Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Department of Radiation Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Clinical Research for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, 300060, China.
Br J Cancer. 2024 Nov;131(10):1683-1693. doi: 10.1038/s41416-024-02863-9. Epub 2024 Oct 5.
Ovarian cancer (OvCa) is the most lethal of the gynecologic malignancies. Immune checkpoint inhibitors, which have revolutionized the treatment of multiple malignancies, have had limited efficacy in OvCa patients. This lack of effectiveness is partly due to the abnormal ovarian tumor microenvironment (TME), displaying a desmoplastic, highly fibrotic extracellular matrix. High extracellular matrix deposition leads to a buildup of compressive forces that cause tumor blood vessel collapse, reduced vessel perfusion, poor delivery of drugs, and compromised trafficking of cytotoxic T-cells to these tumors.
Using two syngeneic OvCa models, we tested the effect of losartan, a widely prescribed anti-hypertensive drug, on reprogramming the TME and chemosensitizing the cancer cells.
Losartan treatment (i) reprograms the TME leading to increased vascular perfusion, and thus enhances drug delivery and immune effector cell intratumoral infiltration and function; and (ii) rewires the OvCa cells by suppressing the IGF-1 signaling, resulting in enhanced chemosensitivity. As a result of the combined tumor and stromal effects, losartan treatment enhances the efficacy of chemo-immunotherapy in OvCa models.
The safety and low cost ( < $1-2/day) of losartan warrant rapid translation of our findings to patients with OvCa.
卵巢癌(OvCa)是妇科恶性肿瘤中最致命的一种。免疫检查点抑制剂已经彻底改变了多种恶性肿瘤的治疗方法,但在 OvCa 患者中的疗效有限。这种效果不佳部分是由于卵巢肿瘤微环境(TME)异常,表现为促结缔组织形成的、高度纤维化的细胞外基质。细胞外基质的高沉积导致压迫力积聚,从而导致肿瘤血管塌陷、血管灌注减少、药物输送不良以及细胞毒性 T 细胞向这些肿瘤的运输受损。
我们使用两种同源卵巢癌模型,测试了广泛用于治疗高血压的药物氯沙坦对重塑 TME 和增强癌细胞化疗敏感性的作用。
氯沙坦治疗(i)重塑 TME,导致血管灌注增加,从而增强药物输送和免疫效应细胞在肿瘤内的浸润和功能;和(ii)通过抑制 IGF-1 信号转导,重新编程 OvCa 细胞,导致化疗敏感性增强。由于肿瘤和基质的综合作用,氯沙坦治疗增强了卵巢癌模型中的化疗免疫治疗效果。
氯沙坦的安全性和低成本(每天<$1-2)保证了我们的研究结果能够迅速转化为 OvCa 患者。