Andrea Sartore‐Bianchi
A5030218831- Colorectal Cancer Treatments and Studies
- Cancer Genomics and Diagnostics
- Genetic factors in colorectal cancer
- Lung Cancer Treatments and Mutations
- Gastric Cancer Management and Outcomes
- HER2/EGFR in Cancer Research
- Cancer Treatment and Pharmacology
- Cancer Research and Treatments
- DNA Repair Mechanisms
- Radiomics and Machine Learning in Medical Imaging
- Cancer Immunotherapy and Biomarkers
- PARP inhibition in cancer therapy
- Hepatocellular Carcinoma Treatment and Prognosis
- BRCA gene mutations in cancer
- Colorectal and Anal Carcinomas
- Epigenetics and DNA Methylation
- Advanced Breast Cancer Therapies
- Helicobacter pylori-related gastroenterology studies
- Glioma Diagnosis and Treatment
- Melanoma and MAPK Pathways
- Colorectal Cancer Surgical Treatments
- Digestive system and related health
- Cancer Cells and Metastasis
- Esophageal Cancer Research and Treatment
- Cancer, Stress, Anesthesia, and Immune Response
University of Milan
2015-2025
Azienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda
2016-2025
Candiolo Cancer Institute
2013-2024
Molecular Oncology (United States)
2024
Mario Negri Institute for Pharmacological Research
2024
European School of Oncology
2023
Istituti di Ricovero e Cura a Carattere Scientifico
2004-2023
Metropolitana Milanese (Italy)
2023
Ospedale Maggiore
2010-2021
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2017-2021
The development of noninvasive methods to detect and monitor tumors continues be a major challenge in oncology. We used digital polymerase chain reaction-based technologies evaluate the ability circulating tumor DNA (ctDNA) 640 patients with various cancer types. found that ctDNA was detectable >75% advanced pancreatic, ovarian, colorectal, bladder, gastroesophageal, breast, melanoma, hepatocellular, head neck cancers, but less than 50% primary brain, renal, prostate, or thyroid cancers. In...
PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% 40% patients who not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, wild-type patients, could have a predictive/prognostic value. PATIENTS AND METHODS retrospectively analyzed objective tumor responses, time progression, overall survival (OS), and mutational status 113 tumors...
Only a fraction of patients with metastatic colorectal cancer receive clinical benefit from therapy anti-epidermal growth factor receptor (EGFR) antibodies, which calls for the identification novel biomarkers better personalized medicine. We produced large xenograft cohorts 85 patient-derived, genetically characterized samples ("xenopatients") to discover determinants therapeutic response and new oncoprotein targets. Serially passaged tumors retained morphologic genomic features their...
Abstract Monoclonal antibodies (mAbs) against the extracellular domain of epidermal growth factor receptor (EGFR) have been introduced for treatment metastatic colorectal cancer (mCRC). We reported recently that increased copy number EGFR can predict response to anti-EGFR mAbs and patients might be selected based on number. Here, we show mutations activating RAS/RAF signaling pathway are also predictive prognostic indicators in mCRC patients, being inversely correlated with mAbs. In cellular...
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies patients with advanced or metastatic solid tumors, including active central nervous system (CNS) disease. Here, we summarize overall safety report antitumor activity entrectinib cohort tumors harboring NTRK1/2/3, ALK gene fusions, naïve to prior TKI treatment targeting specific gene, who were treated at doses that achieved therapeutic exposures consistent recommended II...
Patients with metastatic colorectal cancer who have KRAS codon 12- or 13-mutated tumors are presently excluded from treatment the anti-epidermal growth factor receptor monoclonal antibody cetuximab.To test hypothesis that 13 mutations associated a better outcome after cetuximab than observed other mutations.We studied association between mutation status (p.G13D vs mutations) and response survival in pooled data set of 579 patients chemotherapy-refractory treated 2001 2008. were included...
The monoclonal antibodies (moAb) panitumumab and cetuximab target the epidermal growth factor receptor (EGFR) have proven valuable for treatment of metastatic colorectal cancer (mCRC). EGFR-mediated signaling involves two main intracellular cascades: on one side KRAS activates BRAF, which in turn triggers mitogen-activated protein kinases. On other, membrane localization lipid kinase PIK3CA counteracts PTEN promotes AKT1 phosphorylation, thereby activating a parallel axis. Constitutive...
EGF receptor (EGFR)-targeted monoclonal antibodies are effective in a subset of metastatic colorectal cancers. Inevitably, all patients develop resistance, which occurs through emergence KRAS mutations approximately 50% the cases. We show that amplification MET proto-oncogene is associated with acquired resistance tumors do not during anti-EGFR therapy. Amplification locus was present circulating tumor DNA before relapse clinically evident. Functional studies activation confers to therapy...
How genomic heterogeneity associated with acquired resistance to targeted agents affects response subsequent therapy is unknown. We studied EGFR blockade in colorectal cancer assess whether tissue and liquid biopsies can be integrated radiologic imaging monitor the impact of individual oncogenic alterations on lesion-specific responses. Biopsy a patient's progressing liver metastasis following prolonged cetuximab revealed MEK1(K57T) mutation as novel mechanism resistance. This lesion...
The emergence of drug resistance limits the efficacy targeted therapies in human tumors. prevalent view is that a fait accompli: when treatment initiated, cancers already contain drug-resistant mutant cells. Bacteria exposed to antibiotics transiently increase their mutation rates (adaptive mutability), thus improving likelihood survival. We investigated whether colorectal cancer (CRC) cells likewise exploit adaptive mutability evade therapeutic pressure. found epidermal growth factor...
In a previous cohort study, we proposed that responsiveness of metastatic colorectal cancer (mCRC) to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies has genetic basis, being associated with increased EGFR gene copy number (GCN) as measured by fluorescence in situ hybridization (FISH) individual tumors. The present study was aimed at assessing the predictive role GCN, terms clinical outcome, patients treated panitumumab.Patients mCRC refractory standard therapies were...
ALK, ROS1, and NTRK fusions occur in 0.2% to 2.4% of colorectal cancers. Pioneer cases metastatic cancer (mCRC) patients bearing rearrangements who benefited from anti-ALK, ROS, TrkA-B-C therapies have been reported previously. Here we aimed at characterizing the clinical molecular landscape rearranged mCRC.Clinical features characteristics 27 mCRC tumors were compared with those a cohort 319 not by means Fisher's exact, χ2 test, or Mann-Whitney test as appropriate. Overall survival curves...