Carlo Gambacorti‐Passerini
A5036874214- Chronic Myeloid Leukemia Treatments
- Chronic Lymphocytic Leukemia Research
- Lung Cancer Treatments and Mutations
- Eosinophilic Disorders and Syndromes
- Lymphoma Diagnosis and Treatment
- Acute Lymphoblastic Leukemia research
- Acute Myeloid Leukemia Research
- Cancer Genomics and Diagnostics
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Immunotherapy and Immune Responses
- Immune Cell Function and Interaction
- Cancer therapeutics and mechanisms
- CAR-T cell therapy research
- HER2/EGFR in Cancer Research
- Cancer-related gene regulation
- Lung Cancer Research Studies
- Retinoids in leukemia and cellular processes
- Colorectal Cancer Treatments and Studies
- RNA Interference and Gene Delivery
- Genetic factors in colorectal cancer
- Monoclonal and Polyclonal Antibodies Research
- Ubiquitin and proteasome pathways
- Neuroblastoma Research and Treatments
- PI3K/AKT/mTOR signaling in cancer
- RNA modifications and cancer
University of Milano-Bicocca
2016-2025
Istituti di Ricovero e Cura a Carattere Scientifico
2023-2025
Azienda Ospedaliera San Gerardo
2016-2025
Monash Health
2023
Monash University
2023
ASST Melegnano e della Martesana
2020-2022
Universidad Gerardo Barrios
2021
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2019
The University of Texas MD Anderson Cancer Center
2019
National University of Singapore
2017
Chronic myelogenous leukemia (CML) is caused by the BCR-ABL tyrosine kinase, product of Philadelphia chromosome. Imatinib mesylate, formerly STI571, a selective inhibitor this kinase.
Myelodysplastic syndromes are a diverse and common group of chronic hematologic cancers. The identification new genetic lesions could facilitate diagnostic therapeutic strategies.We used massively parallel sequencing technology to identify somatically acquired point mutations across all protein-coding exons in the genome 9 patients with low-grade myelodysplasia. Targeted resequencing gene encoding RNA splicing factor 3B, subunit 1 (SF3B1), was also performed cohort 2087 myeloid or other...
Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the inhibitor–refractory threonine-to-isoleucine mutation at position 315 (T315I). We conducted phase 2 trial ponatinib in patients chronic myeloid leukemia (CML) or Philadelphia chromosome–positive acute lymphoblastic (Ph-positive ALL).
Several small studies on patients with COVID-19 and haematological malignancies are available showing a high mortality in this population. The Italian Hematology Alliance aimed to collect data from adult who required hospitalisation for COVID-19.This multicentre, retrospective, cohort study included (aged ≥18 years) diagnosis of WHO-defined malignancy admitted 66 hospitals between Feb 25 May 18, 2020, laboratory-confirmed symptomatic COVID-19. Data cutoff analysis was June 22, 2020. primary...
Bosutinib is an oral Src/Abl tyrosine kinase inhibitor. The phase III Efficacy and Safety in Newly Diagnosed Chronic Myeloid Leukemia (BELA) trial compared bosutinib with imatinib newly diagnosed, chronic-phase chronic myeloid leukemia (CML).A total of 502 patients were randomly assigned 1:1 to 500 mg per day or 400 day.The complete cytogenetic response (CCyR) rate at 12 months was not different for (70%; 95% CI, 64% 76%) versus (68%; 62% 74%; two-sided P = .601); therefore, the study did...
Purpose Bosutinib is a potent dual SRC/ABL kinase inhibitor approved for adults with Philadelphia chromosome–positive chronic myeloid leukemia (CML) resistant and /or intolerant to prior therapy. We assessed the efficacy safety of bosutinib versus imatinib first-line treatment chronic-phase CML. Methods In this ongoing, multinational, phase III study, 536 patients newly diagnosed CML were randomly assigned 1:1 receive 400 mg once daily (n = 268) or 268). Per protocol, was in who typical...
Imatinib slows development of chronic myeloid leukemia (CML). However, available information on morbidity and mortality is largely based sponsored trials, whereas independent long-term field studies are lacking. Consecutive CML patients who started imatinib treatment before 2005 were in complete cytogenetic remission (CCyR) after 2 years (±3 months) eligible for enrollment the multicenter Long-Term (Side) Effects (ILTE) study. Incidence first serious nonserious adverse events loss CCyR...
Resistance to imatinib represents an important scientific and clinical issue in chronic myelogenous leukemia. In the present study, effects of novel inhibitor SKI-606 on various models resistance were studied. proved be active Bcr-Abl several leukemia cell lines transfectants, with IC(50) values low nanomolar range, 1 2 logs lower than those obtained imatinib. Cells expressing activated forms KIT or platelet-derived growth factor receptor (PDGFR), two additional targets imatinib, unaffected...
Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome–positive (Ph1-positive) acute lymphocytic (ALL) are 2 fatal BCR/ABL-driven leukemias against which Abl kinase inhibitors fail to induce a long-term response. We recently reported that functional loss of protein phosphatase 2A (PP2A) activity is important for CML blastic transformation. assessed the therapeutic potential PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an...
Anaplastic lymphoma kinase (ALK)-positive lymphomas respond to chemotherapy, but relapses, which bear a poor prognosis, occur. Crizotinib inhibits ALK in vitro and vivo was administered as monotherapy 11 ALK+ patients who were resistant/refractory cytotoxic therapy. The overall response rate 10 of (90.9%; 95% confidence interval [CI] = 58.7% 99.8%). Disease status at the latest follow-up is follows: four are complete (CR) (months >21, >30, >35, >40) under continuous crizotinib...
Imatinib is effective for the treatment of chronic myeloid leukemia (CML). However even undetectable BCR‐ABL1 by Q‐RT‐PCR does not equate to eradication disease. Digital‐PCR (dPCR), able detect 1 positive cell out 10 7 , has been recently developed. The ISAV study a multicentre trial aimed at validating dPCR predict relapses after imatinib discontinuation in CML patients with Q‐RT‐PCR. under therapy since more than 2 years and PCR least 18 months were eligible. Patients monitored standard 36...
Abstract Long non-coding RNAs (lncRNAs) are a growing focus of cancer genomics studies, creating the need for resource lncRNAs with validated roles. Furthermore, it remains debated whether mutated can drive tumorigenesis, and such functions could be conserved during evolution. Here, as part ICGC/TCGA Pan-Cancer Analysis Whole Genomes (PCAWG) Consortium, we introduce Cancer LncRNA Census (CLC), compilation 122 GENCODE causal roles in phenotypes. In contrast to existing databases, CLC requires...
Multi-omics datasets represent distinct aspects of the central dogma molecular biology. Such high-dimensional profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple using statistical fusion, rationalizes contributing evidence highlights associated genes. As part ICGC/TCGA Pan-Cancer Analysis Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing from...
Treatment results for patients with newly diagnosed FMS-like tyrosine kinase 3 (FLT3)-mutated (FLT3mut+) acute myeloid leukemia (AML) ineligible intensive chemotherapy are disappointing. This multicenter, open-label, phase trial randomized (2:1) untreated adults FLT3mut+ AML induction to receive gilteritinib (120 mg/d orally) and azacitidine (GIL + AZA) or (AZA) alone. The primary end point was overall survival (OS). At the interim analysis (August 26, 2020), a total of 123 were treatment...