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Patrick Demkowicz BS Renelle Pointdujour-Lim MD Sofia Miguez BA Yesung Lee BS Bailey S. C. L. Jones BS Christopher A. Barker MD Marcus Bosenberg MD PhD David H. Abramson MD Alexander N. Shoushtari MD Harriet Kluger MD Jasmine H. Francis MD Mario Sznol MD Mathieu F. Bakhoum MD PhD 《Cancer》2023,129(20):3275-3286
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Susanna Zanutto Chiara Maura Ciniselli Antonino Belfiore Mara Lecchi Enzo Masci Gabriele Delconte Massimo Primignani Giulia Tosetti Marco Dal Fante Linda Fazzini Aldo Airoldi Marcello Vangeli Francesca Turpini Giovanni Giuseppe Rubis Passoni Paolo Viaggi Monica Arena Roberta Ilaria Olimpia Motta Anna Maria Cantù Cristiano Crosta Giuseppe De Roberto Francesca Iannuzzi Andrea Cassinotti Valentina Dall'Olio Laura Tizzoni Gabriella Sozzi Emanuele Meroni Luigi Bisanti Marco Alessandro Pierotti Paolo Verderio Manuela Gariboldi 《International journal of cancer. Journal international du cancer》2020,146(4):1164-1173
Colorectal cancer (CRC) screening programs help diagnose cancer precursors and early cancers and help reduce CRC mortality. However, currently recommended tests, the fecal immunochemical test (FIT) and colonoscopy, have low uptake. There is therefore a pressing need for screening strategies that are minimally invasive and consequently more acceptable to patients, most likely blood based, to increase early CRC identification. MicroRNAs (miRNAs) released from cancer cells are detectable in plasma in a remarkably stable form, making them ideal cancer biomarkers. Using plasma samples from FIT-positive (FIT+) subjects in an Italian CRC screening program, we aimed to identify plasma circulating miRNAs that detect early CRC. miRNAs were initially investigated by quantitative real-time PCR in plasma from 60 FIT+ subjects undergoing colonoscopy at Fondazione IRCCS Istituto Nazionale dei Tumori, then tested on an internal validation cohort (IVC, 201 cases) and finally in a large multicenter prospective series (external validation cohort [EVC], 1121 cases). For each endoscopic lesion (low-grade adenoma [LgA], high-grade adenoma [HgA], cancer lesion [CL]), specific signatures were identified in the IVC and confirmed on the EVC. A two-miRNA-based signature for CL and six-miRNA signatures for LgA and HgA were selected. In a multivariate analysis including sex and age at blood collection, the areas under the receiver operating characteristic curve (95% confidence interval) of the signatures were 0.644 (0.607–0.682), 0.670 (0.626–0.714) and 0.682 (0.580–0.785) for LgA, HgA and CL, respectively. A miRNA-based test could be introduced into the FIT+ workflow of CRC screening programs so as to schedule colonoscopies only for subjects likely to benefit most. 相似文献
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Elena Andreucci Anna Laurenzana Silvia Peppicelli Alessio Biagioni Francesca Margheri Jessica Ruzzolini Francesca Bianchini Gabriella Fibbi Mario Del Rosso Chiara Nediani Simona Serratì Livia Fucci Michele Guida Lido Calorini 《Oncology research》2020,28(9):873-884
Malignant melanoma is a highly aggressive skin cancer characterized by an elevated grade of tumor cell plasticity. Such plasticity allows adaptation of melanoma cells to different hostile conditions and guarantees tumor
survival and disease progression, including aggressive features such as drug resistance. Indeed, almost 50% of
melanoma rapidly develop resistance to the BRAFV600E inhibitor vemurafenib, with fast tumor dissemination,
a devastating consequence for patients’ outcomes. Vasculogenic mimicry (VM), the ability of cancer cells to
organize themselves in perfused vascular-like channels, might sustain tumor spread by providing vemurafenibresistant cancer cells with supplementary ways to enter into circulation and disseminate. Thus, this research
aims to determine if vemurafenib resistance goes with the acquisition of VM ability by aggressive melanoma
cells, and identify a driving molecule for both vemurafenib resistance and VM. We used two independent
experimental models of drug-resistant melanoma cells, the first one represented by a chronic adaptation of
melanoma cells to extracellular acidosis, known to drive a particularly aggressive and vemurafenib-resistant
phenotype, the second one generated with chronic vemurafenib exposure. By performing in vitro tube formation assay and evaluating the expression levels of the VM markers EphA2 and VE-cadherin by Western blotting
and flow cytometer analyses, we demonstrated that vemurafenib-resistant cells obtained by both models are
characterized by an increased ability to perform VM. Moreover, by exploiting the CRISPR-Cas9 technique and
using the urokinase plasminogen activator receptor (uPAR) inhibitor M25, we identified uPAR as a driver of
VM expressed by vemurafenib-resistant melanoma cells. Thus, uPAR targeting may be successfully leveraged
as a new complementary therapy to inhibit VM in drug-resistant melanoma patients, to counteract the rapid
progression and dissemination of the disease. 相似文献