在一項(xiàng)突破性研究中，美國科學(xué)家發(fā)現(xiàn)了阻止常用抗乳腺癌藥物起作用的基因,，這一突破每年或能挽救數(shù)百人的生命,。
乳腺癌患者在手術(shù)后通常服用化療藥物來阻止腫瘤擴(kuò)散或反復(fù),，但是,，有些患者卻對此類藥物具有抗藥性，而最新研究結(jié)果則為用以確定這些患者的基因測試鋪平道路,。這樣,，醫(yī)生就可以給檢驗(yàn)結(jié)果呈陽性的患者服用其他的藥物，令其活下來的幾率大增,。
最新研究聚焦于一種名為蒽環(huán)類抗癌藥(Anthracycline),，這種藥物通常作為“輔助”療法給患者服用，有助于抑制患者術(shù)后病情反復(fù),。蒽環(huán)類抗癌藥包括阿霉素,、道諾霉素、表阿霉素等,，在每年確診患有乳腺癌的4.6萬英國女性當(dāng)中,，大約一半服用這種藥物。
美國波士頓丹納·法伯癌癥研究所的研究人員對85名患者的乳腺癌細(xì)胞樣本做了研究,，在大約五分之一的樣本中，有兩種基因過于活躍,，使得癌細(xì)胞對藥物治療具有抗性,。研究結(jié)果刊登在最新一期《自然—醫(yī)學(xué)》（Nature Medicine）雜志上。
醫(yī)療記錄證實(shí),，那些擁有這兩種可疑基因的患者比沒有它們的患者恢復(fù)情況更差,。研究人員安德烈·理查德森(Andrea Richardson)博士說：“這些結(jié)果表明,，對蒽環(huán)類抗癌藥具有抗藥性的腫瘤可能對其它藥劑敏感。所以,，這種方法作為一種測試手段將非常有用,，可以幫助挑選對這些患者最為有效的療法。”（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine 24 January 2010 | doi:10.1038/nm.2090
Amplification of LAPTM4B and YWHAZ contributes to chemotherapy resistance and recurrence of breast cancer
Yang Li1,2,9, Lihua Zou1,3,9, Qiyuan Li4,9, Benjamin Haibe-Kains5,6, Ruiyang Tian1, Yan Li1, Christine Desmedt5, Christos Sotiriou5, Zoltan Szallasi4,7, J Dirk Iglehart1,2, Andrea L Richardson1,8,9 & Zhigang Charles Wang1,2,9
Adjuvant chemotherapy for breast cancer after surgery has effectively lowered metastatic recurrence rates1. However, a considerable proportion of women suffer recurrent cancer at distant metastatic sites despite adjuvant treatment. Identification of the genes crucial for tumor response to specific chemotherapy drugs is a challenge but is necessary to improve outcomes2. By using integrated genomics, we identified a small number of overexpressed and amplified genes from chromosome 8q22 that were associated with early disease recurrence despite anthracycline-based adjuvant chemotherapy. We confirmed the association in an analysis of multiple independent cohorts. SiRNA-mediated knockdown of either of two of these genes, the antiapoptotic gene YWHAZ and a lysosomal gene LAPTM4B, sensitized tumor cells to anthracyclines, and overexpression of either of the genes induced anthracycline resistance. Overexpression of LAPTM4B resulted in sequestration of the anthracycline doxorubicin, delaying its appearance in the nucleus. Overexpression of these two genes was associated with poor tumor response to anthracycline treatment in a neoadjuvant chemotherapy trial in women with primary breast cancer. Our results suggest that 8q22 amplification and overexpression of LAPTM4B and YWHAZ contribute to de novo chemoresistance to anthracyclines and are permissive for metastatic recurrence. Overexpression of these two genes may predict anthracycline resistance and influence selection of chemotherapy.
