neuroendocrine tumors/tyrosine

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Effects of the tyrosine kinase inhibitor imatinib on neuroendocrine tumor cell growth.

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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

Tyrosine hydroxylase indicates cell differentiation of catecholamine biosynthesis in neuroendocrine tumors.

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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

Expression of chromogranin a protein and messenger RNA and tyrosine hydroxylase protein in paraffin-embedded sections of neuroendocrine neoplasms.

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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

Therapy innovations: tyrosine kinase inhibitors for the treatment of pancreatic neuroendocrine tumors.

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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

Pharmacodynamics, clinical findings and approval status of current and emerging tyrosine-kinase inhibitors for pancreatic neuroendocrine tumors.

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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,

Emerging multitarget tyrosine kinase inhibitors in the treatment of neuroendocrine neoplasms.

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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.

Expression of the HER-1-4 family of receptor tyrosine kinases in neuroendocrine tumours.

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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

Sequence, "subtle" alternative splicing and expression of the CYYR1 (cysteine/tyrosine-rich 1) mRNA in human neuroendocrine tumors.

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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

Life-threatening hypoglycemia induced by a tyrosine kinase inhibitor in a patient with neuroendocrine tumor: a case report.

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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

A Phase II Study of Ibrutinib in Advanced Neuroendocrine Neoplasms.

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Ibrutinib is an orally administered inhibitor of Bruton's tyrosine kinase (Btk). Preclinical data suggest that mast cells are recruited within neuroendocrine neoplasms (NENs) where they stimulate angiogenesis and tumor growth. Ibrutinib inhibits mast cell degranulation and has been

Current treatment strategies for patients with advanced gastroenteropancreatic neuroendocrine tumors (GEP-NETs).

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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

Neuroendocrine tumors of the pancreas.

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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

Tyrosine kinase receptors as molecular targets in pheochromocytomas and paragangliomas.

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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

Severe resistant hypoglycemia in a patient with a pancreatic neuroendocrine tumor on sunitinib treatment.

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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

A retrospective review of diagnosis and treatment modalities of neuroendocrine tumors (excluding primary lung cancer) in 10 oncological institutions of the East German Study Group of Hematology and Oncology (OSHO), 2010-2012.

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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,

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