adenocarcinoma/hypoxia

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Overexpression of hypoxia-inducible factor-1 alpha in gastric adenocarcinoma.

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BACKGROUND The transcriptional factor hypoxia-inducible factor 1alpha (HIF-1alpha) controls angiogenesis and metabolism by upregulating hypoxia-induced genes, such as the vascular endothelial growth factor (VEGF) gene and the glucose transporter (GLUT-1) gene. In addition to its regulation by

Hypoxia-inducible factor-1α regulates chemotactic migration of pancreatic ductal adenocarcinoma cells through directly transactivating the CX3CR1 gene.

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CX3CR1 is an important chemokine receptor and regulates the chemotactic migration of pancreatic ductal adenocarcinoma (PDAC) cells. Up to now, its regulatory mechanism remains largely undefined. Here, we report that hypoxia upregulates the expression of CX3CR1 in pancreatic cancer cells. When

[Prolonged hypoxia induces GST-pi expression and drug resistance in lung adenocarcinoma cell line SPCA1].

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OBJECTIVE To investigate the association of hypoxia with GST-pi expression in lung adenocarcinoma cells SPCA1 and the drug resistance in hypoxic condition. METHODS RNA and protein in SPCA1 cells treated with hypoxia (0.5% O(2)) for 16 h were isolated. HIF-1alpha and GST-pi mRNA expression was

Neoangiogenesis and expression of hypoxia-inducible factor 1alpha, vascular endothelial growth factor, and glucose transporter-1 in endometrioid type endometrium adenocarcinomas.

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OBJECTIVE Hypoxia Inducible Factor-1alpha (HIF-1alpha) is a transcriptional factor that activates multiple genes including Vascular Endothelial Growth Factor (VEGF) and glucose transporter-1 (GLUT-1) in response to hypoxia and promotes neoangiogenesis. METHODS Expression of HIF-1alpha VEGF, and

A region within the 5'-untranslated region of hypoxia-inducible factor-1alpha mRNA mediates its turnover in lung adenocarcinoma cells.

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Previously, we showed that CL1-5 cells express more hypoxia-inducible factor-1alpha (HIF-1alpha) than the parental CL1 cells, which bestows CL1-5 cells a stronger invasive activity. Here, we investigated the mechanisms underlying the differential expression of HIF-1alpha mRNA in CL1 and CL1-5 cells.

[Mechanism of regulation of leptin expression in human lung adenocarcinoma cells by hypoxia inducible factor-1alpha: a preliminary study].

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OBJECTIVE To investigate the regulation of leptin expression in human lung adenocarcinoma cells by hypoxia inducible factor-1 (HIF-1alpha) and the mechanism thereof. METHODS Lung adenocarcinoma tissues were collected from 42 patients during operation and samples of corresponding adjacent lung tissue

Differential expression of hypoxia-inducible protein 2 among different histological types of epithelial ovarian cancer and in clear cell adenocarcinomas.

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OBJECTIVE Epithelial ovarian cancer (EOC) can be classified into 5 major histological types. Among them, clear cell adenocarcinoma (CCC) has a poor response to chemotherapy and poor prognosis compared with other histological types. Previously, we reported that the hypoxia-inducible protein 2 (HIG2)

Hypoxia enhances MUC1 expression in a lung adenocarcinoma cell line.

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Expression of a transmembrane mucin MUC1 is emphasized in most cases of carcinoma. High expression of MUC1 is closely associated with cancer progression and metastasis, leading to poor prognosis. However, little is known about how MUC1 is overexpressed in malignant tumor. In this study, we

Expression of carbonic anhydrase IX (CA IX), a hypoxia-related protein, rather than vascular-endothelial growth factor (VEGF), a pro-angiogenic factor, correlates with an extremely poor prognosis in esophageal and gastric adenocarcinomas.

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OBJECTIVE To evaluate the expression of carbonic anhydrase IX (CA IX) and vascular-endothelial growth factor (VEGF) in esophageal and gastric adenocarcinomas and in turn with the histologic subtype. BACKGROUND Tumor hypoxia is an important factor in therapy resistance. A low oxygen concentration in

Hypoxia switches glucose depletion-induced necrosis to phosphoinositide 3-kinase/Akt-dependent apoptosis in A549 lung adenocarcinoma cells.

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In solid tumours, necrosis is commonly found in the core region in response to metabolic stress that results from oxygen and glucose depletion (OGD) due to insufficient vascularization and has been implicated in tumour progression. We have previously shown that metabolic stress due to glucose

Successful pulmonary arterial embolization followed by curative surgery for a lepidic predominant lung adenocarcinoma with severe hypoxemia.

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BACKGROUND Lepidic predominant adenocarcinoma is characterized by frequent refractory hypoxemia due to intrapulmonary shunting. Severe hypoxemia can induce perioperative complications in case of thoracic surgery. METHODS We report a case of a 67 year-old woman with localized lepidic adenocarcinoma

Increasing expression of hypoxia-inducible proteins in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.

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Hypoxia-associated markers are involved in the progression of several malignancies, but are relatively unstudied in Barrett's carcinogenesis. Our aim was to assess the immunohistochemical expression of hypoxia-inducible factor (HIF)-1alpha, HIF-2alpha, erythropoietin (Epo), Epo receptor (Epo-R),

Interaction of heat and hypoxia in modulating transcription of DT diaphorase in human colon adenocarcinoma cells.

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To study the regulation of the human detoxicating enzyme DT diaphorase (DTD) under hypoxic conditions, we examined the effects of heat and hypoxia, and their interaction, on the steady-state levels of mRNA and DTD enzyme activity in human colon adenocarcinoma HT29 cells. We found that a 1-h heat

[Relationship of hypoxia-inducible factor 1 alpha (HIF-1alpha) gene expression with vascular endothelial growth factor (VEGF) and microvessel density (MVD) in human colorectal adenoma and adenocarcinoma].

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OBJECTIVE Hypoxia-inducible factor-1 alpha (HIF-1alpha), a transcriptional factor response to hypoxia plays an important role in tumor angiogenesis. This study was designed to examine the expression of HIF-1alpha gene and its relationship with vascular endothelial growth factor (VEGF) protein and

Herpes simplex virus amplicon delivery of a hypoxia-inducible soluble vascular endothelial growth factor receptor (sFlk-1) inhibits angiogenesis and tumor growth in pancreatic adenocarcinoma.

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BACKGROUND Tumor hypoxia induces vascular endothelial growth factor (VEGF) expression, which stimulates angiogenesis and tumor proliferation. The VEGF signaling pathway is inhibited by soluble VEGF receptors (soluble fetal liver kinase 1; sFlk-1), which bind VEGF and block its interaction with

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