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  • br de la Puente P

    2020-08-07


    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) Erlotinib 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 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