China
Africa
Explore chapters and articles related to this topic
Endocrine Imaging
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Anaplastic thyroid cancer (ATC): Presents more commonly in the elderly and demonstrates a rapid, infiltrative progression.Ultrasound features are that of a large, solid, hypoechoic, ill-defined mass with evidence of extrathyroidal spread and nodal metastases.Core biopsy is superior to fine-needle aspiration cytology (FNAC) for confirming the diagnosis.
Thyroid
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
PTC usually shows single mutations: BRAF 40–45%, RET/PTC rearrangements 10–20%, and RAS point mutations 10–20%. Prognosis is generally very good in these tumors. However tumors with multiple gene mutations, e.g. BRAF V600E together with TERT promoter or TP53, PIK3CA, AKT1, have an adverse prognosis. The coexistence of BRAF V600E and TERT promoter mutations correlates with lymph node metastasis, multifocality, distant metastasis, tumor recurrence, extrathyroidal extension, and disease specific mortality.14 This pattern of mutations is seen in those differentiated thyroid cancers that transform to poorly differentiated or anaplastic thyroid cancer.
Thyroid disease
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
Thyroid cancers comprise a spectrum of tumours arising from either the thyroid follicular cells or the parafollicular cells, or C-cells. The commonest types of thyroid cancers are the differentiated thyroid cancers divided into papillary thyroid cancers (accounting for 80% of thyroid malignancies) and follicular thyroid cancers (10%–20% of thyroid malignancies). These arise from the follicular cells. Medullary thyroid cancer, a neuroendocrine tumour, arises from the C-cells and comprises 6%–8% of thyroid cancers. Anaplastic thyroid cancer, which carries an appalling prognosis, is an aggressive tumour that is believed to develop either from a de-differentiating papillary tumour or de novo. This comprises 1% of thyroid cancers.
LncRNA-IQCH-AS1 sensitizes thyroid cancer cells to doxorubicin via modulating the miR-196a-5p/PPP2R1B signalling pathway
Published in Journal of Chemotherapy, 2023
Thyroid cancer, which is located within the thyroid gland, is a prevalent human endocrine tumour, associating with poor diagnosis and survival rates in worldwide especially for the advanced and aggressive thyroid cancer [1]. Currently, surgery and radioiodine therapy (I-131 therapy) are the primarily therapeutic approaches for thyroid cancer [2]. In addition, chemotherapy with the combination of radiation therapy has been applied for anaplastic thyroid cancer [3]. Doxorubicin, which is an antibiotic derived from the Streptomyces peucetius bacterium, has been widely applied as an anti-cancer agent [4]. Doxorubicin functions through inhibiting the enzyme topoisomerase II to intercalate within DNA base pairs, leading to DNA strands breaking to inhibit both DNA and RNA synthesis [4,5]. Although doxorubicin has achieved improved survival rate for thyroid cancer patients, a large fraction of patients was aggravated by adverse effects and developed doxorubicin resistance, arising a severe challenge for its widely applications [6]. Thus, understanding the underlying molecular mechanisms and specific biotargets of the acquired doxorubicin resistance is an urgent task.
MiR-200c regulates invasion, proliferation and EMT of anaplastic thyroid cancer cells by targeting parathyroid hormone like hormone
Published in Growth Factors, 2022
Yan Zhang, Yuanyuan Duan, Chenguang Wu, Wen Peng, Wenyu Chen, Li Wang, Zhaoqun Deng
Anaplastic thyroid cancer (ATC) is an aggressive and lethal thyroid malignancy. An epidemiological survey showed that the disease-specific survival of patients diagnosed with ATC from 1995 to 2014 was only 4 months (Janz et al. 2019). The characteristics of invasion, metastasis, and low sensitivity to conventional therapy are the main causes of poor prognosis. Moreover, epithelial-to-mesenchymal transition (EMT) has been demonstrated to be responsible for ATC metastasis (Liu et al. 2018). In the EMT process, cancer cells gain motility after losing the cell-cell junction and apical-basal polarity, infiltrate surrounding tissues, or reach distant organs through blood or lymphatic vessels, and eventually form metastatic tumours (Yilmaz and Christofori 2009). During these processes, changes occur in the hallmarks of the EMT expression markers, such as the downregulated expression of E-cadherin (an epithelial marker) and the up-regulated expression of N-cadherin (a mesenchymal marker) (Wang et al. 2018).
Substantial intrinsic variability in chemoradiosensitivity of newly established anaplastic thyroid cancer cell-lines
Published in Acta Oto-Laryngologica, 2020
Sigurdur Gretarsson, Alexander Nygren, Ann H. Rosendahl, Nektaria Mylona, Elisabeth Kjellén, Yuesheng Jin, Kajsa Paulsson, Åke Borg, Eva Brun, Jan Tennvall, Anders Bergenfelz, Lennart Greiff, Johan Wennerberg, Lars Ekblad
Anaplastic thyroid cancer (ATC) is one of the most lethal malignancies with a median survival of about five months and a disease-specific mortality close to 100%. ATC accounts for approximately 5% of all thyroid cancers (TC), but for a substantial part of all deaths from TC. In part based on pilot studies from Skåne University Hospital, a Swedish protocol for treatment of ATC has been defined [1]. The current mainstay is chemoradiotherapy, combining accelerated external radiation therapy and concomitant neoadjuvant chemotherapy. Debulking surgery is performed if the tumour is considered resectable, if the patient is still in good condition after primary treatment, and if distant metastases has not progressed rapidly [1]. The protocol is continuously refined and doxorubicin has recently been replaced by paclitaxel both due to an improved tumour effect as a local radiosensitizer and increased tumour efficacy per se [2]. While this strategy has been successful in decreasing local failure, it has not been shown to prevent or inhibit progression of distant metastases and the survival rates have not increased [1]. Arguably, there is a need for improved strategies, for example, involving optimized treatment combinations or new drugs such as the recently US Food and Drug Administration (FDA) approved combination of dabrafenib and trametinib.