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      Loss of Estrogen Receptors is Associated with Increased Tumor Aggression in Laryngeal Squamous Cell Carcinoma

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          Abstract

          Laryngeal squamous cell carcinoma (LSCC) responds to 17β-estradiol via estrogen-receptor (ER, transcribed from ESR1) dependent mechanisms, but is not recognized as a hormonally responsive cancer. 17β-estradiol production by LSCC cell lines UM-SCC-11A and UM-SCC-12 was examined. Wild type (WT) and ESR1-silenced LSCC cultures and xenografts were examined for 17β-estradiol responsiveness in vivo. 14 LSCC and surrounding epithelial samples at various pathological stages were obtained from patients; ERα and ERβ expression were verified using data from the total cancer genome atlas. UM-SCC-11A and UM-SCC-12 both produce 17β-estradiol, but only UM-SCC-12, not UM-SCC-11A, xenograft tumors grow larger in vivo in response to systemic 17β-estradiol treatments. ERα66 and ERα36 expression inversely correlated with clinical cancer stage and tumor burden. LSCC ERα66 expression was higher compared to surrounding epithelia in indolent samples but lower in aggressive LSCC. ERβ expression was highly variable. High ESR1 expression correlated with improved survival in LSCC. Loss of ERα66 expression inversely correlated with prognosis in LSCC. ERα66 may be a histopathological marker of aggression in LSCC.

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          Mechanisms of tamoxifen resistance.

          Mitch Dowsett, Alistair Ring (2004)
          The anti-oestrogen tamoxifen is the most commonly used treatment for patients with oestrogen-receptor (ER)-positive breast cancer. Although many patients benefit from tamoxifen in the adjuvant and metastatic settings, resistance is an important clinical problem. The target of tamoxifen in vivo is the ER. Over the last decade many advances have been made in our understanding of the biology of the ER which may help to explain how resistance to tamoxifen develops. Such mechanisms may include changes in the expression of ERalpha or ERbeta, alterations in co-regulatory proteins, and the influences of cellular kinase signal transduction pathways. The experimental and clinical evidence supporting these mechanisms of tamoxifen resistance are discussed in this review.
          Article 0 comments Cited 147 times – based on 0 reviews     Review now
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            Endocrine resistance in breast cancer--An overview and update.

            Robert Clarke, John Tyson, J Michael Dixon (2015)
            Tumors that express detectable levels of the product of the ESR1 gene (estrogen receptor-α; ERα) represent the single largest molecular subtype of breast cancer. More women eventually die from ERα+ breast cancer than from either HER2+ disease (almost half of which also express ERα) and/or from triple negative breast cancer (ERα-negative, progesterone receptor-negative, and HER2-negative). Antiestrogens and aromatase inhibitors are largely indistinguishable from each other in their abilities to improve overall survival and almost 50% of ERα+ breast cancers will eventually fail one or more of these endocrine interventions. The precise reasons why these therapies fail in ERα+ breast cancer remain largely unknown. Pharmacogenetic explanations for Tamoxifen resistance are controversial. The role of ERα mutations in endocrine resistance remains unclear. Targeting the growth factors and oncogenes most strongly correlated with endocrine resistance has proven mostly disappointing in their abilities to improve overall survival substantially, particularly in the metastatic setting. Nonetheless, there are new concepts in endocrine resistance that integrate molecular signaling, cellular metabolism, and stress responses including endoplasmic reticulum stress and the unfolded protein response (UPR) that provide novel insights and suggest innovative therapeutic targets. Encouraging evidence that drug combinations with CDK4/CDK6 inhibitors can extend recurrence free survival may yet translate to improvements in overall survival. Whether the improvements seen with immunotherapy in other cancers can be achieved in breast cancer remains to be determined, particularly for ERα+ breast cancers. This review explores the basic mechanisms of resistance to endocrine therapies, concluding with some new insights from systems biology approaches further implicating autophagy and the UPR in detail, and a brief discussion of exciting new avenues and future prospects.
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              Tumor volume in subcutaneous mouse xenografts measured by microCT is more accurate and reproducible than determined by 18F-FDG-microPET or external caliper

              Mette Munk Jensen, Jesper Tranekjær Jørgensen, Tina Binderup … (2008)
              Background In animal studies tumor size is used to assess responses to anticancer therapy. Current standard for volumetric measurement of xenografted tumors is by external caliper, a method often affected by error. The aim of the present study was to evaluate if microCT gives more accurate and reproducible measures of tumor size in mice compared with caliper measurements. Furthermore, we evaluated the accuracy of tumor volume determined from 18F-fluorodeoxyglucose (18F-FDG) PET. Methods Subcutaneously implanted human breast adenocarcinoma cells in NMRI nude mice served as tumor model. Tumor volume (n = 20) was determined in vivo by external caliper, microCT and 18F-FDG-PET and subsequently reference volume was determined ex vivo. Intra-observer reproducibility of the microCT and caliper methods were determined by acquiring 10 repeated volume measurements. Volumes of a group of tumors (n = 10) were determined independently by two observers to assess inter-observer variation. Results Tumor volume measured by microCT, PET and caliper all correlated with reference volume. No significant bias of microCT measurements compared with the reference was found, whereas both PET and caliper had systematic bias compared to reference volume. Coefficients of variation for intra-observer variation were 7% and 14% for microCT and caliper measurements, respectively. Regression coefficients between observers were 0.97 for microCT and 0.91 for caliper measurements. Conclusion MicroCT was more accurate than both caliper and 18F-FDG-PET for in vivo volumetric measurements of subcutaneous tumors in mice.18F-FDG-PET was considered unsuitable for determination of tumor size. External caliper were inaccurate and encumbered with a significant and size dependent bias. MicroCT was also the most reproducible of the methods.
              Article 0 comments Cited 132 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Barbara. D. Boyan: bboyan@vcu.edu
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 6 March 2020
                Publication date PMC-release: 6 March 2020
                Publication date Collection: 2020
                Volume: 10
                Electronic Location Identifier: 4227
                Affiliations
                [1 ]ISNI 0000 0004 0458 8737, GRID grid.224260.0, Department of Biomedical Engineering, , Virginia Commonwealth University, ; Richmond, VA USA
                [2 ]ISNI 0000 0001 0325 0791, GRID grid.415250.7, Department of Otolaryngology, , Meir Hospital, ; Kfar Saba, Israel
                [3 ]ISNI 0000 0004 1937 0546, GRID grid.12136.37, Sackler Faculty of Medicine, , Tel Aviv University, ; Tel Aviv, Israel
                [4 ]ISNI 0000000122483208, GRID grid.10698.36, Department of Otolaryngology – Head and Neck Surgery and Neurosurgery, , University of North Carolina School of Medicine, ; Chapel Hill, NC USA
                [5 ]ISNI 0000 0004 0575 344X, GRID grid.413156.4, Department of Otolaryngology Head and Neck Surgery, Rabin Medical Center, ; Petah-Tikvah, Israel
                [6 ]ISNI 0000 0001 2097 4943, GRID grid.213917.f, Department of Biomedical Engineering, , Georgia Institute of Technology, ; Atlanta, GA USA
                [7 ]ISNI 0000 0001 0629 5880, GRID grid.267309.9, Department of Periodontics, , University of Texas Health Science Center at San Antonio, ; San Antonio, TX USA
                Article
                Publisher ID: 60675
                DOI: 10.1038/s41598-020-60675-2
                PMC ID: 7060328
                PubMed ID: 32144339
                SO-VID: 582fb72a-3c0f-4e0a-975d-72577391c783
                Copyright © © The Author(s) 2020
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 31 July 2019
                Date accepted : 20 January 2020
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Uncategorized
                Keywords: steroid hormones,prognostic markers
                Data availability:
                ScienceOpen disciplines: Uncategorized
                Keywords: steroid hormones, prognostic markers

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