EPHB1
小结
EPHB1编码蛋白是Eph受体酪氨酸激酶家族的一员，在神经和血管系统发育中具有非常重要的作用。脊髓中的EPHB1正向信号转导在骨癌疼痛治疗中的骨癌痛和吗啡耐受的发展起到关键作用。在结直肠癌中观察到EPHB1表达量降低，且此类变化多见于低分化和粘液腺癌，同时表现出更强的侵袭能力。EPHB1蛋白的低表达与胃癌的侵袭，晚期和转移显着相关。研究显示在43.2％的浆液性卵巢癌检测到中EPHB1蛋白的缺失，并且与患者的转移和较差的存活率相关，这表明EPHB1可用作浆液性卵巢癌的预后标志物和治疗靶标。与肾小管正常上皮中的EPHB1表达相比，透明细胞癌（RCC）中EPHB1的表达降低。EPHB1蛋白在嗜铬RCC中适度表达，在透明细胞RCC中弱表达，在乳头状RCC中呈阴性表达，使得EPHB1成为RCC诊断的潜在生物标志物和RCC的治疗靶点。EPHB1和Ephrin-B在46例鳞状细胞/腺鳞癌（SC/ASC）和80例腺癌（AC）中的表达与总生存率呈负相关。对胶质瘤中EphB信号转录水平的研究表明，EPHB1表达水平与恶性星形细胞瘤患者的良好生存率相关。
EPHB1 is a member of the Eph receptor tyrosine kinase family, the largest subgroup of the receptor tyrosine kinase (RTK) family shown to have very important roles in nervous and vascular system development. It is a marker expressed in venous endothelial cells throughout embryonic development to adulthood. EPHB1 forward signaling in the spinal cord plays critical roles in the development of bone cancer pain and morphine tolerance in treating bone cancer pain. Reduced expression of EPHB1 in colorectal cancer was observed, which more often occurred in poorly differentiated and mucinous adenocarcinomas and showed more invasive power. Underexpression of EPHB1 protein is significantly associated with invasion, advanced stage and metastasis in gastric cancer. Loss of EPHB1 protein was shown in 43.2% serous ovarian cancers and associated with metastasis and poor survival in patients, suggesting that EPHB1 may be used as a prognostic marker and a therapeutic target in serous ovarian carcinoma. Decreased expression of EPHB1 was also found in all renal cell carcinomas (RCC) compared with expression in the normal epithelium of renal tubules. EPHB1 protein is moderately expressed in chromophobic RCC, weakly expressed in clear-cell RCC and negatively expressed in papillary RCC, making EPHB1 a potential biomarker in RCC diagnosis and a therapeutic target of RCC. Expression of EPHB1 and Ephrin-B in 46 patients with Squamous cell/adenosquamous carcinoma (SC/ASC) and 80 with adenocarcinoma (AC) showed a negative correlation with overall survival. An in vivo model of EPHB1 function in medulloblastoma, show that the genetic loss of EPHB1 results in a significant delay in tumor recurrence following radiotherapy. In AML cells, EPHB1 was commonly suppressed and its transcript was inversely correlated with EPHB1 promoter methylation. EPHB1 promoter hypermethylation was significantly higher as compared with normal sample controls in many cancers, including breast, lung, cervical, colon, stomach, and prostate cancer. Finally, a study of transcriptional levels of EphB signaling in gliomas demonstrated that EPHB1 expression level is associated with good survival in patients with malignant astrocytomas.