A5028581226- Cancer Cells and Metastasis
- PI3K/AKT/mTOR signaling in cancer
- Melanoma and MAPK Pathways
- Cystic Fibrosis Research Advances
- Cancer Research and Treatments
- MicroRNA in disease regulation
- Cell death mechanisms and regulation
- Cytokine Signaling Pathways and Interactions
- Cancer Mechanisms and Therapy
- Cancer-related Molecular Pathways
- Lung Cancer Treatments and Mutations
- RNA Research and Splicing
- Cancer Genomics and Diagnostics
- Autophagy in Disease and Therapy
- Molecular Biology Techniques and Applications
- Protein Tyrosine Phosphatases
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- Retinoids in leukemia and cellular processes
- Neonatal Respiratory Health Research
- Phytochemistry and biological activity of medicinal plants
- Aquaculture disease management and microbiota
- Extracellular vesicles in disease
- Antibiotic Resistance in Bacteria
- Biomarkers in Disease Mechanisms
Istituto Superiore di Sanità
2004-2023
Health First
2021
Istituto Zooprofilattico Sperimentale delle Venezie
2019-2020
Università Cattolica del Sacro Cuore
2018
University of Palermo
2017
Istituto di Studi sul Mediterraneo (CNR - ISMed)
2006
Adaptation to hypoxia and consequent pro-inflammatory gene expression of prostate breast carcinomas have been implicated in the progression toward cancer malignant phenotype. Only partial data are available for human tumor glioblastoma multiforme (GBM). The aim our study was analyze hypoxic microenvironment GBMs demonstrate that a stem/progenitor cell line derived from (GBM-SCs), activates coordinated inflammatory response, evidencing an invasive migratory phenotype.From each 10 solid...
Question Cystic fibrosis (CF) is due to pathogenic variants in the cystic transmembrane conductance regulator (CFTR) gene. Recent improvements have enabled pharmacological therapy aiming at restoring mutated CFTR expression and function. “modulators” revolutionised CF therapeutic landscape, particularly last approved, Trikafta. This drug combination indicated by United States Food Drug Administration very recently European Medicines Agency for genotypes carrying least one copy of with...
We investigated the membrane localization of CD95 in type I and II cells, which differ their ability to recruit activate caspase-8. found that was preferentially located lipid rafts while it present both raft non-raft plasma sub-domains cells. After stimulation, phospholipid-rich recruited types Similarly, cross-linking resulted caspase-independent translocation FADD/MORT1 caspase-8 rafts, prevented by a death domain-defective receptor. internalization then rapid delayed cells showed...
Abstract Combined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether status determines functional response to combined inhibition. (gene, mRNA, and protein) was extensively characterized a panel cancer cell lines MEK/mTOR displayed highly synergistic pharmacologic interactions almost exclusively PTEN-loss models. Genetic manipulation confirmed mechanistic...
Abstract Fenretinide is a synthetic retinoid characterized by anticancer activity in preclinical models and favorable toxicological profile, but also low bioavailability that hindered its clinical efficacy former trials. We developed new formulation of fenretinide complexed with 2-hydroxypropyl-beta-cyclodextrin (nanofenretinide) an increased therapeutic efficacy. Nanofenretinide was active cell lines derived from multiple solid tumors, primary spheroid cultures xenografts lung colorectal...
Abstract Life expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability kill glioma cell lines in vitro and vivo. Here, we show that, differently from lines, tumors were resistant TRAIL stimulation because they expressed low levels caspase-8 high the death receptor inhibitor PED/PEA-15. Inhibition methyltransferases decitabine...
Abstract Tyrosine kinase inhibitors (TKIs) have shown strong activity against non-small-cell lung cancer (NSCLC) patients harboring activating epidermal growth factor receptor (EGFR) mutations. However, a fraction of EGFR wild-type (WT) may an improvement in terms response rate and progression-free survival when treated with erlotinib, suggesting that factors other than mutation lead to TKI sensitivity. at present, no sufficiently robust clinical or biological parameters been defined...
// Marta Di Martile 1 , Marianna Desideri Teresa De Luca Chiara Gabellini Simonetta Buglioni Adriana Eramo 2 Giovanni Sette Michele Milella 3 Dante Rotili 4 Antonello Mai 4, 5 Simone Carradori Daniela Secci Ruggero Maria 6 Donatella Del Bufalo Trisciuoglio Department of Research, Advanced Diagnostics and Technological Innovation, Regina Elena National Cancer Institute, Rome, Italy Hematology, Oncology Molecular Medicine, Istituto Superiore di Sanità, Clinical Experimental Department, Drug...
An increasing number of anticancer agents has been proposed in recent years with the attempt to overcome treatment-resistant cancer cells and particularly stem (CSC), major culprits for tumour resistance recurrence. However, a huge obstacle treatment success is ineffective delivery drugs within environment due limited solubility, short circulation time or inconsistent stability compounds that, together concomitant dose-limiting systemic toxicity, contribute hamper achievement therapeutic...
Background Tumor cells with stem-like phenotype and properties, known as cancer stem (CSC), have been identified in most solid tumors are presumed to be responsible for driving tumor initiation, chemoresistance, relapse, or metastasis. A subpopulation of increased potential has also within sarcomas. These endowed tumorigenic potential, expression embryonic markers, side population(SP) phenotype. Leiomyosarcomas (LMS) soft tissue sarcomas presumably arising from undifferentiated mesenchymal...
Glioblastoma multiforme (GBM), due to its location, aggressiveness, heterogeneity and infiltrative growth, is characterized by an exceptionally dismal clinical outcome. The small molecule SI113, recently identified as a SGK1 inhibitor, has proven be effective in restraining GBM growth vitro vivo, showing also encouraging results when employed combination with other antineoplastic drugs or radiotherapy. Our aim was explore the pharmacological features of SI113 cells order elucidate pivotal...
Mounting evidence suggests that RAF-mediated MEK activation plays a crucial role in paradox MAPK (re)activation, leading to resistance and therapeutic failure with agents hitting single step along the cascade.We examined molecular functional effects of combined BRAF (dabrafenib), pan-RAF (RAF265), (trametinib) EGFR/HER2 (lapatinib) inhibition, using Western Blot conservative isobologram analysis assess synergism, explored genetic determinants synergistic interactions. Immunoprecipitation...
On behalf of SIFC working group for the revision Consensus document about genetic analysis in cystic fibrosis.pathogen detection, point-of-care (POC) testing and clinical isolate identification with MALDI-TOF MS.Despite advent cutting edge molecular-based (real time PCR, 16S rRNA sequencing, next-generation sequencing) protein-based microbial tools, there is an enormous need to continue culture-based assess susceptibility all antimicrobials identify pathogens mutations that may escape...
Cystic fibrosis (CF) is caused by defects of the cystic transmembrane conductance regulator (CFTR) gene. CFTR-modulating drugs may overcome specific defects, such as case Trikafta, which a clinically approved triple combination Elexacaftor, Tezacaftor and Ivacaftor (ETI) that exhibited strong ability to rescue function most frequent F508del pathogenic variant even in genotypes with mutated allele single copy. Nevertheless, rare lacking are still not eligible for targeted therapies. Via...
Availability of tumor and non‐tumor patient‐derived models would promote the development more effective therapeutics for non‐small cell lung cancer (NSCLC). Recently, conditionally reprogrammed cells (CRC) methodology demonstrated exceptional potential expansion epithelial from patient tissues. However, possibility to expand using CRC protocols is controversial. Here, we used approach non‐tumoral biopsies patients with primary or metastatic NSCLC as well pulmonary metastases colorectal...
Abstract One of the key oncogenic pathways involved in melanoma aggressiveness, development and progression is RAS/BRAF/MEK pathway, whose alterations are found most patients. These molecular anomalies promising targets for more effective anti-cancer therapies. Some Mek inhibitors showed antitumor activity, although schedules doses associated with low systemic toxicity need to be defined. In addition, it now accepted that cancers can arise from maintained by cancer stem cells (CSC) or...