endometrial neoplasms/hypoxia

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Hypoxia-inducible factor-1α, adrenomedullin and Bcl-2 although expected are not related to increased uptake of fluorine-18-fluorodeoxyglucose in endometrial cancer.

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OBJECTIVE To study the relation between SUVmax, hypoxia inducible factor 1α (HIF-1α), angiogenetic factor adrenomedullin (AM) and antiapoptotic factor Bcl-2 in endometrial cancer. METHODS Thirthy eight patients who were diagnosed after a preoperative endometrial biopsy with endometrium cancer

The role of Hypoxia-inducible factor-1 α , glucose transporter-1, (GLUT-1) and carbon anhydrase IX in endometrial cancer patients.

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Hypoxia-inducible factor-1α (HIF-1α), glucose transporter-1 (GLUT-1), and carbon anhydrase IX (CAIX) are important molecules that allow adaptation to hypoxic environments. The aim of our study was to investigate the correlation between HIF-1α, GLUT-1, and CAIX protein level with the

Plausible linkage of hypoxia-inducible factor (HIF) in uterine endometrial cancers.

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OBJECTIVE Angiogenesis is essential for the development, growth and advancement of solid tumors. Angiogenesis is induced by hypoxia with the angiogenic transcription factor hypoxia-inducible factor (HIF). This prompted us to study the clinical implications of HIF relative to angiogenesis in uterine

[Hypoxia inducible factor-1α deSUMOylation reduces the stemness maintenance ability of endometrial cancer stem cell and increases its chemosensitivity].

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Objective: To reduce the stemness maintenance ability of endometrial cancer stem cell and increase its sensitivity to chemotherapy by inducing hypoxia inducible factor 1α (HIF-1α) protein deSUMOylation. Methods: Lentiviral plasmid mediated ubiquitin carrier protein 9 (Ubc9) gene silencing was

SHARP1 suppresses angiogenesis of endometrial cancer by decreasing hypoxia-inducible factor-1α level.

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Recent data support a role for SHARP1, a basic helix-loop-helix transcription repressor, in the regulation of malignant cell behavior in several human cancers. However, the expression and role of SHARP1 during the development of endometrial cancer (EC) remain unclear. Here we show that upregulation

The polymorphism of hypoxia-inducible factor-1a gene in endometrial cancer.

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BACKGROUND Endometral carcinoma is the most common malignant tumor of the female genital tract and the fourth most common cancer in women after breast, colorectal and lung cancers Hypoxia-inducible factor -1 (HIF-1) is a key transcription factor that regulates cellular response to hypoxia HIF-1

An investigation of relationships between hypoxia-inducible factor-1 alpha gene polymorphisms and ovarian, cervical and endometrial cancers.

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BACKGROUND DNA sequence variations in HIF-1 alpha gene might yield changes both in the production outcomes and in the activities of the gene. Overexpression of the HIF-1 alpha subunit, resulting from intratumoral hypoxia and genetic alterations, has been demonstrated in common human cancers and is

Hypoxia and hyperglycaemia determine why some endometrial tumours fail to respond to metformin.

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High expression of Ki67, a proliferation marker, is associated with reduced endometrial cancer-specific survival. Pre-surgical metformin reduces tumour Ki-67 expression in some women with endometrial cancer. Metformin's anti-cancer activity may relate to effects on cellular energy

BNIP3 expression in endometrial cancer relates to active hypoxia inducible factor 1alpha pathway and prognosis.

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OBJECTIVE BNIP3 is a pro-apoptotic mitochondrial protein induced under hypoxic stress, with the BNIP3 gene being under direct regulation of the hypoxia-inducible HIF-1alpha transcription factor. Induction of BNIP3 leads to caspase-independent necrosis-like cell death and an aggressive tumour

Tissue and imaging biomarkers for hypoxia predict poor outcome in endometrial cancer.

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Hypoxia is frequent in solid tumors and linked to aggressive phenotypes and therapy resistance. We explored expression patterns of the proposed hypoxia marker HIF-1α in endometrial cancer (EC) and investigate whether preoperative functional imaging parameters are associated with tumor hypoxia.

Downregulation of Proline Hydroxylase 2 and Upregulation of Hypoxia-Inducible Factor 1α are Associated with Endometrial Cancer Aggressiveness.

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Proline hydroxylase 2 (PHD2) is involved in tumorigenesis. This study aimed to examine PHD2 and hypoxia-inducible factor 1α (HIF-1α) expression in different endometrial tissues and explore the correlations between PHD2 and HIF-1α expression with clinicopathological characteristics of

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro.

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Due to their post-transcriptional regulatory impact on gene expression, microRNAs (miRNA, miRs) influence decisively cellular processes of differentiation, proliferation and apoptosis. In oncogenic pathways various miRNAs exert either oncogenic or tumor suppressor activities in a stage-specific

Expression of leptin, leptin receptor, and hypoxia-inducible factor 1 alpha in human endometrial cancer.

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Recent studies suggested that Ob (Ob) and its receptor (ObR) could be involved in the pathogenesis of various human malignancies, among others in endometrial cancer. Moreover, hypoxia, which is associated with solid tumors, might stimulate, through hypoxia-inducible factor 1alpha (HIF-1alpha),

Hypoxia-inducible factor-1 as a therapeutic target in endometrial cancer management.

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In the Western world, endometrial cancer (EC) is the most common malignant tumor of the female genital tract. Solid tumors like EC outgrow their vasculature resulting in hypoxia. Tumor hypoxia is important because it renders an aggressive phenotype and leads to radio- and chemo-therapy resistance.

Tumor necrosis is an important hallmark of aggressive endometrial cancer and associates with hypoxia, angiogenesis and inflammation responses.

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OBJECTIVE Tumor necrosis is associated with aggressive features of endometrial cancer and poor prognosis. Here, we investigated gene expression patterns and potential treatment targets related to presence of tumor necrosis in primary endometrial cancer lesions. RESULTS By DNA microarray analysis,

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