Janus kinase inhibitors, including tofacitinib, filgotinib, and upadacitinib, have emerged as effective therapeutic options for the management of inflammatory bowel diseases (IBDs). By targeting the JAK-STAT signaling pathway, these agents modulate immune responses and reduce inflammation. However, concerns regarding the potential risk of malignancy associated with their use have gained significant attention. The JAK-STAT pathway is not only critical for inflammatory signaling but also plays a pivotal role in cellular growth, differentiation, and tumor surveillance. Observational studies and clinical trial data in rheumatoid arthritis have reported malignancies, including non-melanoma skin cancer and solid tumors, in patients receiving JAK inhibitors, with evidence suggesting variable risks depending on the selectivity of the agent. Current evidence does not suggest an increased risk of oncogenesis in patients with IBDs. Balancing therapeutic efficacy with long-term safety requires ongoing vigilance; patient stratification based on risk factors; and tailored monitoring strategies to mitigate potential adverse effects, including malignancies, during JAK inhibitor therapy. Long-term follow-up data of up to 10 years offer reassuring evidence that JAK inhibitor therapy in IBD patients does not confer an increased risk of malignancies, supporting their continued use within appropriate clinical settings.
Janus激酶抑制剂，包括托法替尼、菲戈替尼和乌帕替尼，已成为治疗炎症性肠病的有效选择。这些药物通过靶向JAK-STAT信号通路，调节免疫反应并减轻炎症。然而，其使用可能带来的恶性肿瘤风险已引起广泛关注。JAK-STAT通路不仅对炎症信号传导至关重要，还在细胞生长、分化和肿瘤监视中发挥关键作用。类风湿关节炎的观察性研究和临床试验数据显示，接受JAK抑制剂治疗的患者中出现了非黑色素瘤皮肤癌和实体瘤等恶性肿瘤，且证据表明风险因药物选择性而异。现有证据并未表明炎症性肠病患者使用JAK抑制剂会增加肿瘤发生风险。为平衡疗效与长期安全性，需要持续保持警惕，基于风险因素进行患者分层，并制定个体化监测策略以减轻JAK抑制剂治疗期间包括恶性肿瘤在内的潜在不良反应。长达10年的长期随访数据提供了令人安心的证据，表明JAK抑制剂治疗不会增加炎症性肠病患者的恶性肿瘤风险，支持其在适当的临床环境中继续使用。
肿瘤(癌症)患者之家