chemotherapy/hypoxia

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The potential role of hypoxia inducible factor 1alpha in tumor progression after hypoxia and chemotherapy in hepatocellular carcinoma.

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This study investigates the possible molecular basis leading to failure in a treatment that is composed of hypoxia and chemotherapy in a rat orthotopic hepatoma model. Hypoxia was induced by hepatic artery ligation, whereas chemotherapeutic effect was achieved by intraportal injection of cisplatin.

Radiofrequency ablation-induced upregulation of hypoxia-inducible factor-1α can be suppressed with adjuvant bortezomib or liposomal chemotherapy.

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OBJECTIVE To characterize upregulation of hypoxia-inducible factor (HIF)-1α after radiofrequency (RF) ablation and the influence of an adjuvant HIF-1α inhibitor (bortezomib) and nanodrugs on modulating RF ablation-upregulated hypoxic pathways. METHODS Fisher 344 rats (n = 68) were used. First, RF

A redox-activatable biopolymer-based micelle for sequentially enhanced mitochondria-targeted photodynamic therapy and hypoxia-dependent chemotherapy

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A tumor redox-activatable micellar nanoplatform based on the naturally occurring biomacromolecule hyaluronic acid (HA) was developed for complementary photodynamic/chemotherapy against CD44-positive tumors. Here HA was first conjugated with l-carnitine (Lc)-modified zinc phthalocyanine (ZnPc) via

Apoptosis-induced ectodomain shedding of hypoxia-regulated carbonic anhydrase IX from tumor cells: a double-edged response to chemotherapy.

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BACKGROUND Carbonic anhydrase IX (CA IX) is a tumor-associated, highly active, transmembrane carbonic anhydrase isoform regulated by hypoxia and implicated in pH control and adhesion-migration-invasion. CA IX ectodomain (ECD) is shed from the tumor cell surface to serum/plasma of patients, where it

Detection of hypoxia by measurement of DNA damage and repair in human lymphocytes (comet assay): a predictive variable for tumor response during chemotherapy in patients with head and neck squamous cell carcinoma.

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BACKGROUND Only few studies have tried to identify parameters at the time of diagnosis or during treatment that can assist the clinician in predicting the response to Cisplatin, 5-Fluorouracil +/- Folinic acid therapy in patients with head and neck squamous cell carcinoma (HNSCC). METHODS The

Effect of artificial oxygen carrier with chemotherapy on tumor hypoxia and neovascularization.

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In addition to transfusion alternatives, artificial oxygen carriers are a benefit in ischemia disorders. This study aimed at evaluating the possible effects of PEG-conjugated hemoglobin (PEG-Hb) plus cisplatin on tumor hypoxia and neovasculature. METHODS HeLa cells were injected into submucosa of

[Hypoxia increases chemotherapy resistance in nasopharyngeal carcinoma via inducing CDK6 deSUMOylation].

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Objective: To understand the mechanism of chemotherapy resistance in nasopharyngeal carcinoma under hypoxic conditions through the perspective of protein SUMOylation modification. Methods: Cobalt chloride (CoCl(2)) was used to establish the hypoxic model of human nasopharyngeal

[Relationship between the expression of hypoxia-inducible factor-1alpha and chemotherapy response in gastric carcinoma].

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OBJECTIVE To evaluate the relationship of hypoxia-inducible factor (HIF)-1alpha expression with chemotherapy response in gastric cancer and its clinical outcome. METHODS Leucovorin (CF) and 5-fluorouracil (5-FU) in combination with oxaliplatin (L-OHP) were used in 52 patients with gastric carcinoma

[Relationship between the expression of hypoxia-inducible factor-1alpha and chemotherapy response in esophageal squamous cell carcinoma].

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OBJECTIVE To observe the relationship between expression of hypoxia-inducible factor (HIF)-1alpha and chemotherapy response and clinical outcome. METHODS Platixal in combination with cisplatin was used in 48 patients with ESCC at advanced stage. platixal 175 mg/m(2), d1; cisplatin 80 mg/m(2), d 2, d

Hypoxia-inducible factor-1α and excision repair cross-complementing 1 in patients with small cell lung cancer who received front-line platinum-based chemotherapy: a retrospective study.

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BACKGROUND Hypoxia-inducible factor-1α (HIF-1α), which plays an essential role in the adaptive response of cells to hypoxia, is associated with aggressive tumor behavior. Furthermore, a relationship between excision repair cross-complementing 1 (ERCC1) expression and platinum resistance has been

Hypoxia-inducible factor-1alpha suppressing apoptosis and increasing tolerance of lung cancer cells to chemotherapy.

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In order to construct plasmid of hypoxia-inducible factor-1alpha (HIF-1alpha), and transfect into human lung cancer cells A549, the change in sensitivity of lung cancer cells A549 to chemotherapy was observed. HIF-1alpha mRNA structure region was amplified by RT-PCR and inserted into plasmid pcDNA3.

[Acidosis, hypoxia and hypotension in abdominal chemotherapy with blockade of arterial and venous circulation (stop flow)].

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OBJECTIVE A study was performed of the perioperative systemic effects of a recent zoned chemotherapy technique administered in conditions of extreme acidosis, hypoxia and modern hypotension. METHODS METHODS a prospective analysis of the changes compared to basal values using Student's t test for

Light-enhanced Hypoxia-Responsive and Azobenzene Cleavage-Triggered Size-Shrinkable Micelles for Synergistic Photodynamic Therapy and Chemotherapy

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Hypoxia is an important pathological phenomenon due to uncontrolled cancer cell proliferation and insufficient blood flow, which can be used to design hypoxia-responsive nanocarriers for the intelligent treatment of tumor. However, it is difficult to obtain the response of hypoxia-responsive

Multimodal targeting of tumor vasculature and cancer stem-like cells in sarcomas with VEGF-A inhibition, HIF-1α inhibition, and hypoxia-activated chemotherapy.

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Vascular endothelial growth factor A (VEGF-A) inhibition with pazopanib is an approved therapy for sarcomas, but likely results in compensatory pathways such as upregulation of hypoxia inducible factor 1α (HIF-1α). In addition, cancer stem-like cells can preferentially reside in hypoxic regions of

Bortezomib and metformin opposingly regulate the expression of hypoxia-inducible factor alpha and the consequent development of chemotherapy-induced painful peripheral neuropathy.

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Chemotherapy-induced painful peripheral neuropathy is a significant clinical problem that is associated with widely used chemotherapeutics. Unfortunately, the molecular mechanisms by which chemotherapy-induced painful peripheral neuropathy develops have remained elusive. The proteasome inhibitor,

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