Uray Iván P, Brown Powel H
Department of Clinical Cancer Prevention, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77230, USA.
Recent Results Cancer Res. 2011;188:147-62. doi: 10.1007/978-3-642-10858-7_13.
Results from clinical trials have demonstrated that it is possible to prevent estrogen-responsive breast cancers by targeting the estrogen receptor with selective estrogen receptor modulators (SERMs) (tamoxifen, raloxifene, or lasofoxifene) or with aromatase inhibitors (AIs) (anastrozole, letrozole, or exemestene). Results from breast cancer treatment trials suggest that aromatase inhibitors may be even more effective in preventing breast cancer than SERMs. However, while SERMs and aromatase inhibitors do prevent the development of many ER-positive breast cancers, these drugs do not prevent ER-negative breast cancer. These results show that new approaches are needed for the prevention of this aggressive form of breast cancer. Our laboratory and clinical efforts have been focused on identifying critical molecular pathways in breast cells that can be targeted for the prevention of ER-negative breast cancer. Our preclinical studies have demonstrated that other nuclear receptors, such as RXR receptors, vitamin D receptors, as well as others are critical for the growth of ER-negative breast cells and for the transformation of these cells into ER-negative cancers. Other studies show that growth factor pathways including those activated by EGFR, Her2, and IGFR, which are activated in many ER-negative breast cancers, can be targeted for the prevention of ER-negative breast cancer in mice. Clinical studies have also shown that PARP inhibitors are effective for the treatment of breast cancers arising in BRCA-1 or -2 mutation carriers, suggesting that targeting PARP may also be useful for the prevention of breast cancers arising in these high-risk individuals. Most recently, we have demonstrated that ER-negative breast cancers can be subdivided into four distinct groups based on the kinases that they express. These groups include ER-negative/Her-2-positive groups (the MAPK and immunomodulatory groups) and ER-negative/Her2-negative groups (the S6K and the cell cycle checkpoint groups). These groups of ER-negative breast cancers can be targeted with kinase inhibitors specific for each subgroup. These preclinical studies have supported the development of several clinical trials testing targeted agents for the prevention of breast cancer. The results of a completed Phase II cancer prevention trial using the RXR ligand bexarotene in women at high risk of breast cancer will be reviewed, and the current status of an ongoing Phase II trial using the EGFR and Her2 kinase inhibitor lapatinib for the treatment of women with DCIS breast cancer will be presented. It is anticipated that in the future these molecularly targeted drugs will be combined with hormonal agents such as SERMs or aromatase inhibitors to prevent all forms of breast cancer.
临床试验结果表明,通过使用选择性雌激素受体调节剂(SERM)(他莫昔芬、雷洛昔芬或拉索昔芬)或芳香化酶抑制剂(AI)(阿那曲唑、来曲唑或依西美坦)作用于雌激素受体,有可能预防雌激素反应性乳腺癌。乳腺癌治疗试验结果表明,芳香化酶抑制剂在预防乳腺癌方面可能比SERM更有效。然而,虽然SERM和芳香化酶抑制剂确实能预防许多雌激素受体阳性乳腺癌的发生,但这些药物并不能预防雌激素受体阴性乳腺癌。这些结果表明,需要新的方法来预防这种侵袭性乳腺癌。我们实验室和临床研究一直致力于确定乳腺细胞中可作为预防雌激素受体阴性乳腺癌靶点的关键分子途径。我们的临床前研究表明,其他核受体,如视黄酸X受体(RXR)、维生素D受体等,对雌激素受体阴性乳腺细胞的生长以及这些细胞转化为雌激素受体阴性癌症至关重要。其他研究表明,生长因子途径,包括在许多雌激素受体阴性乳腺癌中被激活的表皮生长因子受体(EGFR)、人表皮生长因子受体2(Her2)和胰岛素样生长因子受体(IGFR)所激活的途径,可作为预防小鼠雌激素受体阴性乳腺癌的靶点。临床研究还表明,聚(ADP - 核糖)聚合酶(PARP)抑制剂对治疗携带BRCA - 1或 - 2基因突变的乳腺癌患者有效,这表明靶向PARP可能对预防这些高危个体患乳腺癌也有用。最近,我们已经证明,雌激素受体阴性乳腺癌可根据其表达的激酶分为四个不同的组。这些组包括雌激素受体阴性/Her - 2阳性组(丝裂原活化蛋白激酶(MAPK)和免疫调节组)和雌激素受体阴性/Her2阴性组(核糖体蛋白S6激酶(S6K)和细胞周期检查点组)。这些雌激素受体阴性乳腺癌组可用针对每个亚组的激酶抑制剂进行靶向治疗。这些临床前研究为开展多项测试预防乳腺癌靶向药物的临床试验提供了支持。将回顾一项已完成的II期癌症预防试验的结果,该试验在乳腺癌高危女性中使用RXR配体贝沙罗汀;并介绍一项正在进行的II期试验的现状,该试验使用EGFR和Her2激酶抑制剂拉帕替尼治疗导管原位癌(DCIS)乳腺癌女性患者。预计未来这些分子靶向药物将与SERM或芳香化酶抑制剂等激素药物联合使用,以预防所有类型的乳腺癌。