Molecular markers and therapeutic targets in ductal carcinoma in situ
Molecular markers and therapeutic targets in ductal carcinoma in situ
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DOI：
10.1002/jemt.10172
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发表时间：
2002-10-01
影响因子：
2.5
通讯作者：
Bundred, NJ
中科院分区：
文献类型：
--
作者：
Boland, GP;Knox, WF;Bundred, NJ
乳腺导管原位癌 (DCIS) 是一种癌前病变，约占所有新发乳腺癌的 20%，占乳房 X 光检查检测到的肿瘤病变的 40%。由于 DCIS 保乳手术治疗后复发很常见，因此需要确定预测复发的分子因素。与此同时，随着发现雌激素受体（ER）阳性乳腺癌可以通过抗雌激素来预防，对 DCIS 分子生物学的理解也取得了最新进展。 DCIS 中的受体共表达主要通过免疫组织化学来确定。动物模型为正常乳腺癌和原位癌中参与增殖和凋亡调节和失调的信号通路提供了证据。 ER 阴性 DCIS 已被证明与激素无关。如果乳腺癌化学预防的目标是预防 ER 阴性乳腺癌，那么阻断 ER 阴性 DCIS 中细胞增殖所涉及的途径是可能的，并且是必要的。是要切实实现的。
Ductal carcinoma in situ (DCIS) of the breast is a premalignant condition which accounts for approximately 20% of all new breast cancers and up to 40% of neoplastic lesions detected by mammographic screening. Since recurrence is common after DCIS treated with breast conservation surgery, there is a need to determine molecular factors that predict recurrence. In parallel with this and with the finding that oestrogen receptor (ER) positive breast cancer can be prevented with anti-oestrogens, there have been recent advances in the understanding of the molecular biology of DCIS. Receptor coexpression in DCIS has been determined largely by immunohistochemistry. Animal models have provided evidence for the signalling pathways involved in the regulation and dysregulation of proliferation and apoptosis in both normal breast and in situ cancer. ER-negative DCIS has been shown to be hormone-independent. Blockade of the pathways involved in cell proliferation in ER-negative DCIS is possible and will be necessary to prevent ER-negative breast cancers if the goal of breast cancer chemoprevention. is to be realistically achieved.