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      Cellular and molecular mechanisms of perineural invasion of pancreatic ductal adenocarcinoma

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          Abstract

          Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignant disease with a unique tumor microenvironment surrounded by an interlaced network of cancer and noncancerous cells. Recent works have revealed that the dynamic interaction between cancer cells and neuronal cells leads to perineural invasion (PNI), a clinical pathological feature of PDAC. The formation and function of PNI are dually regulated by molecular (e.g., involving neurotrophins, cytokines, chemokines, and neurotransmitters), metabolic (e.g., serine metabolism), and cellular mechanisms (e.g., involving Schwann cells, stromal cells, T cells, and macrophages). Such integrated mechanisms of PNI not only support tumor development, growth, invasion, and metastasis but also mediate the formation of pain, all of which are closely related to poor disease prognosis in PDAC. This review details the modulation, signaling pathways, detection, and clinical relevance of PNI and highlights the opportunities for further exploration that may benefit PDAC patients.

          Abstract

          This review details the modulation, function, and detection of perineural invasion, and highlights the opportunities for further exploration that may benefit pancreatic cancer patients.

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          Cancer Statistics, 2021

          Rebecca Siegel, Kimberly D Miller, Hannah Fuchs … (2021)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths in the United States and compiles the most recent data on population-based cancer occurrence. Incidence data (through 2017) were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data (through 2018) were collected by the National Center for Health Statistics. In 2021, 1,898,160 new cancer cases and 608,570 cancer deaths are projected to occur in the United States. After increasing for most of the 20th century, the cancer death rate has fallen continuously from its peak in 1991 through 2018, for a total decline of 31%, because of reductions in smoking and improvements in early detection and treatment. This translates to 3.2 million fewer cancer deaths than would have occurred if peak rates had persisted. Long-term declines in mortality for the 4 leading cancers have halted for prostate cancer and slowed for breast and colorectal cancers, but accelerated for lung cancer, which accounted for almost one-half of the total mortality decline from 2014 to 2018. The pace of the annual decline in lung cancer mortality doubled from 3.1% during 2009 through 2013 to 5.5% during 2014 through 2018 in men, from 1.8% to 4.4% in women, and from 2.4% to 5% overall. This trend coincides with steady declines in incidence (2.2%-2.3%) but rapid gains in survival specifically for nonsmall cell lung cancer (NSCLC). For example, NSCLC 2-year relative survival increased from 34% for persons diagnosed during 2009 through 2010 to 42% during 2015 through 2016, including absolute increases of 5% to 6% for every stage of diagnosis; survival for small cell lung cancer remained at 14% to 15%. Improved treatment accelerated progress against lung cancer and drove a record drop in overall cancer mortality, despite slowing momentum for other common cancers.
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            Macrophage diversity enhances tumor progression and metastasis.

            Bin-Zhi Qian, Jeffrey W Pollard (2010)
            There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and malignant progression. During tumor initiation, they create an inflammatory environment that is mutagenic and promotes growth. As tumors progress to malignancy, macrophages stimulate angiogenesis, enhance tumor cell migration and invasion, and suppress antitumor immunity. At metastatic sites, macrophages prepare the target tissue for arrival of tumor cells, and then a different subpopulation of macrophages promotes tumor cell extravasation, survival, and subsequent growth. Specialized subpopulations of macrophages may represent important new therapeutic targets. Copyright 2010 Elsevier Inc. All rights reserved.
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              Pancreatic cancer.

              Jörg Kleeff, Murray Korc, Minoti V. Apte … (2016)
              Pancreatic cancer is a major cause of cancer-associated mortality, with a dismal overall prognosis that has remained virtually unchanged for many decades. Currently, prevention or early diagnosis at a curable stage is exceedingly difficult; patients rarely exhibit symptoms and tumours do not display sensitive and specific markers to aid detection. Pancreatic cancers also have few prevalent genetic mutations; the most commonly mutated genes are KRAS, CDKN2A (encoding p16), TP53 and SMAD4 - none of which are currently druggable. Indeed, therapeutic options are limited and progress in drug development is impeded because most pancreatic cancers are complex at the genomic, epigenetic and metabolic levels, with multiple activated pathways and crosstalk evident. Furthermore, the multilayered interplay between neoplastic and stromal cells in the tumour microenvironment challenges medical treatment. Fewer than 20% of patients have surgically resectable disease; however, neoadjuvant therapies might shift tumours towards resectability. Although newer drug combinations and multimodal regimens in this setting, as well as the adjuvant setting, appreciably extend survival, ∼80% of patients will relapse after surgery and ultimately die of their disease. Thus, consideration of quality of life and overall survival is important. In this Primer, we summarize the current understanding of the salient pathophysiological, molecular, translational and clinical aspects of this disease. In addition, we present an outline of potential future directions for pancreatic cancer research and patient management.
              Article 0 comments Cited 461 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Daolin Tang:
                ORCID: https://orcid.org/0000-0002-1903-6180
                daolin.tang@utsouthwestern.edu
                Journal
                Journal ID (nlm-ta): Cancer Commun (Lond)
                Journal ID (iso-abbrev): Cancer Commun (Lond)
                Journal ID (doi): 10.1002/(ISSN)2523-3548
                Journal ID (publisher-id): CAC2
                Title: Cancer Communications
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2523-3548
                Publication date (Electronic): 15 July 2021
                Publication date Collection: August 2021
                Volume: 41
                Issue: 8 ( doiID: 10.1002/cac2.v41.8 )
                Pages: 642-660
                Affiliations
                [ 1 ] Department of Surgery UT Southwestern Medical Center Dallas Texas 75390 USA
                Author notes
                [*] [* ] Correspondence

                Daolin Tang, Department of Surgery, UT Southwestern Medical Center, Dallas, Texas 75390, USA.

                Email: daolin.tang@ 123456utsouthwestern.edu

                Author information
                https://orcid.org/0000-0002-1903-6180
                Article
                Publisher ID: CAC212188
                DOI: 10.1002/cac2.12188
                PMC ID: 8360640
                PubMed ID: 34264020
                SO-VID: 75ba1203-f5f3-46fd-b3a2-4e65b70b487f
                Copyright © © 2021 The Authors. Cancer Communications published by John Wiley & Sons Australia, Ltd. on behalf of Sun Yat‐sen University Cancer Center
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date revision received : 11 May 2021
                Date received : 17 March 2021
                Date accepted : 18 June 2021
                Page count
                Figures: 4, Tables: 3, Pages: 19, Words: 11996
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                cover-date August 2021
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.5 mode:remove_FC converted:12.08.2021

                Keywords: neurotrophins,pancreatic ductal adenocarcinoma,perineural invasion,schwann cells,tumor microenvironment
                Data availability:
                Keywords: neurotrophins, pancreatic ductal adenocarcinoma, perineural invasion, schwann cells, tumor microenvironment

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