1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The endogenous erythropoietin in correlation with other erythrocytic parameters in patients with head and neck squamous cell carcinoma treated with platinum-based induction chemotherapy

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Between January 2017 and July 2018 103 patients were included in a prospective study of erythropoietin (EPO) monitoring. The group consisted of 33% patients with oropharynx, 29% with oral cavity, 13% with nasopharynx, 6% with larynx, 6% with hypopharynx, 8% with unknown primary cancer, 4% with nasal cavity, and 1% with salivary gland cancer. Clinic stage: T4 – 50, T3 – 21, T2 – 14, T1 – 10, T0 – 8, and N3 – 19, N2 – 61, N1 – 10, N0 – 13. All patients received from one to four cycles of induction chemotherapy. EPO was measured in blood serum by enzyme-labelled chemiluminescent immunometric assay, using an Immulite 2000XPi analyser before the administration and on day 11 of each chemotherapy cycle.

          During induction chemotherapy the EPO level was elevated in all patients, which is expressed by means of medians: 10.7 ( p = 0.000001) in the middle of cycle 1; 10.9 ( p = 0.66) before cycle 2; 14.35 ( p = 0.000177) in the middle of cycle 2; 14.95 ( p = 0.39) before cycle 3, 17.00 ( p = 0.00078) in the middle of cycle 3, and 20.9 after cycle 3 ( p = 0.41).

          The correlation analysis conducted indicates that the administration of one chemotherapy dose results in higher EPO release (two-fold increase in EPO concentration) which intensifies reticulocytes (REC) production but without haemoglobin concentration in reticulocytes (HGB-REC) growth. In consequence, it leads to a decrease in RBC and HGB concentration (29–32 cases). The administration of two and three chemotherapy doses results in the subsequent higher release of EPO, which does not intensify REC production. In consequence, anaemia increases (35 cases).

          Related collections

          Most cited references18

          • Record: found
          • Abstract: found
          • Article: not found

          Erythropoietin and erythropoietin receptor expression in human cancer.

          Erythropoietin (EPO) stimulates the growth of erythroblasts in the bone marrow (C. Lacombe and P. Mayeux, NEPHROL: DIAL: TRANSPLANT:, 14 (SUPPL: 2): 22-28, 1999). We report basal and hypoxia-stimulated expression of EPO and its receptor, EPOR, in human breast cancer cells, and we demonstrate EPO-stimulated tyrosine phosphorylation and the proliferation of these cells in vitro. In 50 clinical specimens of breast carcinoma, we report high levels of EPO and EPOR associated with malignant cells and tumor vasculature but not with normal breast, benign papilloma, or fibrocystic tissue. Hypoxic tumor regions display the highest levels of EPO and EPOR expression. Enhanced EPO signaling may contribute to the promotion of human cancer by tissue hypoxia.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Impact of hemoglobin levels on tumor oxygenation: the higher, the better?

            Tumor hypoxia has been linked to tumor progression, the development of treatment resistance, and thus poor prognosis. Since anemia is a major factor causing tumor hypoxia, the association between blood hemoglobin concentration (cHb) and tumor oxygenation status has been examined. Published data on the relationship between pretreatment cHb values and tumor oxygenation (in terms of median pO(2) values, hypoxic fractions) have been summarized. Pretreatment O(2) tension measurements were performed in histologically proven experimental tumors, human breast cancers, squamous cell carcinomas of the head and neck, and cancers of the uterine cervix and of the vulva. In order to allow for a comparison between solid tumors and normal tissues, pO(2) measurements were also performed in healthy tissue in anemic and nonanemic patients. cHb was determined at the time of the pO(2) measurements. Based on current information from experimental and clinical studies there is increasing evidence that anemia is associated with a detrimental tumor oxygenation status. Increasing cHb values are correlated with significantly higher pO(2) values and lower hypoxic fractions. Maximum tumor oxygenation in squamous cell carcinomas is observed at normal (gender-specific) cHb values (approximately 14 g/dl in women and approximately 15 g/dl in men). Above this "optimal" Hb range, the oxygenation status tends to worsen again. In anemic patients, tumor oxygenation is compromised due to a decreased O(2) transport capacity of the blood. At the upper edge of the Hb scale, a substantial increase in the blood's viscous resistance to flow in "chaotic" tumor microvessels is thought to be mainly responsible for the observed restriction of O(2) supply. Review of relevant clinical data suggests that a maximum oxygenation status in solid tumors is to be expected in the range 12 g/dl < cHb < 14 g/dl for women and 13 g/dl < cHb < 15 g/dl for men. Considering the "optimal" cHb range with regard to tumor oxygenation, the concept of "the higher, the better" is therefore no longer valid. This finding has potentially far-reaching implications in the clinical setting (e. g., inappropriate erythropoietin treatment of nonanemic tumor patients).
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Functional erythropoietin receptor is undetectable in endothelial, cardiac, neuronal, and renal cells.

              Erythropoiesis stimulating agents (ESAs) have been reported to activate erythropoietin receptors (EpoR) on cell types, including endothelial, neuronal, renal tubule, and cardiac cells. ESAs have also been reported to promote angiogenesis. However, those findings are controversial and confounded by methodologic issues. We show that EpoR mRNA was detected in essentially all cell types examined, including primary human endothelial, renal, cardiac, and neuronal cells but 10- to 100-fold lower than Epo-responsive cells using quantitative reverse-transcribed polymerase chain reaction. Total endothelial EpoR protein examined using a new monoclonal antibody was low to undetectable. Surface EpoR on endothelial cells was not detected using [(125)I]-rHuEpo surface-binding studies. There was no evidence of ESA-induced intracellular signaling in endothelial cells. There was a similar lack of EpoR expression and signaling in other cell types examined. Experiments were performed examining ESA function on these cells. An in vivo rat corneal angiogenesis assay demonstrated neo-vessel formation in response to recombinant human vascular endothelial growth factor (rHuVEGF). However, recombinant mouse Epo did not induce vessel formation. Similarly, ESAs did not reproducibly provide cytoprotection to neuronal, renal, or cardiac cells. Taken together, our data challenge the notion of presence or function of EpoR on nonhematopoietic cells, and call into question the preclinical basis for clinical studies exploring direct, "pleiotropic" actions of ESAs.
                Bookmark

                Author and article information

                Journal
                Contemp Oncol (Pozn)
                Contemp Oncol (Pozn)
                WO
                Contemporary Oncology
                Termedia Publishing House
                1428-2526
                1897-4309
                31 October 2019
                2019
                : 23
                : 3
                : 178-182
                Affiliations
                [1 ]I Department of Radiotherapy and Chemotherapy, Maria Skłodowska-Curie Memorial Cancer Centre and Institute of Oncology, Gliwice Branch, Gliwice, Poland
                [2 ]Department of Bone Marrow Transplantation and Haematology-Oncology, Maria Skłodowska-Curie Memorial Cancer Centre and Institute of Oncology, Gliwice Branch, Gliwice, Poland
                [3 ]I Department of Radiotherapy and Chemotherapy, Maria Skłodowska-Curie Memorial Cancer Centre and Institute of Oncology, Gliwice Branch, Gliwice, Poland
                Author notes
                Address for correspondence Dominika Leś, I Department of Radiotherapy and Chemotherapy, Maria Skłodowska-Curie Memorial Cancer Centre and Institute of Oncology, Gliwice Branch, 15 Wybrzeże Armii Krajowej St., 44-100 Gliwice, Poland. e-mail: dominika.les@ 123456io.gliwice.pl
                Article
                89247
                10.5114/wo.2019.89247
                6883964
                8cb695a1-5dfb-458e-8969-19e740d7b484
                Copyright: © 2019 Termedia Sp. z o. o.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                : 22 March 2019
                : 21 June 2019
                Categories
                Original Paper

                erythropoietin,cisplatin,carboplatin,erythropoietin receptor

                Comments

                Comment on this article