国际病理科学与临床杂志
國際病理科學與臨床雜誌
국제병이과학여림상잡지
JOURNAL OF INTERNATIONAL PATHOLOGICAL AND CLINICAL MEDICINE
2013年
4期
327-331
,共5页
李晓营%刘春霞%李锋(综述)
李曉營%劉春霞%李鋒(綜述)
리효영%류춘하%리봉(종술)
横纹肌肉瘤%成纤维生长因子受体%上皮间叶转化
橫紋肌肉瘤%成纖維生長因子受體%上皮間葉轉化
횡문기육류%성섬유생장인자수체%상피간협전화
rhabdomyosarcoma%ifbroblast growth factor receptor%epithelial-mesenchymal transition
横纹肌肉瘤是起源于骨骼肌的间叶源性肿瘤,常发生于15岁以下的儿童和青少年。由于不同类型横纹肌肉瘤的组织学特征、发病年龄、部位和预后各具差异,迄今为止横纹肌肉瘤的分子机制仍不明确。近年来,关于其分子机制的研究主要集中于关键基因和信号通路等方面,研究发现成纤维生长因子受体信号通路与横纹肌肉瘤的生长及转移密切相关,在多数上皮源性肿瘤中已证实上皮间叶转化促进了肿瘤增生与转移,因此笔者提出在横纹肌肉瘤中上皮间叶转化可能通过成纤维生长因子受体信号通路促进肿瘤增生和转移的假设,结合成纤维生长因子受体信号通路和上皮间叶转化来试着解释横纹肌肉瘤的发生、发展,以期为其治疗和预后评估提供一定的帮助。
橫紋肌肉瘤是起源于骨骼肌的間葉源性腫瘤,常髮生于15歲以下的兒童和青少年。由于不同類型橫紋肌肉瘤的組織學特徵、髮病年齡、部位和預後各具差異,迄今為止橫紋肌肉瘤的分子機製仍不明確。近年來,關于其分子機製的研究主要集中于關鍵基因和信號通路等方麵,研究髮現成纖維生長因子受體信號通路與橫紋肌肉瘤的生長及轉移密切相關,在多數上皮源性腫瘤中已證實上皮間葉轉化促進瞭腫瘤增生與轉移,因此筆者提齣在橫紋肌肉瘤中上皮間葉轉化可能通過成纖維生長因子受體信號通路促進腫瘤增生和轉移的假設,結閤成纖維生長因子受體信號通路和上皮間葉轉化來試著解釋橫紋肌肉瘤的髮生、髮展,以期為其治療和預後評估提供一定的幫助。
횡문기육류시기원우골격기적간협원성종류,상발생우15세이하적인동화청소년。유우불동류형횡문기육류적조직학특정、발병년령、부위화예후각구차이,흘금위지횡문기육류적분자궤제잉불명학。근년래,관우기분자궤제적연구주요집중우관건기인화신호통로등방면,연구발현성섬유생장인자수체신호통로여횡문기육류적생장급전이밀절상관,재다수상피원성종류중이증실상피간협전화촉진료종류증생여전이,인차필자제출재횡문기육류중상피간협전화가능통과성섬유생장인자수체신호통로촉진종류증생화전이적가설,결합성섬유생장인자수체신호통로화상피간협전화래시착해석횡문기육류적발생、발전,이기위기치료화예후평고제공일정적방조。
Rabdomyosarcoma (RMS), common in the children and adolescence, is a mesenchymal malignancy derived from skeletal muscle. RMS can be classiifed into 3 main subtypes, more aggressive alveolar rhabdomyosarcoma (ARMS), more common, and better outcome embryonal rhabdomyosarcoma (ERMS) and the rare pleomorphic rhabdomyosarcoma (PRMS). The molecular mechanism for RMS is still unclear due to the different types of RMS with differences in histologic characteristic, age of onset, location, and prognosis. Recent studies are mainly focused on the key genes and signaling pathways in RMS. It has been found that ifbroblast growth factor receptor (FGFR) signaling pathway is strongly associated with the proliferation and metastasis of RMS. More interestingly, it has been conifrmed that epithelial-mesenchymal transition (EMT) promotes the proliferation and metastasis in lots of epithelial tumors. So we hypothesize that EMT promotes proliferation and metastasis via FGFR signaling pathway in RMS. In this article we tried to understand the development of RMS via EMT and FGFR signaling pathway. Hopefully, it can offer a new view for the treatment and prognosis assessment of RMS.