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Tumor Tissue-Derived Formaldehyde and Acidic Microenvironment Synergistically Induce Bone Cancer Pain

机译:肿瘤组织衍生的甲醛和酸性微环境协同诱导骨癌疼痛。

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摘要

BackgroundThere is current interest in understanding the molecular mechanisms of tumor-induced bone pain. Accumulated evidence shows that endogenous formaldehyde concentrations are elevated in the blood or urine of patients with breast, prostate or bladder cancer. These cancers are frequently associated with cancer pain especially after bone metastasis. It is well known that transient receptor potential vanilloid receptor 1 (TRPV1) participates in cancer pain. The present study aims to demonstrate that the tumor tissue-derived endogenous formaldehyde induces bone cancer pain via TRPV1 activation under tumor acidic environment.
机译:背景技术当前有兴趣了解肿瘤引起的骨痛的分子机制。累积的证据表明,乳腺癌,前列腺癌或膀胱癌患者的血液或尿液中内源性甲醛浓度升高。这些癌症通常与癌症疼痛有关,尤其是在骨转移之后。众所周知,瞬态受体电位类香草受体1(TRPV1)参与了癌痛。本研究旨在证明在肿瘤酸性环境下,肿瘤组织来源的内源甲醛通过TRPV1激活诱导骨癌疼痛。

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