Background Around 70% of breast cancers (BCs) are estrogen receptor-α (ERα)-positive. Adjuvant endocrine therapy is used to reduce estrogen levels and inhibit signal transduction through the ER. The anti-estrogen drugs that are most commonly used in endocrine therapy belong to the selective ER modulator (SERM) class and include tamoxifen. Although it has been used for three decades in cases of early-stage and ERα-positive BC, resistance to tamoxifen is a common problem. microRNAs (miRNAs) have a potential role in demonstrating BC resistance to tamoxifen therapy. Hence, there is a need to investigate the expression of miRNA-221 (miR-221) in luminal-subtype BC patients receiving tamoxifen therapy. Methods This case-control study investigated luminal-subtype BC patients who had undergone endocrine therapy for at least 1 year. The case group comprised patients with local or metastatic recurrence, and the control group comprised patients without local or metastatic recurrence. Results There was a significant difference in miR-221 expression ( p = 0.005) between the case and control groups. There were no significant differences between the groups that were positive and negative for the progesterone receptor (PR) ( p = 0.25), had high and low marker of proliferation Ki-67 levels ( p = 0.60), were positive and negative for lymphovascular invasion ( p = 0.14), and had stage 2 and stage 3 cancer ( p = 0.25). Conclusion miR-221 expression was higher in tamoxifen-resistant BC cases. miR-221 is a potential biomarker of tamoxifen resistance.
IntroductionHypoxic 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).MethodologyWe 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 discussionWe observed an increase in the SP of cells within the thyroid cancer cell lines following induction of hypoxia.
Thyroid carcinoma showing thymic-like differentiation (CASTLE) is a rare malignancy of the thyroid gland, and it accounts for 0.1–0.15% of all thyroid cancers. As the name suggests, it has a histological and immunophenotypic resemblance to thymic carcinoma. Preoperative diagnosis of CASTLE can be difficult as its clinical manifestations, and histological characteristic resembles other aggressive and advanced thyroid carcinomas. It is essential to distinguish CASTLE from other aggressive neoplasms as the former has a more favourable prognosis. Immunohistochemical staining with CD5 can help to differentiate thyroid CASTLE from other aggressive thyroid neoplasms. Due to the rarity of this disease, there is no clear definitive treatment strategy. Surgical resection of CASTLE is usually attempted initially. Nodal involvement and extrathyroidal extension are shown to be the main prognostic factors that influenced the survival of patients. Therefore, complete resection of the tumour is vital to reduce local recurrence rates and to improve the chance of long-term survival. Radiotherapy (RT) for CASTLE is an effective treatment. Curative surgery followed by adjuvant RT should be considered in cases with extrathyroidal extension and nodal metastases. With RT, shrinkage of the tumour and reduction of local recurrence rate is possible. With that in mind, we present a case of CASTLE who presented with airway compression symptoms three years after thyroid surgery. He subsequently underwent tumour debulking surgery and a tracheostomy. The patient refused adjuvant chemoradiotherapy, and during our serial follow-up, he is well and symptom-free.
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