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您的检索式：作者名="Daniela Carbone"
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| 1 | Alterations of negative regulators of cytokine signalling in immunodeficiency‐related non‐Hodgkin lymphoma显示文摘 | Daniela Capello Annunziata Gloghini Gianluca Baldanzi Maurizio Martini Clara Deambrogi Marco Lucioni Daniela Piranda Rosella Famà Andrea Graziani Michele Spina Umberto Tirelli Marco Paulli Luigi Maria Larocca Gianluca Gaidano Antonino Carbone Fabiola Sini | 2012 | Hematol Oncol2012，，1： | 1 |
| 2 | SF3B1 modulators affect key genes in metastasis and drug influx: a new approach to fight pancreatic cancer chemoresistance显示文摘Aim:Because mutations of splicing factor 3B subunit-1(SF3B1)have been identified in 4%of pancreatic ductal adenocarcinoma(PDAC)patients,we investigated the activity of new potential inhibitors of SF3B1 in combination with gemcitabine,one of the standard drugs,in PDAC cell lines.Methods:One imidazo[2,1-b][1,3,4]thiadiazole derivative(IS1)and three indole derivatives(IS2,IS3 and IS4),selected by virtual screening from an in-house library,were evaluated by the sulforhodamine-B and wound healing assay for their cytotoxic and antimigratory activity in the PDAC cells SUIT-2,Hs766t and Panc05.04,the latter harbouring the SF3B1 mutations.The effects on the splicing pattern of proto-oncogene recepteur d’origine nantais(RON)and the gemcitabine transporter human equilibrative nucleoside transporter-1(hENT1)were assessed by PCR,while the ability to reduce tumour volume was tested in spheroids of primary PDAC cells.Results:The potential SF3B1 modulators inhibited PDAC cell proliferation and prompted induction of cell death.All compounds showed an interesting anti-migratory ability,associated with splicing RON/ΔRON shift in SUIT-2 cells after 24 h exposure.Moreover,IS1 and IS4 potentiated the sensitivity to gemcitabine in both conventional 2D monolayer and 3D spheroid cultures,and these results might be explained by the statistically significant increase in hENT1 expression(P<0.05 vs.untreated control cells),potentially reversing PDAC chemoresistance.Conclusion:These results support further studies on new SF3B1 inhibitors and the role of RON/hENT1 modulation to develop effective drug combinations against PDAC. | Ornella Randazzo Stella M.Cascioferro Camilla Pecoraro Widad Ait Iddouch Amir Avan Barbara Parrino Daniela Carbone Ugo Perricone Godefridus J.Peters Patrizia Diana Elisa Giovannetti | 2021 | Cancer Drug Resistance2021，4，4： | 0 |
| 3 | Resistance to epidermal growth factor receptor inhibition in non-small cell lung cancer显示文摘Aberrant activation of the epidermal growth factor receptor(EGFR)is a driving force for cancer growth in a subgroup of non-small cell lung cancer patients.These patients can be identified by the presence of activating EGFR mutations.Currently three generations of EGFR-tyrosine kinase inhibitors(TKIs)have been approved by the Food and Drug Administration and European Medicine Agency.This paper reviews the structure of EGFR and the downstream signaling pathways of EGFR and describes the mechanisms of intrinsic and acquired resistance against EGFR-TKIs.These mechanisms include secondary or tertiary mutations in EGFR,the activation of bypassing signaling pathways or a histological transformation to small cell lung cancer.Moreover,drug efflux transporters will affect the cellular accumulation of EGFR-TKIs and penetration of the first generation of EGFR-TKI into the brain.Lysosomal sequestration of some EGFR-TKIs may also prevent the drugs to reach their target.In conclusion,resistance to EGFR-TKIs is multifactorial,including primary and acquired mutations in the EGFR gene,activation of bypassing pathways and limited uptake of drugs in the cells or target tissues.More pharmacological studies are needed in order to develop new specific compounds targeted to overcome new resistance mechanisms in order to enable a personalized treatment approach. | Nele Van Der Steen Elisa Giovannetti Daniela Carbone Alessandro Leonetti Christian D.Rolfo Godefridus J.Peters | 2018 | Cancer Drug Resistance2018，1，4： | 0 |
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