1,721,035 research outputs found
Dual dichotomies--when thyroid dysfunction and thyroid hormones get into the skin.
No full textGuest Editorial Dual Dichotomiessâ When Thyroid Dysfunction and Thyroid Hormones Ge tinto the Skin Monica Dentice1 and Giuseppe Monfrecola 2 his issue of Thyroid features three brief reports illustrating related but rare complications of thyroid disease: cutaneous and subcutaneous invasion by thyroid cancer metastasis.
Santarpia et al. (1) describe several patients with skin metastasis from medullary thyroid carcinomas (MTC). They suggest that dissemination of this tumor be included in the differential diagnosis of cutaneous eruptions and nodules, especially when they are located in the upper part of the body in patients with a history of MTC. In another paper, Lou et al. report a patient with what appeared to be slin contamination after radioactive iodine therapy. Further investigation showed that the aberrant papillary carcinoma. Finally. Harish et al. (3) present a 60-year-old woman with an ulcerating cutaneous lesion of the neck due to contiguous extension of a non-hodgkinâs lymphoma of the thyroid. They were unable to ï-nd other published examples of this complication in thyroid lymphoma. Because of their rarity, few clinicians would even list metastasis of thyroid tumors to be one of the skin manifestations
Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone inactivation
No full textDeiodination is a critical process by which the minimally active thyroxine (T4) molecule is converted into the favorite ligand for thyroid hormone (TH) receptors, triiodothyronine (T3). The iodothyronine deiodinases type 1, 2, and 3 (D1, D2, and D3) constitute a potent mechanism of TH activation (D1 and D2) or inactivation (D3), which functions by tissue specifically regulating TH bioavailability. D2 and D3 are widely expressed and in a dynamically and tightly coordinated fashion, thereby allowing cells to customize their own TH activity. D3, the major T3 and T4 inactivating deiodinase, catalyzes their conversion to 3,3′-diiodothyronine and to reverse T3 respectively. According to common wisdom, D3 plays a major role in lowering serum TH concentrations during development, as supported by the much wider D3 tissue expression in the embryo structures than in the adult tissues. However, several recent studies show that D3 is reexpressed in adult life in various pathophysiological contexts, which strengthens the concept that cell-specific TH inactivation is a critical mediator in cellular TH metabolism. This review focuses on the progress made in understanding the physiological function and significance of D3. It summarizes the intriguing evidence that D3 plays a pivotal role in defining local TH concentration in the developing fetus and in several conditions in adult life.</jats:p
Activation and inactivation of thyroid hormone by deiodinases: local action with general consequences
No full textThe impact of the tumor microenvironment in the dual burden of obesity-cancer link
Full text linkObesity induces systemic perturbations of tissue homeostasis, leading to dyslipidemia, insulin resistance and chronic state of inflammation. Evidence from clinical and preclinical studies links excess of adiposity with increased cancer incidence and suggests that chronic inflammation may contribute to increased cancer risk in obese patients. Over the last decades of obesity research, multifaced and complicated effects of abnormal or excessive expansion of Adipose Tissue have been uncovered. In particular, it is widely described how obesity can exacerbate the tumorigenesis for instance by fueling soluble signals and adipokines and by enhancing tissue inflammation and altering the hormonal balance. Less is known about the paracrine effects of the cancer-associated adipocytes on the tumor cells and still poorly explored is the reciprocal communication between cancer cells and the adipose component of the tumor microenvironment (TME). In this review, we will address the mechanisms by which the peritumoral Adipose Tissue can influence the dynamics of tumoral cells. We will discuss how obesity-induced changes in the tumor microenvironment may enhance tumor growth and aggressive characteristics leading to increased invasiveness and metastatic progression of cancer that leads to a worsen cancer survival in obese subjects. We conclude that targeting the peritumoral adipose component of the TME would be a therapeutic option to prevent cancer development
The deiodinases and the control of intracellular thyroid hormone signaling during cellular differentiation.
No full textDeiodinases and Cancer
Full text link: Hormones are key drivers of cancer development, and alteration of the intratumoral concentration of thyroid hormone (TH) is a common feature of many human neoplasias. Besides the systemic control of TH levels, the expression and activity of deiodinases constitute a major mechanism for the cell-autonomous, prereceptoral control of TH action. The action of deiodinases ensures tight control of TH availability at intracellular level in a time- and tissue-specific manner, and alterations in deiodinase expression are frequent in tumors. Research over the past decades has shown that in cancer cells, a complex and dynamic expression of deiodinases is orchestrated by a network of growth factors, oncogenic proteins, and miRNA. It has become increasingly evident that this fine regulation exposes cancer cells to a dynamic concentration of TH that is functional to stimulate or inhibit various cellular functions. This review summarizes recent advances in the identification of the complex interplay between deiodinases and cancer and how this family of enzymes is relevant in cancer progression. We also discuss whether deiodinase expression could represent a diagnostic tool with which to define tumor staging in cancer treatment or even a therapeutic tool against cancer
Thyroid hormone promotes differentiation of colon cancer stem cells
Full text linkTumor formation and maintenance depend on a small fraction of cancer stem cells (CSCs) that can self-renew and generate a wide variety of differentiated cells. CSCs are resistant to chemotherapy and radiation, and can represent a reservoir of cancer cells that often cause relapse after treatment. Evidence suggests that CSCs also give rise to metastases. Thyroid hormone (TH) controls a variety of biological processes including the development and functioning of most adult tissues. Recent years has seen the emergence of an intimate link between TH and multiple steps of tumorigenesis. Thyroid hormone controls the balance between the proliferation and differentiation of CSCs, and may thus be a druggable anti-cancer agent. Here, we review current understanding of the effects of TH on colorectal CSCs, including the cross regulatory loops between TH and regulators of CSC stemness. Targeting TH in the tumor microenvironment may improve treatment strategies
- …
