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      Is Open Access

      Hypoxia Increases Thyroid Cancer Stem Cell-Enriched Side Population

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          Abstract

          Introduction

          Hypoxic stress is a feature of rapidly growing thyroid tumours. Cancer progression is thought to be driven by a small population of tumour cells possessing stem cell properties. Hypoxia-inducible factors (HIFs) are important mediators of hypoxia. Both HIF-1alpha and HIF-2alpha have been reported to be expressed in thyroid cancers. There is growing evidence that the HIF pathway plays a significant role in the maintenance of thyroid cancer stem cells (CSC).

          Methodology

          We have isolated thyroid CSC from a papillary thyroid cancer-derived cell line (BCPAP) and an anaplastic thyroid cancer-derived cell line (SW1736) as side population (SP) cells (a putative stem cell population) and treated them with cobalt chloride (II) to induce hypoxia.

          Results and discussion

          We observed an increase in the SP of cells within the thyroid cancer cell lines following induction of hypoxia.

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          Hypoxia-inducible factors and the response to hypoxic stress.

          Amar Majmundar, Waihay J. Wong, M. Celeste Simon (2010)
          Oxygen (O(2)) is an essential nutrient that serves as a key substrate in cellular metabolism and bioenergetics. In a variety of physiological and pathological states, organisms encounter insufficient O(2) availability, or hypoxia. In order to cope with this stress, evolutionarily conserved responses are engaged. In mammals, the primary transcriptional response to hypoxic stress is mediated by the hypoxia-inducible factors (HIFs). While canonically regulated by prolyl hydroxylase domain-containing enzymes (PHDs), the HIFα subunits are intricately responsive to numerous other factors, including factor-inhibiting HIF1α (FIH1), sirtuins, and metabolites. These transcription factors function in normal tissue homeostasis and impinge on critical aspects of disease progression and recovery. Insights from basic HIF biology are being translated into pharmaceuticals targeting the HIF pathway. Copyright © 2010 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 420 times – based on 0 reviews     Review now
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            BRAF mutation in thyroid cancer.

            M Xing (2005)
            Genetic alteration is the driving force for thyroid tumorigenesis and progression, based upon which novel approaches to the management of thyroid cancer can be developed. A recent important genetic finding in thyroid cancer is the oncogenic T1799A transversion mutation of BRAF (the gene for the B-type Raf kinase, BRAF). Since the initial report of this mutation in thyroid cancer 2 years ago, rapid advancements have been made. BRAF mutation is the most common genetic alteration in thyroid cancer, occurring in about 45% of sporadic papillary thyroid cancers (PTCs), particularly in the relatively aggressive subtypes, such as the tall-cell PTC. This mutation is mutually exclusive with other common genetic alterations, supporting its independent oncogenic role, as demonstrated by transgenic mouse studies that showed BRAF mutation-initiated development of PTC and its transition to anaplastic thyroid cancer. BRAF mutation is mutually exclusive with RET/PTC rearrangement, and also displays a reciprocal age association with this common genetic alteration in thyroid cancer. The T1799A BRAF mutation occurs exclusively in PTC and PTC-derived anaplastic thyroid cancer and is a specific diagnostic marker for this cancer when identified in cytological and histological specimens. This mutation is associated with a poorer clinicopathological outcome and is a novel independent molecular prognostic marker in the risk evaluation of thyroid cancer. Moreover, preclinical and clinical evaluations of the therapeutic value of novel specific mitogen-activated protein kinase pathway inhibitors in thyroid cancer are anticipated. This newly discovered BRAF mutation may prove to have an important impact on thyroid cancer in the clinic.
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              The changing incidence of thyroid cancer.

              Cari M. Kitahara, Julie Sosa (2016)
              During the past few decades, the incidence of thyroid cancer has increased substantially in many countries, including the USA. The rise in incidence seems to be attributable both to the growing use of diagnostic imaging and fine-needle aspiration biopsy, which has led to enhanced detection and diagnosis of subclinical thyroid cancers, and environmental factors. The latest American Thyroid Association (ATA) practice guidelines for the management of adult patients with thyroid nodules and differentiated thyroid cancer differ substantially from the previous ATA guidelines published in 2009. Specifically, the problems of overdiagnosis and overtreatment of a disease that is typically indolent, where treatment-related morbidity might not be justified by a survival benefit, now seem to be acknowledged. As few modifiable risk factors for thyroid cancer have been established, the specific environmental factors that have contributed to the rising incidence of thyroid cancer remain speculative. However, the findings of several large, well-designed epidemiological studies have provided new information about exposures (such as obesity) that might influence the development of thyroid cancer. In this Review, we describe the changing incidence of thyroid cancer, suggest potential explanations for these trends, emphasize the implications for patients and highlight ongoing and potential strategies to combat this growing clinical and public health issue.
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                Author and article information

                Contributors
                A. Meeson: +44-0191-241-8856 , Annette.Meeson@ncl.ac.uk
                Journal
                Journal ID (nlm-ta): World J Surg
                Journal ID (iso-abbrev): World J Surg
                Title: World Journal of Surgery
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 0364-2313
                ISSN (Electronic): 1432-2323
                Publication date (Electronic): 22 November 2017
                Publication date PMC-release: 22 November 2017
                Publication date (Print): 2018
                Volume: 42
                Issue: 2
                Pages: 350-357
                Affiliations
                [1 ]ISNI 0000 0001 0462 7212, GRID grid.1006.7, Institute of Genetic Medicine, Faculty of Medical Sciences, , Newcastle University, ; Newcastle-upon-Tyne, NE1 3BZ UK
                [2 ]ISNI 0000 0004 0402 1394, GRID grid.416512.5, Northumbria Healthcare NHS Foundation Trust, , North Tyneside General Hospital, ; Rake Lane, North Shields, NE29 8NH UK
                Article
                Publisher ID: 4331
                DOI: 10.1007/s00268-017-4331-x
                PMC ID: 5762807
                PubMed ID: 29167950
                SO-VID: 38bd0c6f-9ccf-49ae-b2ae-2b661cac2c51
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

                History
                Funding
                Funded by: Get Ahead charitable trust
                Award ID: BH164226
                Funded by: FundRef 10.13039/100010378, British Association of Endocrine and Thyroid Surgeons;
                Award ID: BH154364
                Categories
                Subject: Original Scientific Report
                Custom metadata
                issue-copyright-statement © Société Internationale de Chirurgie 2018

                ScienceOpen disciplines: Surgery
                Data availability:
                ScienceOpen disciplines: Surgery

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