1,721,234 research outputs found

    The role of Insulin-like Growth Factor (IGF) system in the adrenocortical tumors

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    The different presentation of adrenocortical tumors in benign adenoma (ACA) or adrenocortical carcinoma (ACC) is related to the variability at the molecular level. The insulin-like growth factor (IGF) system is one of the most frequently altered pathways in ACC. In this review we will critically analyze the evidence regarding the pathogenic role of the IGF system in adrenal tumorigenesis, focusing on ACC. We will also examine the pre-clinical and clinical studies which investigated the targeting of the IGF system as a therapeutic approach in ACC

    Diabetes and cancer

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    The multiform relation between DM and cancer is far away to be definitively understood and all the studies of the next years will have to reckon with the complexity of both DM and neoplasms and consider the heterogeneity of the population involved. But, in the third millenium medicine, all the scientist are called to make an effort in order to give a solution to the emerging health questions of our society

    The metabolic syndrome and cardiovascular risk in Cushing's syndrome

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    Cushing's syndrome (CS) is characterized by a series of systemic complications that increase cardiovascular risk and cause severe atherosclerotic damage that develops in parallel with an acquired metabolic syndrome. Short-term remission from hypercortisolism improves metabolic and vascular damages, but long-term remission from CS seems to be associated with similar or worse metabolic and vascular damage, probably because of persistent abdominal obesity or insulin resistance years after normalization of cortisol secretion. Study results suggest that an increased cardiovascular risk also may persist in patients who undergo treatment with exogenous glucocorticoids after therapy withdrawal. Considering the many patients subjected to corticosteroid treatment, this could be of great clinical relevance and should be investigated thoroughly

    Application of molecular biology of differentiated thyroid cancer for clinical prognostication

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    Although cancer outcome results from the interplay between genetics and environment, researchers are making a great effort for applying molecular biology in the prognostication of differentiated thyroid cancer (DTC). Nevertheless, role of molecular characterisation in the prognostic setting of DTC is still nebulous. Among the most common and well-characterised genetic alterations related to DTC, including mutations of BRAF and RAS and RET rearrangements, BRAF(V600E) is the only mutation showing unequivocal association with clinical outcome. Unfortunately, its accuracy is strongly limited by low specificity. Recently, the introduction of next-generation sequencing techniques led to the identification of TERT promoter and TP53 mutations in DTC. These genetic abnormalities may identify a small subgroup of tumours with highly aggressive behaviour, thus improving specificity of molecular prognostication. Although knowledge of prognostic significance of TP53 mutations is still anecdotal, mutations of the TERT promoter have showed clear association with clinical outcome. Nevertheless, this genetic marker needs to be analysed according to a multigenetic model, as its prognostic effect becomes negligible when present in isolation. Given that any genetic alteration has demonstrated, taken alone, enough specificity, the co-occurrence of driving mutations is emerging as an independent genetic signature of aggressiveness, with possible future application in clinical practice. DTC prognostication may be empowered in the near future by non-tissue molecular prognosticators, including circulating BRAF(V600E) and miRNAs. Although promising, use of these markers needs to be refined by the technical sight, and the actual prognostic value is still yet to be validated

    Management of functional pancreatic neuroendocrine neoplasms

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    : Functional pancreatic neuroendocrine neoplasms (pNENs) are rare and heterogeneous diseases in terms of both clinical and pathological aspects. These tumors secrete hormones or peptides, which may cause a wide variety of symptoms related to a clinical syndrome. The management of functional pNENs is still challenging for clinicians due to the need to control both tumor growth and specific symptoms. Surgery remains the cornerstone in the management of local disease because it can definitively cure the patient. However, when the disease is not resectable, a broad spectrum of therapeutic options, including locoregional therapy, somatostatin analogs (SSAs), targeted therapies, peptide-receptor radionuclide therapy (PRRT), and chemotherapy, are available. The present review summarizes the main key issues regarding the clinical management of these tumors, providing a specific highlight on their therapeutic approach

    Somatostatin analogues: treatment of pituitary and neuroendocrine tumors.

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    This chapter summarizes the most recent data on the use of the somatostatin analogues (SSAs), octreotide (OCT) and lanreotide for the treatment of patients with pituitary and neuroendocrine tumors (NETs). These two analogues have a high affinity for somatostatin receptor (SSR) sub-types 2 and 5. The major indications of these compounds are GH- and TSH-secreting pituitary adenomas, secreting NETs and non-functioning NETs in progression. Pasireotide is a new analogue, with a receptor pattern different from previous analogues since it binds with high affinity to SSR types 1, 2, 3 and 5. This analogue will be available to treat patients with ACTH-secreting adenomas in a short time. A recent study has also demonstrated a beneficial effect of OCT long-acting release in patients with non-functioning NETs independently from their progression status. These data open the treatment with SSAs in all NET patients
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