Benedetta Picciani

ORCID: 0000-0002-4023-5547
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About
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Research Areas
  • Colorectal Cancer Treatments and Studies
  • Cancer Genomics and Diagnostics
  • Lung Cancer Treatments and Mutations
  • Radiomics and Machine Learning in Medical Imaging
  • Medical Imaging Techniques and Applications
  • Cellular transport and secretion
  • Cancer Cells and Metastasis
  • Cellular Mechanics and Interactions
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Endoplasmic Reticulum Stress and Disease
  • Bacterial Infections and Vaccines
  • Ion channel regulation and function
  • Cytokine Signaling Pathways and Interactions
  • Computational Drug Discovery Methods
  • Genetic factors in colorectal cancer
  • Glycosylation and Glycoproteins Research
  • Melanoma and MAPK Pathways

Fondazione IRCCS Istituto Nazionale dei Tumori
2015-2017

Mario Negri Sud Foundation
2014

Purpose: Even if RAS-BRAF wild-type and HER2/MET-negative metastatic colorectal cancer (mCRC) patients frequently respond to anti-EGFR mAbs, acquired resistance almost invariably occurs. Mechanisms of EGFR blockade include the emergence KRAS, NRAS, extracellular domain mutations as well HER2/MET alterations. However, these findings derive from retrospective studies that analyzed one single mechanism at a time; moreover, it is still unclear how molecular heterogeneity affects clonal evolution...

10.1158/1078-0432.ccr-16-1863 article EN Clinical Cancer Research 2016-10-26

// Carmen Ruggiero 1,4,* , Giorgia Fragassi 1,* Mauro Grossi 1 Benedetta Picciani Rosaria Di Martino 3 Mirco Capitani Roberto Buccione 2 Alberto Luini and Michele Sallese Unit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy Laboratory Tumour Cell Invasion, Institute Protein Biochemistry National Research Council, Naples, 4 Current address: Institut de Pharmacologie Moléculaire et Cellulaire CNRS Associated International (LIA) NEOGENEX...

10.18632/oncotarget.3270 article EN Oncotarget 2014-12-18

// Ilaria Penna 1, 2 , Alessandra Molla Giulia Grazia Loredana Cleris Gabriella Nicolini Federica Perrone 3 Benedetta Picciani Michele Del Vecchio 4 Filippo de Braud Roberta Mortarini 2, * Andrea Anichini 1 Human Tumors Immunobiology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy Department of Experimental Oncology and Molecular Medicine, Laboratory Pathology, Pathology Medical Unit Oncology, These authors contributed equally to this work Correspondence to: Anichini,...

10.18632/oncotarget.6600 article EN Oncotarget 2015-12-14

Whether invasive mucinous adenocarcinoma (IMA) and colloid (ICA) of the lung represent separate tumour entities, or simply lie within a spectrum phenotypic variability, is worth investigating. Fifteen ICA, 12 IMA, 9 ALK-rearranged adenocarcinomas (ALKA), 8 non-mucinous KRAS-mutated (KRASA) breast (MBA) were assessed by immunohistochemistry for alveolar (TTF1, cytoplasmic MUC1), intestinal (CDX-2, MUC2), gastric (membrane MUC1, MUC6), bronchial (MUC5AC), mesenchymal (vimentin), neuroendocrine...

10.1002/cjp2.67 article EN cc-by-nc-nd The Journal of Pathology Clinical Research 2017-02-25

Neisseria meningitidis adhesin A (NadA) is a meningococcus surface protein thought to assist in the adhesion of bacterium host cells. We have previously shown that NadA also promotes bacterial internalization heterologous expression system. Here we used soluble recombinant (rNadA) lacking membrane anchor region characterize its route Chang epithelial Added culture medium, rNadA internalizes through PI3K-dependent endocytosis process not mediated by canonical clathrin or caveolin scaffolds,...

10.1371/journal.pone.0110047 article EN cc-by PLoS ONE 2014-10-27

Abstract Background: Acquired resistance to anti-EGFR MoAbs (cetuximab and panitumumab) represents a challenge in the treatment of mCRC, but its molecular mechanisms are not completely understood. Even presence RAS-BRAF-PI3KCA ”quadruple wt” HER-2/MET negative status for protein expression gene amplification, pts who primarily respond will eventually develop secondary resistance. Prior retrospective small series uniquely investigated single biomarker, showing some cases emergence KRAS...

10.1158/1535-7163.targ-15-b57 article EN Molecular Cancer Therapeutics 2015-12-01

<p>Supplementary Figure 1: Patients with acquired MET amplification have shorter PFS as compared to those MET-negative tumors. duration expressed month time units is shown for individual patients (blue histograms) and (red tumors (panel A). Kaplan Meier curves show median of MET-amplified (blue) (red) patients; moreover, around 40% 15% (but none subjects) were still progression-free at 10 even 20 months, respectively B).</p>

10.1158/1078-0432.22466544 preprint EN cc-by 2023-03-31

<p>Supplementary Figure 1: Patients with acquired MET amplification have shorter PFS as compared to those MET-negative tumors. duration expressed month time units is shown for individual patients (blue histograms) and (red tumors (panel A). Kaplan Meier curves show median of MET-amplified (blue) (red) patients; moreover, around 40% 15% (but none subjects) were still progression-free at 10 even 20 months, respectively B).</p>

10.1158/1078-0432.22466544.v1 preprint EN cc-by 2023-03-31

<div>Abstract<p><b>Purpose:</b> Even if <i>RAS-BRAF</i> wild-type and <i>HER2/MET</i>–negative metastatic colorectal cancer (mCRC) patients frequently respond to anti-EGFR mAbs, acquired resistance almost invariably occurs. Mechanisms of EGFR blockade include the emergence <i>KRAS</i>, <i>NRAS</i>, <i>EGFR</i> extracellular domain mutations as well <i>HER2/MET</i> alterations. However, these...

10.1158/1078-0432.c.6526347.v1 preprint EN 2023-03-31

<div>Abstract<p><b>Purpose:</b> Even if <i>RAS-BRAF</i> wild-type and <i>HER2/MET</i>–negative metastatic colorectal cancer (mCRC) patients frequently respond to anti-EGFR mAbs, acquired resistance almost invariably occurs. Mechanisms of EGFR blockade include the emergence <i>KRAS</i>, <i>NRAS</i>, <i>EGFR</i> extracellular domain mutations as well <i>HER2/MET</i> alterations. However, these...

10.1158/1078-0432.c.6526347 preprint EN 2023-03-31
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