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      Antitumor effects of anlotinib in thyroid cancer

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          Abstract

          There is no effective treatment for patients with poorly differentiated papillary thyroid cancer or anaplastic thyroid cancer (ATC). Anlotinib, a multi-kinase inhibitor, has already shown antitumor effects in various types of carcinoma in a phase I clinical trial. In this study, we aimed to better understand the effect and efficacy of anlotinib against thyroid carcinoma cells in vitro and in vivo. We found that anlotinib inhibits the cell viability of papillary thyroid cancer and ATC cell lines, likely due to abnormal spindle assembly, G2/M arrest, and activation of TP53 upon anlotinib treatment. Moreover, anlotinib suppresses the migration of thyroid cancer cells in vitro and the growth of xenograft thyroid tumors in mice. Our data demonstrate that anlotinib has significant anticancer activity in thyroid cancer, and potentially offers an effective therapeutic strategy for patients of advanced thyroid cancer type.

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          Association between BRAF V600E mutation and mortality in patients with papillary thyroid cancer.

          Mingzhao Xing, Ali Alzahrani, Kathryn Carson … (2013)
          BRAF V600E is a prominent oncogene in papillary thyroid cancer (PTC), but its role in PTC-related patient mortality has not been established. To investigate the relationship between BRAF V600E mutation and PTC-related mortality. Retrospective study of 1849 patients (1411 women and 438 men) with a median age of 46 years (interquartile range, 34-58 years) and an overall median follow-up time of 33 months (interquartile range, 13-67 months) after initial treatment at 13 centers in 7 countries between 1978 and 2011. Patient deaths specifically caused by PTC. Overall, mortality was 5.3% (45/845; 95% CI, 3.9%-7.1%) vs 1.1% (11/1004; 95% CI, 0.5%-2.0%) (P < .001) in BRAF V600E-positive vs mutation-negative patients. Deaths per 1000 person-years in the analysis of all PTC were 12.87 (95% CI, 9.61-17.24) vs 2.52 (95% CI, 1.40-4.55) in BRAF V600E-positive vs mutation-negative patients; the hazard ratio (HR) was 2.66 (95% CI, 1.30-5.43) after adjustment for age at diagnosis, sex, and medical center. Deaths per 1000 person-years in the analysis of the conventional variant of PTC were 11.80 (95% CI, 8.39-16.60) vs 2.25 (95% CI, 1.01-5.00) in BRAF V600E-positive vs mutation-negative patients; the adjusted HR was 3.53 (95% CI, 1.25-9.98). When lymph node metastasis, extrathyroidal invasion, and distant metastasis were also included in the model, the association of BRAF V600E with mortality for all PTC was no longer significant (HR, 1.21; 95% CI, 0.53-2.76). A higher BRAF V600E-associated patient mortality was also observed in several clinicopathological subcategories, but statistical significance was lost with adjustment for patient age, sex, and medical center. For example, in patients with lymph node metastasis, the deaths per 1000 person-years were 26.26 (95% CI, 19.18-35.94) vs 5.93 (95% CI, 2.96-11.86) in BRAF V600E-positive vs mutation-negative patients (unadjusted HR, 4.43 [95% CI, 2.06-9.51]; adjusted HR, 1.46 [95% CI, 0.62-3.47]). In patients with distant tumor metastasis, deaths per 1000 person-years were 87.72 (95% CI, 62.68-122.77) vs 32.28 (95% CI, 16.14-64.55) in BRAF V600E-positive vs mutation-negative patients (unadjusted HR, 2.63 [95% CI, 1.21-5.72]; adjusted HR, 0.84 [95% CI, 0.27-2.62]). In this retrospective multicenter study, the presence of the BRAF V600E mutation was significantly associated with increased cancer-related mortality among patients with PTC. Because overall mortality in PTC is low and the association was not independent of tumor features, how to use BRAF V600E to manage mortality risk in patients with PTC is unclear. These findings support further investigation of the prognostic and therapeutic implications of BRAF V600E status in PTC.
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            International patterns and trends in thyroid cancer incidence, 1973-2002.

            Briseis A Kilfoy, Tongzhang Zheng, Theodore R. Holford … (2009)
            During the past several decades, an increasing incidence of thyroid cancer has been reported in many parts of the world. To date, no study has compared the trends in thyroid cancer incidence across continents. We examined incidence data from cancer incidence in five continents (CI5) over the 30-year period 1973-2002 from 19 populations in the Americas, Asia, Europe, and Oceania. Thyroid cancer rates have increased from 1973-1977 to 1998-2002 for most of the populations except Sweden, in which the incidence rates decreased about 18% for both males and females. The average increase was 48.0% among males and 66.7% among females. More recently, the age-adjusted international thyroid cancer incidence rates from 1998 to 2002 varied 5-fold for males and nearly 10-fold for females by geographic region. Considerable variation in thyroid cancer incidence was present for every continent but Africa, in which the incidence rates were generally low. Our analysis of published CI5 data suggests that thyroid cancer rates increased between 1973 and 2002 in most populations worldwide, and that the increase does not appear to be restricted to a particular region of the world or by the underlying rates of thyroid cancer.
            Article 0 comments Cited 225 times – based on 0 reviews     Review now
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              Pathogenetic mechanisms in thyroid follicular-cell neoplasia.

              Tetsuo Kondo, Shereen Ezzat, Sylvia L Asa (2006)
              Thyroid cancer is one of the few malignancies that are increasing in incidence. Recent advances have improved our understanding of its pathogenesis; these include the identification of genetic alterations that activate a common effector pathway involving the RET-Ras-BRAF signalling cascade, and other unique chromosomal rearrangements. Some of these have been associated with radiation exposure as a pathogenetic mechanism. Defects in transcriptional and post-transcriptional regulation of adhesion molecules and cell-cycle control elements seem to affect tumour progression. This information can provide powerful ancillary diagnostic tools and can also be used to identify new therapeutic targets.
              Article 0 comments Cited 224 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocr Relat Cancer
                Journal ID (iso-abbrev): Endocr. Relat. Cancer
                Journal ID (hwp): ERC
                Title: Endocrine-Related Cancer
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Print): 1351-0088
                ISSN (Electronic): 1479-6821
                Publication date Collection: January 2019
                Publication date (Electronic): 21 August 2018
                Volume: 26
                Issue: 1
                Pages: 153-164
                Affiliations
                [1 ]Department of Thyroid and Neck Tumor Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China
                [2 ]State Key Laboratory of Medicinal Chemical Biology Key Laboratory of Bioactive Materials, Ministry of Education, Collaborative Innovation Center for Biotherapy, Tianjin Key Laboratory of Protein Sciences, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics and College of Life Sciences, Nankai University, Tianjin, China
                [3 ]Department of Diagnostic and Therapeutic Ultrasonography Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China
                Author notes
                Correspondence should be addressed to L Chen or M Gao: lingyichen@ 123456nankai.edu.cn or gaoming68@ 123456aliyun.com

                *(X Ruan and X Shi contributed equally to this work)

                Article
                Publisher ID: ERC170558
                DOI: 10.1530/ERC-17-0558
                PMC ID: 6215907
                PubMed ID: 30139768
                SO-VID: 080c2c46-02a1-43cc-8013-11f5ff9ef0df
                Copyright © © 2018 The authors
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date received : 05 July 2018
                Date accepted : 21 August 2018
                Categories
                Subject: Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: anlotinib,multi-kinase inhibitor,thyroid cancer,apoptosis,migration
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: anlotinib, multi-kinase inhibitor, thyroid cancer, apoptosis, migration

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