Salvatore Cortellino

ORCID: 0000-0001-8331-3800
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About
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Research Areas
  • Dietary Effects on Health
  • Diet and metabolism studies
  • Nutrition, Genetics, and Disease
  • Cancer, Stress, Anesthesia, and Immune Response
  • DNA Repair Mechanisms
  • Nutrition and Health in Aging
  • Genetic factors in colorectal cancer
  • Epigenetics and DNA Methylation
  • Cancer-related molecular mechanisms research
  • Ovarian cancer diagnosis and treatment
  • Cancer Genomics and Diagnostics
  • Cellular Mechanics and Interactions
  • Genomics and Chromatin Dynamics
  • DNA and Nucleic Acid Chemistry
  • Cellular transport and secretion
  • Cancer Immunotherapy and Biomarkers
  • Metabolism, Diabetes, and Cancer
  • Neuroendocrine Tumor Research Advances
  • Intraperitoneal and Appendiceal Malignancies
  • Circadian rhythm and melatonin
  • Cell Adhesion Molecules Research
  • Renal and related cancers
  • Microtubule and mitosis dynamics
  • Vitamin C and Antioxidants Research
  • Cancer Cells and Metastasis

Translational Research in Oncology
2025

Scuola Superiore Meridionale
2024-2025

Temple University
2003-2025

Istituti di Ricovero e Cura a Carattere Scientifico
2023-2024

Centro di Riferimento Oncologico della Basilicata
2023-2024

Istituto Universitario di Studi Superiori di Pavia
2024

Institute for Scientific Interchange
2024

Candiolo Cancer Institute
2024

World Health Organization - Italy
2024

IFOM
2013-2023

Abstract In tumor-bearing mice, cyclic fasting or fasting-mimicking diets (FMD) enhance the activity of antineoplastic treatments by modulating systemic metabolism and boosting antitumor immunity. Here we conducted a clinical trial to investigate safety biological effects cyclic, five-day FMD in combination with standard therapies. 101 patients, was safe, feasible, resulted consistent decrease blood glucose growth factor concentration, thus recapitulating metabolic changes that mediate...

10.1158/2159-8290.cd-21-0030 article EN cc-by-nc-nd Cancer Discovery 2021-11-17

The degradation of extracellular matrix (ECM) by metalloproteases is crucial in physiological and pathological cell invasion alike. Degradation occurs at specific sites where invasive cells make contact with the ECM via specialized plasma membrane protrusions termed invadopodia. Herein, we show that dynamin 2 (Dyn2), a GTPase implicated control actin-driven cytoskeletal remodeling events transport, necessary for focalized Dynamin was inhibited using two approaches: 1) expression dominant...

10.1091/mbc.e02-05-0308 article EN Molecular Biology of the Cell 2003-03-01

The mechanisms by which tumor cells metastasize and the role of endocytic proteins in this process are not well understood. We report that overexpression GTPase RAB5A, a master regulator endocytosis, is predictive aggressive behavior metastatic ability human breast cancers. RAB5A necessary sufficient to promote local invasion distant dissemination various mammary nonmammary cell lines, prometastatic associated with increased intratumoral motility. Specifically, for formation invadosomes,...

10.1083/jcb.201403127 article EN cc-by-nc-sa The Journal of Cell Biology 2014-07-21

Immunotherapy is improving the prognosis and survival of cancer patients, but despite encouraging outcomes in different cancers, majority tumors are resistant to it, immunotherapy combinations often accompanied by severe side effects. Here, we show that a periodic fasting-mimicking diet (FMD) can act on tumor microenvironment increase efficacy (anti-PD-L1 anti-OX40) against poorly immunogenic triple-negative breast (TNBCs) expanding early exhausted effector T cells, switching metabolism from...

10.1016/j.celrep.2022.111256 article EN cc-by-nc-nd Cell Reports 2022-08-01

Immune checkpoint inhibitors cause side effects ranging from autoimmune endocrine disorders to severe cardiotoxicity. Periodic Fasting mimicking diet (FMD) cycles are emerging as promising enhancers of a wide range cancer therapies including immunotherapy. Here, either FMD alone or in combination with anti-OX40/anti-PD-L1 much more effective than immune delaying melanoma growth mice. also show trend for increased against lung model. As importantly, the cardiac fibrosis, necrosis and...

10.1038/s41467-023-41066-3 article EN cc-by Nature Communications 2023-09-08

Inflammation is a key contributor to both the initiation and progression of tumors, it can be triggered by genetic instability within as well lifestyle dietary factors. The inflammatory response plays critical role in epigenetic reprogramming tumor cells, cells that comprise microenvironment. Cells microenvironment acquire phenotype promotes immune evasion, progression, metastasis. We will review mechanisms pathways involved interaction between inflammation, nutrition, limitations current...

10.3390/ijms25052750 article EN International Journal of Molecular Sciences 2024-02-27

Cytotoxicity of methylating agents is caused mostly by methylation the O 6 position guanine in DNA to form –methylguanine ( –meG). –meG can direct misincorporation thymine during replication, generating –meG:T mismatches. Recognition these mispairs mismatch repair (MMR) system leads cell cycle arrest and apoptosis. MMR also modulates sensitivity other antitumor drugs. The base excision (BER) enzyme MED1 (also known as MBD4) interacts with protein MLH1. was found exhibit glycosylase activity...

10.1073/pnas.2334585100 article EN Proceedings of the National Academy of Sciences 2003-11-12

Abstract The base excision repair protein MED1 (also known as MBD4), an interactor with the mismatch MLH1, has a central role in maintenance of genomic stability dual functions DNA damage response and repair. acts thymine uracil N-glycosylase on T:G U:G mismatches that occur at cytosine-phosphate-guanine (CpG) methylation sites due to spontaneous deamination 5-methylcytosine cytosine, respectively. To elucidate mechanisms underlie sequence discrimination by MED1, we did single-turnover...

10.1158/0008-5472.can-05-4488 article EN Cancer Research 2006-08-01

// Rossella Tricarico 1 , Salvatore Cortellino 2 Antonio Riccio 3 Shantie Jagmohan-Changur 4 Heleen Van der Klift 5 Juul Wijnen David Turner 6 Andrea Ventura 7 Valentina Rovella 8 Percesepe 9 Emanuela Lucci-Cordisco 10 Paolo Radice 11 Lucio Bertario Monica Pedroni 12 Maurizio Ponz de Leon Pietro Mancuso 1, 13 Karthik Devarajan 14 Kathy Q. Cai 15 Andres J.P. Klein-Szanto Giovanni Neri Pål Møller 16 Alessandra Viel 17 Genuardi Riccardo Fodde Alfonso Bellacosa Cancer Epigenetics...

10.18632/oncotarget.5740 article EN Oncotarget 2015-10-16

Thymine DNA Glycosylase (TDG) is a base excision repair enzyme that acts as thymine and uracil N-glycosylase on G:T G:U mismatches, thus protecting CpG sites in the genome from mutagenesis by deamination. In addition, TDG has an epigenomic function removing novel cytosine derivatives 5-formylcytosine 5-carboxylcytosine (5caC) generated Ten-Eleven Translocation (TET) enzymes during active demethylation. We others previously reported essential for mammalian development. However, its...

10.18632/oncotarget.21219 article EN Oncotarget 2017-09-23
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