耶鲁大学癌症中心的一个研究团队已经证实，10-20%的被分类为雌激素受体（ER）阴性的乳腺癌其实是阳性的。了解何时以及为什么乳腺癌可能被错误的分类对诊断患有乳腺癌的妇女的治疗和预后具有重要意义。
其研究结果在线发表在6月28日的《Journal of Clinical Oncology》上。
一名被诊断患有乳腺癌的妇女可以通过免疫组织化学（IHC）进行测试，IHC是可检测出癌组织中特定蛋白质存在的一个过程。那些ER检测为阳性的患者会被给予内分泌治疗，如他莫昔芬、Letrazol或类似的药物。10-20%的被错误的分类为ER阴性的癌症患者，可能会被给予缺乏疗效的治疗。
在耶鲁大学医学院病理学教授，医学博士David Rimm的领导下，研究小组强调了IHC评估乳腺癌雌激素受体的局限性，并确定了标准的ER测量的新方法。他们使用了一种结合一系列标准控件的荧光检测技术来检测雌激素受体。研究小组报道说，这个更加敏感、重复性好的方法发现了那些最初被称为“阴性”但其实为“阳性”的病例。
Rimm说：“我们的研究表明，雌激素受体测定的常规方法可能会导致10-20%的假阴性率，这可能会导致乳腺癌患者的治疗不足，并且由于不恰当的测试，我们可能会错过利用我们最好的药物之一（他莫昔芬）的机会。”
该测试已授权给康涅狄格州Branford的HistoRx公司。该测定方法将会在临床实验室改进修正案认证的实验室很快的应用于患者。第一个发布测试的实验室将是加利福尼亚州Carlsbad的Genoptix公司。
这项研究的其他作者包括Allison Welsh，Sudha Kumar，Peter Gershkovich和Malini Harigopal。（生物谷Bioon.com）
生物谷推荐原文出处：
Journal of Clinical Oncology DOI: 10.1200/JCO.2010.30.3552
Loss of Nuclear Localized and Tyrosine Phosphorylated Stat5 in Breast Cancer Predicts Poor Clinical Outcome and Increased Risk of Antiestrogen Therapy Failure
y R. Peck, Agnieszka K. Witkiewicz, Chengbao Liu, Ginger A. Stringer, Alexander C. Klimowicz, Edward Pequignot, Boris Freydin, Thai H. Tran, Ning Yang, Anne L. Rosenberg, Jeffrey A. Hooke, Albert J. Kovatich, Marja T. Nevalainen, Craig D. Shriver, Terry Hyslop, Guido Sauter, David L. Rimm, Anthony M. Magliocco and Hallgeir Rui
Purpose To investigate nuclear localized and tyrosine phosphorylated Stat5 (Nuc-pYStat5) as a marker of prognosis in node-negative breast cancer and as a predictor of response to antiestrogen therapy.
Patients and Methods Levels of Nuc-pYStat5 were analyzed in five archival cohorts of breast cancer by traditional diaminobenzidine-chromogen immunostaining and pathologist scoring of whole tissue sections or by immunofluorescence and automated quantitative analysis (AQUA) of tissue microarrays.
Results Nuc-pYStat5 was an independent prognostic marker as measured by cancer-specific survival (CSS) in patients with node-negative breast cancer who did not receive systemic adjuvant therapy, when adjusted for common pathology parameters in multivariate analyses both by standard chromogen detection with pathologist scoring of whole tissue sections (cohort I; n = 233) and quantitative immunofluorescence of a tissue microarray (cohort II; n = 291). Two distinct monoclonal antibodies gave concordant results. A progression array (cohort III; n = 180) revealed frequent loss of Nuc-pYStat5 in invasive carcinoma compared to normal breast epithelia or ductal carcinoma in situ, and general loss of Nuc-pYStat5 in lymph node metastases. In cohort IV (n = 221), loss of Nuc-pYStat5 was associated with increased risk of antiestrogen therapy failure as measured by univariate CSS and time to recurrence (TTR). More sensitive AQUA quantification of Nuc-pYStat5 in antiestrogen-treated patients (cohort V; n = 97) identified by multivariate analysis patients with low Nuc-pYStat5 at elevated risk for therapy failure (CSS hazard ratio [HR], 21.55; 95% CI, 5.61 to 82.77; P < .001; TTR HR, 7.30; 95% CI, 2.34 to 22.78; P = .001).
Conclusion Nuc-pYStat5 is an independent prognostic marker in node-negative breast cancer. If confirmed in prospective studies, Nuc-pYStat5 may become a useful predictive marker of response to adjuvant hormone therapy.
