大多數癌症患者到晚期後，例如結腸直腸癌，胰臟癌，食道癌和肺癌，通常患者身體體態都非常瘦弱，此現象稱為癌症惡質病(Cachexia)。惡質病是一個多重複雜的代謝疾病，最常見的臨床特徵是非自願性的體重明顯減輕以及肌肉和脂肪被耗損殆盡。然而，胰臟癌死亡率極高，相較於其他癌症，早期並沒有特別症狀，當診斷發現時已經是晚期，不僅加上腫瘤轉移特性及預後不佳的情形，若病患同時又患有惡質病是否也是造成高死亡率的原因之一。先前研究報導代謝因子和發炎因子如IL-6，TNF-α和IL-1β等，藉由肌肉細胞受體接收後進而活化蛋白降解訊號路徑造成肌肉萎縮。在臨床上，利用抑制蛋白降解訊號路徑抑制劑或是營養補充方式治療，但是僅限於解緩惡質病帶來的症狀，對於惡質病本身治療機制仍然不清楚。惡質病病患明顯有肌肉萎縮現象，為了了解其中造成肌肉萎縮的原因，在我們的研究中，先建立一個胰臟癌誘導惡質病的小鼠模型並利用觀察體重變化，抓力測量及螢光染色鑑定惡質病的小鼠模型及進行肌肉組織分析，藉此，希望能夠改善癌症誘發惡質病病患嚴重肌肉萎縮現象。

SUMMARY
Most patients in advance stage cancers such as colorectal, pancreatic, esophageal, and lung cancers often have emaciated body figures, known as cancer cachexia. Cachexia is a complex metabolic syndrome, and the most common clinical feature is the apparent weight loss rate and decreased muscle and fat mass. However, the prognosis was poor when diagnosed with pancreatic cancer in the late stage. Cancer-induced cachexia in pancreatic cancer patients is one of the causes of high mortality in pancreatic cancer. Previous studies reported that catabolic factors and inflammatory factors, such as IL-6, TNF-α and IL-1, can activate protein degradation pathway via binding to muscle cell receptors, and thus lead to muscle atrophy. In clinical care, by inhibition of protein degradation pathway or by nutritional supplement only reliefs symptoms, with limited benefits in reversing the cachexia symptoms. In patients with cachexia, there is obvious muscle atrophy. In order to understand and disease mechanisms the cause is needed system-wide analyses of muscle atrophy, to establish an available pancreatic cancer cachexia mouse model. Body weight changes, grip strength measurement and fluorescent staining in cachexia mouse model. Therefore, it is hoped that the severe muscle atrophy of cancer induced cachexia patients can be improved.

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