A5076007073- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Prostate Cancer Treatment and Research
- RNA Research and Splicing
- Hedgehog Signaling Pathway Studies
- Cytokine Signaling Pathways and Interactions
- Cancer Genomics and Diagnostics
- DNA Repair Mechanisms
- PI3K/AKT/mTOR signaling in cancer
- Ubiquitin and proteasome pathways
- Microtubule and mitosis dynamics
- Genomics and Chromatin Dynamics
- Cancer-related molecular mechanisms research
- Molecular Biology Techniques and Applications
- NF-κB Signaling Pathways
- MicroRNA in disease regulation
- Cancer, Hypoxia, and Metabolism
- PARP inhibition in cancer therapy
- Cancer Immunotherapy and Biomarkers
- Natural product bioactivities and synthesis
- Effects of Radiation Exposure
- Radiation Therapy and Dosimetry
- Cancer Cells and Metastasis
- Immunotherapy and Immune Responses
University of Trento
2015-2024
Istituto Nazionale di Fisica Nucleare, Trento Institute for Fundamental Physics And Applications
2023
University of Modena and Reggio Emilia
2022
Vilnius University
2022
Universidade Federal do Rio de Janeiro
2017
Universidade de São Paulo
2017
Hospital Federal dos Servidores do Estado
2017
Universidade Federal de São Paulo
2017
Universidade de Ribeirão Preto
2017
National Institutes of Health
2013
Many recent studies using ChIP-seq approaches cross-referenced to trascriptome data and also potentially unbiased in vitro DNA binding selection experiments are detailing with increasing precision the p53-directed gene regulatory network that, nevertheless, is still expanding. However, most have been conducted established cell lines subjected specific p53-inducing stimuli, both factors biasing results. We developed p53retriever, a pattern search algorithm that maps p53 response elements...
Cancer treatment consists today of surgery, chemotherapy, radiation, and most recently immunotherapy. Combination immunotherapy-radiotherapy (CIR) has experienced a surge in public attention due to numerous clinical publications outlining the reduction or elimination metastatic disease following with specifically ipilimumab radiotherapy. The mechanism behind CIR, however, remains unclear, though it is hypothesized that radiation transforms tumor into an in-situ vaccine, which immunotherapy...
Germline TP53 mutations result in cancer proneness syndromes known as Li-Fraumeni, Li-Fraumeni-like, and nonsyndromic predisposition with or without family history. To explore genotype/phenotype associations, we previously adopted a functional classification of all germline mutant alleles based on transactivation. Severe deficiency (SD) were associated more severe syndromes, larger number tumors, compared partial (PD) alleles. Because p53 can exert dominant-negative (DN) effects, addressed...
Abstract Brain tumors are the leading cause of cancer‐related death in children. Experimental vitro models that faithfully capture hallmarks and tumor heterogeneity pediatric brain cancers limited hard to establish. We present a protocol enables efficient generation, expansion, biobanking cancer organoids. Utilizing our protocol, we have established patient‐derived organoids (PDOs) from ependymomas, medulloblastomas, low‐grade glial tumors, xenograft (PDXOs) medulloblastoma xenografts. PDOs...
Abstract Background The tumor suppressor p53 is a sequence-specific transcription factor that regulates an extensive network of coding genes, long non-coding RNAs and microRNAs, establish intricate gene regulatory circuits influencing many cellular responses beyond the prototypical control cell cycle, apoptosis DNA repair. Methods Using bioinformatic approaches, we identified additional group candidate microRNAs (miRs) under direct transcriptional control. To validate family-mediated...
// Joana Soares 1, 2 , Liliana Raimundo Nuno A.L. Pereira 4 Ângelo Monteiro Sara Gomes Cláudia Bessa Clara Glória Queiroz 3 Alessandra Bisio 5 João Fernandes 6 Célia Flávio Reis Jorge Gonçalves Alberto Inga Maria M.M. Santos Lucília Saraiva 1 UCIBIO/REQUIMTE, Universidade do Porto, Portugal Laboratório de Microbiologia, Departamento Ciências Biológicas, Faculdade Farmácia, Farmacologia, Medicamento, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Lisboa, CIBIO, Centre...
The transcription factor ETV7 is an oncoprotein that up-regulated in all breast cancer (BC) types. We have recently demonstrated promoted progression by increasing cell proliferation and stemness was also involved the development of chemo- radio-resistance. However, roles inflammation yet to be studied. Gene ontology analysis previously performed on BC cells stably over-expressing suppression innate immune inflammatory responses. To better decipher involvement these signaling pathways, this...
Germline CDKN2A mutations are observed in 20 -50% of melanoma-prone families.We identified melanoma patients that were heterozygous for non-coding germline variants the 5 0 -UTR of) and examined their impact on p16 INK4a activity using two luciferase-based reporter vectors differ basal transcription level transfected into melanoma-derived WM266-4 breast cancer-derived MCF7 cells.The wild-type sequence, containing a reported SNP (c.-33G > C) known melanoma-predisposing mutation (c.-34G T),...
Background The p53 tumor suppressor, which is altered in most cancers, a sequence-specific transcription factor that able to modulate the expression of many target genes and influence variety cellular pathways. Inactivation pathway cancer frequently occurs through mutant protein. In tumors retain wild type p53, can be by upstream modulators, particularly negative regulators MDM2 MDM4. Methodology/Principal Findings Given factors might function, including levels, mutations, cofactor proteins...
Structural and biochemical studies have demonstrated that p73, p63 p53 recognize DNA with identical amino acids similar binding affinity. Here, measuring transactivation activity for a large number of response elements (REs) in yeast human cell lines, we show family proteins also overlapping profiles. We identified mutations at conserved loops L1 L3 the DNA-binding domain tune potential nearly equally p53. For example, mutant S139F p73 has higher towards selected REs, enhanced cooperativity...
Loss-of-function, partial-function, altered-function, dominant-negative, temperature sensitive, interfering, contact, structural, unfolded, misfolded, dimeric, monomeric, non-cooperative, unstable, supertrans, superstable, intragenic suppressor. TP53 mutants are many, more than 2,000 in fact, and they can be very diverse. Sporadic; germline; gain-of-function (GoF); oncogenic; rebel-angel; yin yang; prion-like; metastasis-inducer; mediator of chemo-resistance; modifier stemness. impact...
Estrogen receptors (ERs) and p53 can interact via cis-elements to regulate the angiogenesis-related VEGFR-1 (FLT1) gene, as we reported previously. Here, address cooperation between these transcription factors on a global scale. Human breast adenocarcinoma MCF7 cells were exposed single or combinatorial treatments with chemotherapeutic agent doxorubicin ER ligand 17β-estradiol (E2). Whole-genome transcriptome changes measured by expression microarrays. Nearly 200 differentially expressed...
The tumor suppressor p53 was previously shown to markedly up-regulate the expression of PRODH gene, encoding proline dehydrogenase (PRODH) enzyme, which catalyzes first step in degradation. Also PRODH2, degrades 4-hydroxy-L-proline, a product protein (e.g. collagen) catabolism, recently described as target. Here, we confirmed p53-dependent induction endogenous response genotoxic damage cell lines different histological origin. We established that over-expression TAp73β or TAp63β is...
Half of human cancers harbor TP53 mutations that render p53 inactive as a tumor suppressor. In these cancers, reactivation mutant (mutp53) through restoration wild-type-like function constitutes valuable anticancer therapeutic strategy. order to search for mutp53 reactivators, small library tryptophanol-derived oxazoloisoindolinones was synthesized and the potential compounds reactivators agents investigated in cells xenograft mouse models. By analysis their anti-proliferative effect on...
// Alessandra Bisio 1 , Judit Zámborszky 1, 3 Sara Zaccara Mattia Lion 4 Toma Tebaldi 2 Vasundhara Sharma Ivan Raimondi Federica Alessandrini Yari Ciribilli Alberto Inga Laboratory of Transcriptional Networks, Centre for Integrative Biology, CIBIO, University Trento, 38123, Italy Translational Genomics, Institute Enzymology, Research Natural Sciences, Budapest, Hungary Department Genetics, Massachusetts General Hospital, Boston, MA, USA Correspondence to: Ciribilli, e-mail:...
// Paola Monti 1,* , Yari Ciribilli 2,* Alessandra Bisio *2 Giorgia Foggetti 1 Ivan Raimondi 2,3 Campomenosi 3,4 Menichini Gilberto Fronza 1,** Alberto Inga 2,** Mutagenesis Unit, Istituto di Ricerca e Cura a Carattere Scientifico Azienda Ospedaliera Universitaria San Martino-IST-Istituto Nazionale per la sul Cancro, Genoa, Italy; 2 Laboratory of Transcriptional Networks, Centre for Integrative Biology, CIBIO, University Trento, 3 Department Biotechnology and Life Sciences, DBSV, Insubria,...
// Alessandra Bisio 1 , Elisa Latorre 2 Virginia Andreotti 3 Brigitte Bressac-de Paillerets 4 Mark Harland 5 Giovanna Bianchi Scarra Paola Ghiorzo Robert C. Spitale 6 Alessandro Provenzani Alberto Inga Laboratory of Transcriptional Networks, Centre for Integrative Biology, CIBIO, University Trento, Italy Genomic Screening, Genetics Rare Hereditary Cancers, DiMI, Genoa, and IRCCS AOU San Martino-IST, Service de Génétique, Institut Gustave Roussy, Villejuif, France Section Epidemiology...
Abstract Therapy resistance is a major roadblock in oncology. Exacerbation of molecular dysfunctions typical cancer cells have proven effective twisting oncogenic mechanisms to lethal conditions, thus offering new therapeutic avenues for treatment. Here, we demonstrate that selective agonists Transient Receptor Potential cation channel subfamily M member 8 (TRPM8), characteristic the prostate epithelium frequently overexpressed advanced stage III/IV cancers (PCa), sensitize therapy...
Abstract 53BP1 acts at the crossroads between DNA repair and p53‐mediated stress response. With its interactors p53 USP28, it is part of mitotic surveillance (or stopwatch) pathway (MSP), a sensor that monitors duration cell division, promoting p53‐dependent cycle arrest when critical time threshold surpassed. Here, we show Polo‐like kinase 1 (PLK1) activity essential for time‐dependent release from kinetochores. PLK1 inhibition, which leads to persistence kinetochores, prevents cytosolic...