neuroendocrine tumors/tyrosine

OBJECTIVE We investigated the effects of the tyrosine kinase inhibitor imatinib (Gleevec) on neuroendocrine tumor cells. METHODS Neuroendocrine tumor cells were incubated without and with imatinib. The effects on growth were examined by methylthiazoletetrazolium (MTT) assay. The c-Kit expression in

The intracellular localization of tyrosine hydroxylase (TH), which is the rate limiting enzyme in catecholamine (CA) biosynthesis, and its activity in various adrenal and other neuroendocrine tumors was studied. TH was strongly localized in adrenal medulla, pheochromocytoma, and paraganglioma, but

Forty-three neuroendocrine neoplasms were analyzed by immunohistochemistry for tyrosine hydroxylase and chrornogranin A and by in situ hybridization (ISH) for chrornogranin A messenger RNA (mRNA) using formalin-fixed paraffin-embedded tissue sections. These included pheochromocytomas (7), medullary

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) show limited sensitivity to cytotoxic agents, requiring the search for novel therapies. Recently, data from a phase III trial demonstrated that sunitinib produces a clinically significant improvement in progression-free survival in patients

Introduction: Pancreatic neuroendocrine tumors (panNETs) represent a rare group of malignancies. For decades, chemotherapy, somatostatin analogs (SSAs) and interferon (IFN) represented the only systemic therapies, however over previous years, new options were registered, including Everolimus,

In the last few years, the therapeutic approach for neuroendocrine neoplasms (NENs) has changed dramatically following the approval of several novel targeted treatments. The multitarget tyrosine kinase inhibitor (MTKI), sunitinib malate, has been approved by Regulatory Agencies in pancreatic NENs.

The type I receptor tyrosine kinase family comprises four homologous members: Epidermal growth factor receptor (EGFR), HER-2, HER-3 and HER-4. Studies have shown that EGFR and HER-2 play a critical role in oncogenesis. In this study we sought to determine the pattern of expression and the prognostic

BACKGROUND CYYR1 is a recently identified gene located on human chromosome 21 whose product has no similarity to any known protein and is of unknown function. Analysis of expressed sequence tags (ESTs) have revealed high human CYYR1 expression in cells belonging to the diffuse neuroendocrine system

We describe a case of a patient who was confronted with two life-threatening conditions: extensive neuroendocrine tumor and hypoglycemia induced by sunitinib administration, as an anti-neoplastic agent. Administration of small dose of prednisolone could prevent severe hypoglycemia and improve

UNASSIGNED Neuroendocrine tumors (NETs) are rare neoplasms, with an estimated annual incidence of ~ 6.9/100,000. NETs arise throughout the body from cells of the diffuse endocrine system. More than half originate from endocrine cells of the gastrointestinal tract and the pancreas, thus being

OBJECTIVE Pancreatic neuroendocrine tumors (PNETs) are rare tumors, with an incidence of one per 100, 000 individuals per year, and they account for 1-2% of all pancreatic neoplasms. PNETs are a heterogeneous group with varying clinical presentation, tumor biology and prognosis. This article reviews

Pheochromocytomas and paragangliomas are neuroendocrine tumors shown to be responsive to multitargeted tyrosine kinase inhibitor (TKI) treatment. Despite growing knowledge regarding their genetic basis, the ability to predict behavior in these tumors remains challenging. There is also limited

OBJECTIVE Sunitinib is a tyrosine kinase inhibitor used in the therapy of pancreatic neuroendocrine tumors (PNETs), metastatic renal cancer and gastrointestinal stromal tumors. We describe a patient with PNET who presented with severe hypoglycemia following sunitinib administration. METHODS A

BACKGROUND There is a paucity of data on the incidence of neuroendocrine tumors (NET) outside pulmonary primaries and on treatment modalities applied to patients with NET in clinical practice. Only very little therapeutic progress has been made with respect to response and overall survival,