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目的：观察３６ 例（Ｅ２ ＋ ） 乳腺癌患者组织ＰＲ 和ＥＲ ＤＮＡ 结合功能的关系，进而探讨（Ｅ２ ＋ ／ＰＲ＋ ） 表型内分泌治疗无反应的分子机制。方法：用激素结合法和迁移率改变法。结果：１） 用含有ＥＲ 的ＭＣＦ－ ７ 细胞株作为阳性对照，２２ ℃Ｍｇ２ ＋ 存在条件下，迁移率改变法中ＥＲ－ ＥＲＥ 复合物的形成是激素依赖性的，证实了ＥＲ－ ＥＲＥ 复合物的特性。２） 激素结合法和迁移率改变法检测结果显示，３６ 例（Ｅ２ ＋ ） 乳腺癌中有２５ 例相一致，其中两种方法都是阳性者（ＰＲ＋ ／ＥＲＥ＋ ）１７ 例，都是阴性者（ＰＲ－ ／ＥＲＥ－ ）８ 例。３ 例肿瘤，激素结合法阳性而迁移率改变法阴性（ＰＲ＋ ／ＥＲＥ－ ） 。８ 例肿瘤，激素结合法阴性而迁移率改变法阳性（ＰＲ－ ／ＥＲＥ＋ ） 。结论：乳腺癌组织中依赖ＥＲ 的ＰＲ 表达还有其它途径（ＰＲ＋ ／ＥＲＥ－ ） ，且ＰＲ 阴性不能表示ＥＲ ＤＮＡ 结合功能状态有缺陷（ＰＲ－ ／ＥＲＥ＋ ） ，利用ＰＲ 评估ＥＲ ＤＮＡ 结合功能状态以指导乳腺癌的内分泌治疗存在约３０ ％ （１１／３６） 的误差率。因此，传统的激素结合法检测结果（Ｅ２ 、ＰＲ） 同迁移率改变法检测结果（ＥＲＥ） 相结合，能更准确地反应ＥＲ 功
OBJECTIVE: To investigate the relationship between PR and ER DNA binding function in 36 (E2 +) breast cancer patients, and to explore the molecular mechanism of the (E2 + /PR+) phenotype endocrine therapy nonresponsiveness. Methods: Hormone binding and mobility changes. RESULTS: 1) The formation of ER-ERE complex in the mobility shift assay was hormone-dependent in the presence of the ER-containing MCF-7 cell line as a positive control in the presence of 22 °C Mg2+, confirming the ER-ERE complex The characteristics. 2) The results of hormone binding assay and mobility shift assay showed that 25 of 36 (E2 +) breast cancers were consistent, and both of them were positive (PR+/ERE+) 17 and were negative ( PR-/ERE-) 8 cases. Three tumors were positive for hormone binding and negative for migration (PR+/ERE-). In 8 tumors, the hormone binding method was negative and the mobility shift method was positive (PR-/ERE+). Conclusion: There are other pathways of PR-dependent ER expression in breast cancer (PR+/ERE-), and PR-negative cannot indicate the defective ER DNA-binding function status (PR-/ERE+). Use PR to evaluate ER-DNA binding function status. There is an error rate of about 30% (11/36) for endocrine therapy to guide breast cancer. Therefore, the traditional hormone binding assay results (E2, PR) combined with the mobility shift assay (ERE) can more accurately reflect ER performance.