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本文引用的文献

1
Castration-resistant prostate cancer: from new pathophysiology to new treatment targets.去势抵抗性前列腺癌:从新的病理生理学到新的治疗靶点。
Eur Urol. 2009 Oct;56(4):594-605. doi: 10.1016/j.eururo.2009.06.027. Epub 2009 Jun 24.
2
Antitumor activity with CYP17 blockade indicates that castration-resistant prostate cancer frequently remains hormone driven.CYP17阻断的抗肿瘤活性表明,去势抵抗性前列腺癌通常仍由激素驱动。
Cancer Res. 2009 Jun 15;69(12):4937-40. doi: 10.1158/0008-5472.CAN-08-4531. Epub 2009 Jun 9.
3
Bone sialoprotein stimulates focal adhesion-related signaling pathways: role in migration and survival of breast and prostate cancer cells.骨唾液蛋白刺激粘着斑相关信号通路:在乳腺癌和前列腺癌细胞迁移及存活中的作用
J Cell Biochem. 2009 Aug 15;107(6):1118-28. doi: 10.1002/jcb.22211.
4
Phase I study of concurrent weekly docetaxel and repeated samarium-153 lexidronam in patients with castration-resistant metastatic prostate cancer.多西他赛每周一次与重复使用钐-153 来昔单抗同步治疗去势抵抗性转移性前列腺癌患者的 I 期研究。
J Clin Oncol. 2009 Jul 10;27(20):3319-24. doi: 10.1200/JCO.2008.20.5393. Epub 2009 May 4.
5
The role of 'notch' in urological cancers.“Notch”在泌尿系统癌症中的作用。
BJU Int. 2009 Jul;104(1):1-2. doi: 10.1111/j.1464-410X.2009.08479.x. Epub 2009 Apr 21.
6
Targeting TGF-beta in prostate cancer: therapeutic possibilities during tumor progression.靶向前列腺癌中的转化生长因子-β:肿瘤进展过程中的治疗可能性
Expert Opin Ther Targets. 2009 Feb;13(2):227-34. doi: 10.1517/14728220802705696.
7
Phase II trial of neoadjuvant nab-paclitaxel in high risk patients with prostate cancer undergoing radical prostatectomy.纳布紫杉醇新辅助治疗在接受根治性前列腺切除术的高危前列腺癌患者中的II期试验。
J Urol. 2009 Apr;181(4):1672-7; discussion 1677. doi: 10.1016/j.juro.2008.11.121. Epub 2009 Feb 23.
8
Phase III trial of androgen ablation with or without three cycles of systemic chemotherapy for advanced prostate cancer.晚期前列腺癌雄激素剥夺联合或不联合三个周期全身化疗的III期试验。
J Clin Oncol. 2008 Dec 20;26(36):5936-42. doi: 10.1200/JCO.2007.15.9830. Epub 2008 Nov 24.
9
Androgen receptor is a tumor suppressor and proliferator in prostate cancer.雄激素受体在前列腺癌中既是一种肿瘤抑制因子,也是一种增殖因子。
Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12182-7. doi: 10.1073/pnas.0804700105. Epub 2008 Aug 22.
10
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms.雄激素受体阴性的人前列腺癌细胞通过FGF9介导的机制在小鼠体内诱导成骨。
J Clin Invest. 2008 Aug;118(8):2697-710. doi: 10.1172/JCI33093.

以临床观察为基础的前列腺癌治疗新模式。

A new therapy paradigm for prostate cancer founded on clinical observations.

机构信息

Department of Genitourinary Medical Oncology and David H Koch Center for Applied Research of Genitourinary Cancers, University of Athens, Athens, Greece.

出版信息

Clin Cancer Res. 2010 Feb 15;16(4):1100-7. doi: 10.1158/1078-0432.CCR-09-1215. Epub 2010 Feb 9.

DOI:10.1158/1078-0432.CCR-09-1215
PMID:20145177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3891669/
Abstract

Efficacy equivalent to that reported in other common adult solid tumors considered to be chemotherapy-sensitive has been reported with Docetaxel in patients with castrate-resistant prostate cancer. However, in contrast to other cancers, the expected increase in efficacy with the use of chemotherapy in earlier disease states has not been reported to date in prostate cancer. On the basis of these observations, we speculated that the therapy development paradigm used successfully in other cancers may not apply to the majority of prostate cancers. Several lines of supporting clinical and experimental observations implicate the tumor microenvironment in prostate carcinogenesis and resistance to therapy. We conclude that a foundation to guide the development of therapy for prostate cancer is required. The therapy paradigm we propose accounts for the central role of the tumor microenvironment in bone and, if correct, will lead to microenvironment-targeted therapy.

摘要

在去势抵抗性前列腺癌患者中,多西他赛在其他被认为对化疗敏感的常见成人实体肿瘤中的疗效与报告的疗效相当。然而,与其他癌症不同的是,迄今为止,在前列腺癌中,尚未报告在疾病早期使用化疗会提高疗效。基于这些观察结果,我们推测在其他癌症中成功应用的治疗开发范例可能不适用于大多数前列腺癌。几条支持的临床和实验观察结果暗示肿瘤微环境在前列腺癌发生和对治疗的抵抗中起作用。我们得出结论,需要一个指导前列腺癌治疗开发的基础。我们提出的治疗范例考虑了肿瘤微环境在骨骼中的核心作用,如果正确,将导致针对微环境的治疗。