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      Bone metastasis as primary presentation of pancreatic ductal adenocarcinoma: A case report and literature review

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          Abstract

          PDAC bone metastases represent a clinical challenge characterized by multifaceted biological entity.

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          Most cited references33

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          Tumor metastasis: molecular insights and evolving paradigms.

          Scott Valastyan, Robert A Weinberg (2011)
          Metastases represent the end products of a multistep cell-biological process termed the invasion-metastasis cascade, which involves dissemination of cancer cells to anatomically distant organ sites and their subsequent adaptation to foreign tissue microenvironments. Each of these events is driven by the acquisition of genetic and/or epigenetic alterations within tumor cells and the co-option of nonneoplastic stromal cells, which together endow incipient metastatic cells with traits needed to generate macroscopic metastases. Recent advances provide provocative insights into these cell-biological and molecular changes, which have implications regarding the steps of the invasion-metastasis cascade that appear amenable to therapeutic targeting. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring

            Yu. Shi, Weina Gao, Nikki K Lytle … (2019)
            Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis largely due to inefficient diagnosis and tenacious drug resistance. Activation of pancreatic stellate cells (PSCs) and consequent development of dense stroma are prominent features accounting for this aggressive biology 1,2 . The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains their own activation, facilitating a vicious cycle to exacerbate tumourigenesis and drug resistance 3–7 . Moreover, PSC activation occurs very early during PDAC tumourigenesis 8–10 , and activated PSCs comprise a significant fraction of the tumour mass, providing a rich source of readily detectable factors. Therefore, we hypothesized that the communication between PSCs and PCCs could be an Achilles’ heel exploitable to develop effective strategies for PDAC therapy and diagnosis. Here, starting with systematic proteomic investigation of secreted disease mediators and underlying molecular mechanisms, we reveal that leukemia inhibitory factor (LIF) is a key paracrine factor from activated PSCs acting on cancer cells. Both pharmacologic LIF blockade and genetic Lifr deletion significantly slow tumour progression and augment chemotherapy efficacy to prolong survival of PDAC mouse models, mainly by modulating cancer cell differentiation and EMT status. Moreover, we show that, consistently in both mouse models and human PDAC, aberrant production of LIF in the pancreas is unique to pathological conditions and correlates with PDAC pathogenesis, and circulating LIF level changes correlate well with tumour response to therapy. Collectively, these findings uncover a previously unappreciated function of LIF in PDAC tumourigenesis, and suggest its translational potential as an attractive therapeutic target and circulating marker. These studies underscore how a better understanding of cell-cell communications within the tumour microenvironment promotes novel strategies for cancer therapy.
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              Microenvironment drug resistance in multiple myeloma: emerging new players

              Lucia Di Marzo, Vanessa Desantis, Antonio Solimando … (2016)
              Multiple myeloma (MM) drug resistance (DR) is a multistep transformation process based on a powerful interplay between bone marrow stromal cells and MM cells that allows the latter to escape anti-myeloma therapies. Here we present an overview of the role of the bone marrow microenvironment in both soluble factors-mediated drug resistance (SFM-DR) and cell adhesion-mediated drug resistance (CAM-DR), focusing on the role of new players, namely miRNAs, exosomes and cancer-associated fibroblasts.
              Article 0 comments Cited 87 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Antonella Argentiero:
                ORCID: https://orcid.org/0000-0001-9187-3891
                argentieroantonella@gmail.com
                Journal
                Journal ID (nlm-ta): Clin Case Rep
                Journal ID (iso-abbrev): Clin Case Rep
                Journal ID (doi): 10.1002/(ISSN)2050-0904
                Journal ID (publisher-id): CCR3
                Title: Clinical Case Reports
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2050-0904
                Publication date (Electronic): 05 September 2019
                Publication date Collection: October 2019
                Volume: 7
                Issue: 10 ( doiID: 10.1002/ccr3.v7.10 )
                Pages: 1972-1976
                Affiliations
                [ 1 ] Medical Oncology Unit National Cancer Research Centre Istituto Tumori "Giovanni Paolo II" Bari Italy
                [ 2 ] Radiology Unit National Cancer Research Centre Istituto Tumori "Giovanni Paolo II" Bari Italy
                [ 3 ] Department of Biomedical Sciences and Human Oncology Section of Internal Medicine “G. Baccelli” University of Bari Medical School Bari Italy
                [ 4 ] Nuclear Medicine Unit SS Annunziata Hospital, Taranto Bari Italy
                [ 5 ] Division of Anatomic Pathology SS Annunziata Hospital, Taranto Bari Italy
                Author notes
                [*] [* ] Correspondence

                Antonella Argentiero, Medical Oncology Unit, Cancer Institute "Giovanni Paolo II", Viale Orazio Flacco, 65, 70124, Bari, Italy.

                Email: argentieroantonella@ 123456gmail.com

                Author information
                https://orcid.org/0000-0001-9187-3891
                https://orcid.org/0000-0002-2293-9698
                https://orcid.org/0000-0002-7014-6828
                Article
                Publisher ID: CCR32412
                DOI: 10.1002/ccr3.2412
                PMC ID: 6787833
                PubMed ID: 31624620
                SO-VID: b3b799a3-df4f-4005-bf17-60b30caa9e0b
                Copyright © © 2019 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 23 May 2019
                Date revision received : 27 July 2019
                Date accepted : 13 August 2019
                Page count
                Figures: 3, Tables: 0, Pages: 5, Words: 2733
                Categories
                Subject: Case Report
                Subject: Case Reports
                Custom metadata
                source-schema-version-number 2.0
                component-id ccr32412
                cover-date October 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.0 mode:remove_FC converted:11.10.2019

                Keywords: bone metastases,pancreatic ductal adenocarcinoma,pdac,zoledronic acid
                Data availability:
                Keywords: bone metastases, pancreatic ductal adenocarcinoma, pdac, zoledronic acid

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