cholangiocarcinoma/prolina

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Lack of promoting effect of proline on bile duct cancer development in dimethylnitrosamine-initiated hamster livers.

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Bile duct hyperplasia caused by proline is believed to represent a chemical effect of the liver fluke, Fasciola hepatica, and the resultant cell division might be expected to play a role as a tumor promoter. To investigate the potential promoting effect of proline on bile duct cancer development,

Adenosine Suppresses Cholangiocarcinoma Cell Growth and Invasion in Equilibrative Nucleoside Transporters and Proline-Rich Homeodomain Protein-Dependent Pathway.

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Cholangiocarcinoma (CCA) is a lethal disease with increasing incidence worldwide. Previous study showed that CCA was sensitive to adenosine. Thereby, molecular mechanisms of CCA inhibition by adenosine were examined in this study. Our results showed that adenosine inhibited CCA cells via an uptake

Screening of Molecular Targets of Action of Atractylodin in Cholangiocarcinoma by Applying Proteomic and Metabolomic Approaches.

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Cholangiocarcinoma (CCA) is cancer of the bile duct and the highest incidence of CCA in the world is reported in Thailand. Our previous in vitro and in vivo studies identified Atractylodeslancea (Thunb) D.C. as a promising candidate for CCA treatment. The present study aimed to examine

Expression of peptidyl-prolyl isomerase PIN1 and its role in the pathogenesis of extrahepatic cholangiocarcinoma.

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The phosphorylation of proteins on serine/threonine residues that immediately precede proline (pSer/Thr-Pro) is a key signaling mechanism by which cell cycle regulation and cell differentiation and proliferation occur. The peptidyl-prolyl isomerase PIN1-catalyzed conformational changes of the

Opisthorchis viverrini infestation and endogenous nitrosamines as risk factors for cholangiocarcinoma in Thailand.

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Cholangiocarcinoma (CCA) is one of the most common cancers in north-east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12-hr overnight urine (after dosing with proline and ascorbic acid or proline alone) were collected from 20

Endogenous nitrosamines and liver fluke as risk factors for cholangiocarcinoma in Thailand.

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Cholangiocarcinoma (CCA) is one of the most prevalent cancers in north-east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12-h overnight urine (after dosing with 500 mg proline and 200 mg ascorbic acid or 500 mg proline alone) were

SPRR2A expression in cholangiocarcinoma increases local tumor invasiveness but prevents metastasis.

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Cholangiocarcinoma morbidity and mortality is attributable to local invasiveness and regional lymph node and distant organ metastasis. Cholangiocarcinoma progression follows a series of sequential events that resemble wound healing reactions: local invasion resembles the epithelial migration phase

Small proline rich protein 2a in benign and malignant liver disease.

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STAT3-driven expression of small proline rich protein 2a (SPRR2a), which acts as an src homology 3 (SH3) domain ligand, induces biliary epithelial cell (BEC) epithelial-mesenchymal transition (EMT), which, in turn, promotes wound healing. SPRR2a also quenches free radicals and protects against

Thiocyanate-independent nitrosation in humans with carcinogenic parasite infection.

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Infection with the liver fluke, Opisthorchis viverrini, is a causative agent of cholangiocarcinoma. One possible contributing factor in this carcinogenesis is the chronic, local generation of nitric oxide by inflammatory cells expressing inducible nitric oxide synthase and the production of

Suppression of aquaporin, a mediator of water channel control in the carcinogenic liver fluke, Opisthorchis viverrini.

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BACKGROUND Opisthorchiasis and Opisthorchis viverrini-associated bile duct cancer represent major public health threats in Thailand and Laos. The tegument of this food borne fluke plays pivotal roles in parasite metabolism, homeostasis and osmoregulation. Excretory/secretory products also pass from

SPRR2A enhances p53 deacetylation through HDAC1 and down regulates p21 promoter activity.

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BACKGROUND Small proline rich protein (SPRR) 2A is one of 14 SPRR genes that encodes for a skin cross-linking protein, which confers structural integrity to the cornified keratinocyte cell envelope. New evidence, however, shows that SPRR2A is also a critical stress and wound repair modulator: it

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