Alberto Bardelli researcher
Bardelli, Alberto.
VIAF ID: 2926150869798722190009 (Personal)
Permalink: http://viaf.org/viaf/2926150869798722190009
Preferred Forms
-
100 0 _
‡a
Alberto Bardelli
‡c
researcher
-
100 1 _ ‡a Bardelli, Alberto
-
100 1 _
‡a
Bardelli, Alberto
-
100 1 _ ‡a Bardelli, Alberto.
4xx's: Alternate Name Forms (5)
5xx's: Related Names (2)
Works
| Title | Sources |
|---|---|
| Cancer evolution : a subject collection from Cold Spring Harbor perspectives in medicine |
|
| Digital PCR quantification of MGMT methylation refines prediction of clinical benefit from alkylating agents in glioblastoma and metastatic colorectal cancer. |
|
| The molecular landscape of colorectal cancer cell lines unveils clinically actionable kinase targets |
|
| Molecular profiling of the "plexinome" in melanoma and pancreatic cancer |
|
| Monitoring tumor-derived cell-free DNA in patients with solid tumors: clinical perspectives and research opportunities |
|
| Mouse models of Kras-mutant colorectal cancer: valuable GEMMs for drug testing? |
|
| Multi-determinants analysis of molecular alterations for predicting clinical benefit to EGFR-targeted monoclonal antibodies in colorectal cancer |
|
| Mutant Met-mediated transformation is ligand-dependent and can be inhibited by HGF antagonists |
|
| Mutation-Enrichment Next-Generation Sequencing for Quantitative Detection of KRAS Mutations in Urine Cell-Free DNA from Patients with Advanced Cancers |
|
| Mutational analysis of the tyrosine kinome in colorectal cancers |
|
| Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas |
|
| Novel somatic and germline mutations in cancer candidate genes in glioblastoma, melanoma, and pancreatic carcinoma |
|
| Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature |
|
| Oncogenes and angiogenesis: a way to personalize anti-angiogenic therapy? |
|
| Oncogenic KRAS sensitizes premalignant, but not malignant cells, to Noxa-dependent apoptosis through the activation of the MEK/ERK pathway |
|
| p21(WAF1/CIP1) mediates the growth response to TGF-beta in human epithelial cells |
|
| Parallel Evaluation of Circulating Tumor DNA and Circulating Tumor Cells in Metastatic Colorectal Cancer |
|
| Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer |
|
| Phase II study of cetuximab in combination with cisplatin and docetaxel in patients with untreated advanced gastric or gastro-oesophageal junction adenocarcinoma (DOCETUX study). |
|
| Phase II study of panitumumab, oxaliplatin, 5-fluorouracil, and concurrent radiotherapy as preoperative treatment in high-risk locally advanced rectal cancer patients (StarPan/STAR-02 Study). |
|
| Phosphatase Protein Homologue to Tensin Expression and Phosphatidylinositol-3 Phosphate Kinase Mutations in Colorectal Cancer |
|
| PIK3CA-activating mutations and chemotherapy sensitivity in stage II-III breast cancer |
|
| PIK3CA cancer mutations display gender and tissue specificity patterns. |
|
| PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor-positive breast cancer |
|
| A point mutation in the MET oncogene abrogates metastasis without affecting transformation. |
|
| Preclinical models for precision oncology |
|
| PRL-3: a phosphatase for metastasis? |
|
| PRL-3 expression in metastatic cancers |
|
| PRL-3 phosphatase is implicated in ovarian cancer growth |
|
| The prognostic IDH1( R132 ) mutation is associated with reduced NADP+-dependent IDH activity in glioblastoma |
|
| Protein tyrosine phosphatase PTP-S binds to the juxtamembrane region of the hepatocyte growth factor receptor Met. |
|
| PTPN11 Is a Central Node in Intrinsic and Acquired Resistance to Targeted Cancer Drugs |
|
| RAF/RAS oncogenes and mismatch-repair status |
|
| RAF suppression synergizes with MEK inhibition in KRAS mutant cancer cells |
|
| Receptor tyrosine kinases as therapeutic targets: the model of the MET oncogene. |
|
| Regulation of the urokinase-type plasminogen activator gene by the oncogene Tpr-Met involves GRB2. |
|
| Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses |
|
| Restoring PUMA induction overcomes KRAS-mediated resistance to anti-EGFR antibodies in colorectal cancer |
|
| RET fusions in a small subset of advanced colorectal cancers at risk of being neglected. |
|
| Retreatment with anti-EGFR monoclonal antibodies in metastatic colorectal cancer: Systematic review of different strategies |
|
| Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma |
|
| Review: Peering through a keyhole: liquid biopsy in primary and metastatic central nervous system tumours |
|
| The road to resistance: EGFR mutation and cetuximab. |
|
| Scatter factor and hepatocyte growth factor are indistinguishable ligands for the MET receptor |
|
| Scatter factor receptors are key players in a unique multistep program leading to invasive growth. |
|
| Selective cytotoxicity of a bicyclic Ras inhibitor in cancer cells expressing K-Ras(G13D). |
|
| Sensitivity to Entrectinib Associated With a Novel LMNA-NTRK1 Gene Fusion in Metastatic Colorectal Cancer |
|
| Sequential HER2 blockade as effective therapy in chemorefractory, HER2 gene-amplified, RAS wild-type, metastatic colorectal cancer: learning from a clinical case. |
|
| SHP2 is required for growth of KRAS-mutant non-small-cell lung cancer in vivo. |
|
| SMAC/Diablo-dependent apoptosis induced by nonsteroidal antiinflammatory drugs (NSAIDs) in colon cancer cells |
|
| Somatic alterations as the basis for resistance to targeted therapies |
|
| Specific uncoupling of GRB2 from the Met receptor. Differential effects on transformation and motility |
|
| A Subset of Colorectal Cancers with Cross-Sensitivity to Olaparib and Oxaliplatin |
|
| Targeted knock-in of the polymorphism rs61764370 does not affect KRAS expression but reduces let-7 levels |
|
| Targeted therapies: how personal should we go? |
|
| Targeting c-MET in gastrointestinal tumours: rationale, opportunities and challenges |
|
| Targeting EGFR/HER2 pathways enhances the antiproliferative effect of gemcitabine in biliary tract and gallbladder carcinomas |
|
| Targeting oncogenic serine/threonine-protein kinase BRAF in cancer cells inhibits angiogenesis and abrogates hypoxia |
|
| Targeting the human epidermal growth factor receptor 2 (HER2) oncogene in colorectal cancer. |
|
| TAS-120 Overcomes Resistance to ATP-Competitive FGFR Inhibitors in Patients with FGFR2 Fusion-Positive Intrahepatic Cholangiocarcinoma |
|
| TGFα and amphiregulin paracrine network promotes resistance to EGFR blockade in colorectal cancer cells |
|
| Therapeutic implications of resistance to molecular therapies in metastatic colorectal cancer. |
|
| Tivantinib (ARQ197) displays cytotoxic activity that is independent of its ability to bind MET. |
|
| Toll-like receptor 9 agonist IMO cooperates with cetuximab in K-ras mutant colorectal and pancreatic cancers |
|
| Toward understanding and exploiting tumor heterogeneity |
|
| Trabectedin and olaparib in patients with advanced and non-resectable bone and soft-tissue sarcomas (TOMAS): an open-label, phase 1b study from the Italian Sarcoma Group |
|
| Tracking a CAD-ALK gene rearrangement in urine and blood of a colorectal cancer patient treated with an ALK inhibitor. |
|
| Tracking colorectal cancer evolution in time and space. |
|
| Tracking the genomic evolution of breast cancer metastasis |
|
| TRK Fusions Are Enriched in Cancers with Uncommon Histologies and the Absence of Canonical Driver Mutations |
|
| Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition |
|
| Tumor Evolution as a Therapeutic Target |
|
| Tumor Heterogeneity and Lesion-Specific Response to Targeted Therapy in Colorectal Cancer |
|
| Tumor MGMT promoter hypermethylation changes over time limit temozolomide efficacy in a phase II trial for metastatic colorectal cancer |
|
| Uncoupling signal transducers from oncogenic MET mutants abrogates cell transformation and inhibits invasive growth |
|
| Understanding how kinase-targeted therapies work |
|
| Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR. |
|
| Vertical suppression of the EGFR pathway prevents onset of resistance in colorectal cancers. |
|
| A Vulnerability of a Subset of Colon Cancers with Potential Clinical Utility. |
|
| Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer |
|
