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      Low Pre-ChemoradiotherapyPan-Immune-Inflammation Value (PIV) Measures Predict Better Survival Outcomes in Locally Advanced Pancreatic Adenocarcinomas

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          Abstract

          Objective

          This study sought to determine whether pretreatment pan-immune-inflammation value (PIV) could be used to predict prognosis in patients with locally advanced pancreatic adenocarcinoma (LA-PAC) following definitive concurrent chemoradiotherapy (C-CRT).

          Methods

          The outcomes of 178 LA-PAC patients who received definitive C-CRT were analyzed retrospectively. For all patients, the PIV was calculated using the peripheral blood platelet (P), monocyte (M), neutrophil (N), and lymphocyte (L) counts obtained on the first day of C-CRT: PIV=P×M×N÷L. The optimum cutoff values for PIV connected to progression-free (PFS) and overall survival (OS) results were sought using receiver operating characteristic (ROC) curve analysis. The OS and PFS differences between the PIV groups constituted the primary and secondary endpoints, respectively.

          Results

          ROC curve analysis indicated that the ideal PIV cutoff was 464 (AUC: 75.9%, sensitivity: 74.1%, specificity: 71.9%), which categorized patients into two groups based on PFS and OS results: low PIV (L-PIV; N = 69) and high PIV (H-PIV; N = 109). According to comparative survival analyses, patients in the L-PIV group had significantly longer median PFS (14.3 vs 7.3 months; HR: 3.04; P<0.001) and OS (25.9 vs 13.3 months; HR: 2.86; P<0.001) than those in the H-PIV group. Although none of the H-PIV patients could survive beyond 5 years, the estimated 5-year OS rate was 29.7% in the L-PIV cohort. In multivariate analyses, besides the L-PIV, N 0 nodal stage, and CA 19–9 ≤ 90 U/mL appeared to be the independent predictors of better PFS (P < 0.05 for each) and OS (P < 0.05 for each) results.

          Conclusion

          The present results indicated that pre-C-CRT L-PIV measures were associated with favorable median and long-term PFS and OS results in LA-PAC patients, suggesting that the PIV is a potent and independent novel prognostic biomarker.

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          Hallmarks of Cancer: The Next Generation

          Douglas Hanahan, Robert A. Weinberg (2011)
          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Cancer-related inflammation.

            Alberto Mantovani, Paola Allavena, Antonio Sica … (2008)
            The mediators and cellular effectors of inflammation are important constituents of the local environment of tumours. In some types of cancer, inflammatory conditions are present before a malignant change occurs. Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours. Regardless of its origin, 'smouldering' inflammation in the tumour microenvironment has many tumour-promoting effects. It aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents. The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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              Pancreatic cancers require autophagy for tumor growth.

              Shenghong Yang, Xiaoxu Wang, Gianmarco Contino … (2011)
              Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer is complex and may differ depending on tumor type or context. Here we show that pancreatic cancers have a distinct dependence on autophagy. Pancreatic cancer primary tumors and cell lines show elevated autophagy under basal conditions. Genetic or pharmacologic inhibition of autophagy leads to increased reactive oxygen species, elevated DNA damage, and a metabolic defect leading to decreased mitochondrial oxidative phosphorylation. Together, these ultimately result in significant growth suppression of pancreatic cancer cells in vitro. Most importantly, inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models. These results suggest that, unlike in other cancers where autophagy inhibition may synergize with chemotherapy or targeted agents by preventing the up-regulation of autophagy as a reactive survival mechanism, autophagy is actually required for tumorigenic growth of pancreatic cancers de novo, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on autophagy. As chloroquine and its derivatives are potent inhibitors of autophagy and have been used safely in human patients for decades for a variety of purposes, these results are immediately translatable to the treatment of pancreatic cancer patients, and provide a much needed, novel vantage point of attack.
              Article 0 comments Cited 585 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Inflamm Res
                Journal ID (iso-abbrev): J Inflamm Res
                Journal ID (publisher-id): jir
                Title: Journal of Inflammation Research
                Publisher: Dove
                ISSN (Electronic): 1178-7031
                Publication date (Electronic): 18 September 2022
                Publication date Collection: 2022
                Volume: 15
                Pages: 5413-5423
                Affiliations
                [1 ]Department of Radiation Oncology, Baskent University Medical Faculty , Adana, Turkey
                [2 ]Department of Radiation Oncology, Koc University School of Medicine , Istanbul, Turkey
                [3 ]Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center , Houston, TX, USA
                [4 ]Clinic of Radiation Oncology, Mersin Education and Research Hospital , Mersin, Turkey
                [5 ]Department of Radiation Oncology, Bahcesehir University , Istanbul, Turkey
                Author notes
                Correspondence: Erkan Topkan, Department of Radiation Oncology, Baskent University Medical Faculty , Adana, 01120, Turkey, Tel +90-533-7381069, Fax +90-322-3444452, Email docdretopkan@gmail.com
                Author information
                http://orcid.org/0000-0001-8120-7123
                http://orcid.org/0000-0001-8087-3140
                http://orcid.org/0000-0002-5361-364X
                http://orcid.org/0000-0001-8253-488X
                Article
                Publisher ID: 385328
                DOI: 10.2147/JIR.S385328
                PMC ID: 9499729
                PubMed ID: 36158517
                SO-VID: e629ec57-e6af-482b-84bc-6af67c13cb55
                Copyright © © 2022 Topkan et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 06 August 2022
                Date accepted : 10 September 2022
                Page count
                Figures: 3, Tables: 3, References: 47, Pages: 11
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Immunology
                Keywords: pancreas cancer,pan-immune-inflammation value,biomarker,prognosis,survival
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: pancreas cancer, pan-immune-inflammation value, biomarker, prognosis, survival

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