台灣地區大腸直腸癌發生、死亡人數，每年呈快速增加的趨勢，居所有癌症發生率及死亡率的第三大原因。在臨床上治療包括化學治療、放射線療法、標靶治療以及最主要的手術切除，不過對於大腸直腸癌後期轉移性的患者來說，一直到目前為止還尚未發現有效的治療策略。目前認為大腸直腸癌是一種異質性疾病，涉及了多種複雜的發病機制，包括致癌基因的活化，以及未活化的抑癌基因，基因突變及轉變。目前需要更清楚的理解大腸直腸癌的分子機制，回顧大腸直腸癌的病理生理學以及目前已知的分子機制是相當重要的，由於近年來分子生物學進展快速，從正常的上皮細胞-瘜肉-腺瘤-腺癌的生成機制逐漸明朗。目前已知APC (Adenomatous polyposis coli) 基因的突變發生在大腸瘜肉的早期，致癌基因KRAS則是發生在中期腺瘤階段而後期大腸癌的發生則伴隨著TP53基因的突變，其他基因突變也陸續在大腸直腸癌不同階段被發現。在這篇文章中，首先我們介紹幾種常見的大腸直腸癌 (遺傳性以及散發性大腸直腸癌)，以及大腸直腸癌常見的分期法，接著會逐步描述典型的大腸直腸癌基因轉變之發病過程，以及已知的大腸直腸癌的基因突變包括，KRAS，P53，APC，錯誤修復基因等許多基因。另外，我們也會整理數種已知的大腸直腸癌涉及的訊息傳遞路徑包括Wnt訊息傳遞路徑、TGF-beta路徑、K-RAS路徑、LKB路徑、Notch以及Hedgehog路徑，最後一部分會討論在許多研究中已發現穿膜受體酪氨酸激酶RTK的過度表現會造成癌症的發生，並且在大腸直腸癌中發現TAM家族的酪氨酸激酶接受器TYRO3過度表現，以及細胞核內TYRO3可能參與調控了致癌基因的表現，不過TYRO3入核調控機制尚不清楚，因此我們認為未來應該靶向TYRO3來進行更進一步的研究以及治療上的策略，提供大腸直腸癌的治療能夠多一個新的治療方向。

We sorted several pathogenesis, signal pathway, mutated oncogene and tumor suppressor gene of colorectal cancer (CRC) which can offer new treatment direction for clinicians.The past studies have found that the overexpression of many transmembrane receptor tyrosine kinase (RTK)s can cause cancer. Due to TAM family receptor tyrosine kinase TYRO3 is positive correlation with severity of CRC. Through animal experiment, TYRO3 antibody combined with anticancer drugs 5-Fluorouracil treatment had good results, but it was not completely inhibited. Therefore, we believe that there should be other mechanisms involved, and subsequent studies found that TYRO3 enters the nucleus and the nucleus TYRO3 is also proportional to the malignancy of CRC. Therefore, we suggest that TYRO3 in the nucleus should be targeted as a research direction in the future.

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