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      The Role of Activator Protein-1 (AP-1) Family Members in CD30-Positive Lymphomas

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          Abstract

          The Activator Protein-1 (AP-1) transcription factor (TF) family, composed of a variety of members including c-JUN, c-FOS and ATF, is involved in mediating many biological processes such as proliferation, differentiation and cell death. Since their discovery, the role of AP-1 TFs in cancer development has been extensively analysed. Multiple in vitro and in vivo studies have highlighted the complexity of these TFs, mainly due to their cell-type specific homo- or hetero-dimerization resulting in diverse transcriptional response profiles. However, as a result of the increasing knowledge of the role of AP-1 TFs in disease, these TFs are being recognized as promising therapeutic targets for various malignancies. In this review, we focus on the impact of deregulated expression of AP-1 TFs in CD30-positive lymphomas including Classical Hodgkin Lymphoma and Anaplastic Large Cell Lymphoma.

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          AP-1: a double-edged sword in tumorigenesis.

          Robert Eferl, Erwin F. Wagner (2003)
          Article 0 comments Cited 568 times – based on 0 reviews     Review now
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            Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma.

            Michael Green, Stefano Monti, Scott J. Rodig … (2010)
            Classical Hodgkin lymphoma (cHL) and mediastinal large B-cell lymphoma (MLBCL) are lymphoid malignancies with certain shared clinical, histologic, and molecular features. Primary cHLs and MLBCLs include variable numbers of malignant cells within an inflammatory infiltrate, suggesting that these tumors escape immune surveillance. Herein, we integrate high-resolution copy number data with transcriptional profiles and identify the immunoregulatory genes, PD-L1 and PD-L2, as key targets at the 9p24.1 amplification peak in HL and MLBCL cell lines. We extend these findings to laser-capture microdissected primary Hodgkin Reed-Sternberg cells and primary MLBCLs and find that programmed cell death-1 (PD-1) ligand/9p24.1 amplification is restricted to nodular sclerosing HL, the cHL subtype most closely related to MLBCL. Using quantitative immunohistochemical methods, we document the association between 9p24.1 copy number and PD-1 ligand expression in primary tumors. In cHL and MLBCL, the extended 9p24.1 amplification region also included the Janus kinase 2 (JAK2) locus. Of note, JAK2 amplification increased protein expression and activity, specifically induced PD-1 ligand transcription and enhanced sensitivity to JAK2 inhibition. Therefore, 9p24.1 amplification is a disease-specific structural alteration that increases both the gene dosage of PD-1 ligands and their induction by JAK2, defining the PD-1 pathway and JAK2 as complementary rational therapeutic targets.
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              Role of the CXCL8-CXCR1/2 Axis in Cancer and Inflammatory Diseases

              Helen Ha, Bikash Debnath, Nouri Neamati (2017)
              The chemokine receptors CXCR1/2 and their ligand CXCL8 are essential for the activation and trafficking of inflammatory mediators as well as tumor progression and metastasis. The CXCL8-CXCR1/2 signaling axis is involved in the pathogenesis of several diseases including chronic obstructive pulmonary diseases (COPD), asthma, cystic fibrosis and cancer. Interaction between CXCL8 secreted by select cancer cells and CXCR1/2 in the tumor microenvironment is critical for cancer progression and metastasis. The CXCL8-CXCR1/2 axis may play an important role in tumor progression and metastasis by regulating cancer stem cell (CSC) proliferation and self-renewal. During the past two decades, several small-molecule CXCR1/2 inhibitors, CXCL8 releasing inhibitors, and neutralizing antibodies against CXCL8 and CXCR1/2 have been reported. As single agents, such inhibitors are expected to be efficacious in various inflammatory diseases. Several preclinical studies suggest that combination of CXCR1/2 inhibitors along with other targeted therapies, chemotherapies, and immunotherapy may be effective in treating select cancers. Currently, several of these inhibitors are in advanced clinical trials for COPD, asthma, and metastatic breast cancer. In this review, we provide a comprehensive analysis of the role of the CXCL8-CXCR1/2 axis and select genes co-expressed in this pathway in disease progression. We also discuss the latest progress in developing small-molecule drugs targeting this pathway.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 28 March 2018
                Publication date Collection: April 2018
                Volume: 10
                Issue: 4
                Electronic Location Identifier: 93
                Affiliations
                [1 ]Ludwig Boltzmann Institute for Cancer Research, 1090 Vienna, Austria; Ines.Garces@ 123456lbicr.lbg.ac.at
                [2 ]Unit of Laboratory Animal Pathology, University of Veterinary Medicine Vienna, 1210 Vienna, Austria; Sabine.Lagger@ 123456vetmeduni.ac.at
                [3 ]Clinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria; huan-chang.liang@ 123456meduniwien.ac.at (H.-C.L.); Olaf.merkel@ 123456meduniwien.ac.at (O.M.)
                [4 ]Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB21QP, UK; sdt36@ 123456cam.ac.uk
                Author notes
                [†]

                Co-first authors.

                [‡]

                Co-last authors.

                Author information
                https://orcid.org/0000-0003-2612-3714
                https://orcid.org/0000-0002-8439-4507
                Article
                Publisher ID: cancers-10-00093
                DOI: 10.3390/cancers10040093
                PMC ID: 5923348
                PubMed ID: 29597249
                SO-VID: c2f5880d-f522-40fa-87c7-53c4260f5a70
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 February 2018
                Date accepted : 25 March 2018
                Categories
                Subject: Review

                Keywords: activator protein-1 (ap-1),transcription factors (tfs),anaplastic large cell lymphoma (alcl),cd-30,classical hodgkin lymphoma (chl),peripheral t-cell lymphoma (ptcl)
                Data availability:
                Keywords: activator protein-1 (ap-1), transcription factors (tfs), anaplastic large cell lymphoma (alcl), cd-30, classical hodgkin lymphoma (chl), peripheral t-cell lymphoma (ptcl)

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