basket Trial.

The Genomic Landscape of Endocrine-Resistant Advanced Breast Cancers.

p95HER2-T cell bispecific antibody for breast cancer treatment.

Neratinib is effective in breast tumors bearing both amplification and mutation of ERBB2 (HER2).

NTRK fusion-positive cancers and TRK inhibitor therapy.

and Amplifications Determine Response to HER2 Inhibition in -Amplified Esophagogastric Cancer.

Loss of the FAT1 Tumor Suppressor Promotes Resistance to CDK4/6 Inhibitors via the Hippo Pathway.

Colorectal Carcinomas Containing Hypermethylated MLH1 Promoter and Wild-Type BRAF/KRAS Are Enriched for Targetable Kinase Fusions.

MET activation confers resistance to cetuximab, and prevents HER2 and HER3 upregulation in head and neck cancer.

Author Correction: HER kinase inhibition in patients with HER2- and HER3-mutant cancers.

PI3K Inhibition Activates SGK1 via a Feedback Loop to Promote Chromatin-Based Regulation of ER-Dependent Gene Expression.

Prevalence and role of HER2 mutations in cancer.

Solid pseudopapillary neoplasms of the pancreas are dependent on the Wnt pathway.

Cell-free DNA analysis in healthy individuals by next-generation sequencing: a proof of concept and technical validation study.

Resistance to TRK inhibition mediated by convergent MAPK pathway activation.

Double mutations in cis increase oncogenicity and sensitivity to PI3Kα inhibitors.

Efficacy and Determinants of Response to HER Kinase Inhibition in HER2-Mutant Metastatic Breast Cancer.

TRK Fusions are Enriched in Cancers with Uncommon Histologies and the Absence of Canonical Driver Mutations.