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  • br de la Puente P

    2020-08-18


    160. de la Puente P, Luderer MJ, Federico C, et al. Enhancing proteasome-inhibitory activity and specificity of bortezomib by CD38 targeted nanoparticles in multiple myeloma. Journal of controlled release : official journal of the Controlled Release Society. Jan 28 2018;270:158-176.
    162. Huang YH, Vakili MR, Molavi O, et al. Decoration of Anti-CD38 on Nanoparticles Carrying a STAT3 Inhibitor Can Improve the Therapeutic Efficacy Against Myeloma. Cancers. Feb 20 2019;11(2).
    Tables
    Table 1: Targeted Nanomedicines for Cell Type-Specific Delivery
    ACCEPTED MANUSCRIPT
    Cell-Type Targeted Targeted Receptor Targeting Moiety Examples
    Tumor PSMA Antibody 30-32
    Cells/Endothelium EGFR Peptide 26-28
    Antibody
    Folate Receptor Folate 141,142
    P-selectin Fucoidan 41
    Polysaccharide
    CD44 Antibody 36
    M2 Tumor Associated Mannose Receptor Monosaccharide 102,109
    Sialic Acid Receptor Sialic Acid 111
    SR-B1 Receptor Apo-1 Peptide 144
    Th2 Regulatory T-cells GITR Peptide 112,113
    Nrp1 Peptide 145
    Tumor-Associated Sigma-Receptor Anisamide 118-120
    Fibroblasts (TAFs)
    Dendritic Cells SR-B1 Receptor Peptide 144
    T-Lymphocytes CD3 Antibody 146,147
    CD4 Antibody 148
    B-Lymphocytes/Plasma CD19 Antibody 151-154
    Graphical abstract
    Figure 1
    Figure 2
    Figure 3
    Contents lists available at ScienceDirect
    EBioMedicine
    Research paper
    Biomarker concordance between primary colorectal cancer and its metastases
    Colorectal & Peritoneal Oncology Centre, The Christie NHS Foundation Trust, Manchester, UK
    Division of Cancer Sciences, School of Medical Science, Faculty of Biology, Medicine and Health, University of Manchester, UK
    Article history:
    Keywords:
    Biomarker
    Concordance
    Colorectal cancer
    RAS
    BRAF
    PIK3CA 
    Background: The use of biomarkers to target anti-EGFR treatments for metastatic colorectal cancer (CRC) 9064-57-7 well-established, requiring molecular analysis of primary or metastatic biopsies. We aim to review concordance between primary CRC and its metastatic sites.
    Methods: A systematic review and meta-analysis of all published studies (1991–2018) reporting on biomarker concordance between primary CRC 9064-57-7 and its metastatic site(s) was undertaken according to PRISMA guidelines using several medical databases. Studies without matched samples or using peripheral blood for biomarker anal-ysis were excluded.
    © 2019 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).
    1. Introduction
    Advances in biological therapies such as anti-epidermal growth factor receptor (EGFR) antibodies (cetuximab and panitumumab) have resulted in biomarkers being used to target metastatic CRC (mCRC) [11]. KRAS is a key proto-oncogene downstream of EGFR and is activated in up to 50% of sporadic mCRC patients, with 95% of activa-tions occurring in codons 12/13 of exon 2 [12]. Importantly, KRAS exon
    Corresponding author at: Consultant Colorectal Surgeon, Colorectal and Peritoneal Oncology Centre, The Christie NHS Foundation Trust, Wilmslow Road, Manchester M20 4BX, United Kingdom.
    E-mail address: [email protected] (O. Aziz).
    1 Signifies co-first authors.
    2–4 mutations (involving codons 12, 13, 161, 117 & 146) demonstrate a significantly lower response to cetuximab and panitumumab [13,14]. Some studies have also indicated that KRAS mutations may confer resis-tance to bevacizumab [15,16]. The extended RAS family of oncogenes includes NRAS, with exon 2–4 mutations occurring in 3–5% of CRC's and similarly resulting in a lower response [17,18]. BRAF, a RAF gene kinase and immediate downstream effector of KRAS, shows mutations in nearly 10% of colorectal adenocarcinomas and is also a strong nega-tive prognostic marker, predicting resistance to both cytotoxic and anti-EGFR therapy [19–21].
    Mutations in genes other than those constituting the RAS/RAF path-way include PIK3CA and PTEN [22]. Approximately 15–20% of patients with mCRC, have mutations in exon 20 of PIK3CA and demonstrate resistance to cetuximab even in the presence of KRAS wild type [23]. Loss of expression of PTEN, a natural inhibitor of PI3K-initiated signal-ling, has itself also been associated with unresponsiveness to cetuximab and reduced OS [24,25]. Beyond the factors associated with EGFR signal-ling pathways, a number of other genes are significantly mutated in CRC, including APC (51–81%), TP53 (20–60%), and SMAD4 (10–20%) [12]. APC is the most prevalent gene in the establishment of sporadic co-lorectal malignancy [26]. Similar to APC, the TP53 gene is heavily