这些癌细胞仿佛在等待一个信号，而病毒引发的炎症，正是那个"启动密码"。美国科罗拉多大学安 舒茨医学分校的科学家在小鼠模型上做了实验：当乳腺癌小鼠呼吸道感染后，原本平静的肺部迅速变 得"热闹"起来，休眠的癌细胞在几天内开始苏醒、分裂，短短两周，转移病灶就明显扩大。 科学家们紧接着分析了英国生物样本库（4837人，所有癌症类型）和美国Flatiron健康数据库 （36845人，乳腺癌患者），发现人类世界的数据也有类似的警报：呼吸道感染后的癌症患者，其癌症 相关死亡风险是未感染者的一倍；而在乳腺癌患者中，感染后肺部转移的风险上升了40%以上。 这意味着，呼吸道感染可能"开门"让癌细胞趁虚而入。或许，人体免疫系统在全力抗敌时，无意中 为癌细胞创造了"温床"，炎症信号就像"营养液"，刺激它们重新活跃。 研究无止境，科学无定论。这一研究还有待进一步扩大样本和深入分析。它也不是让人们恐慌的理 由，而是提醒人们：健康是一场精密的平衡游戏。对于癌症康复者来说，预防呼吸道感染，比以往任何 时候都更重要。戴口罩、打疫苗、勤洗手，这些看似简单的动作，可能就是在为自己的身体筑起一 道"防火墙"。 《自然》杂志最近发表了一项重磅研究，揭 ...

Core Viewpoint - The study highlights the significant impact of respiratory viral infections, such as influenza and SARS-CoV-2, on the awakening and proliferation of dormant disseminated cancer cells (DCC) in the lungs, which may lead to increased cancer-related mortality and metastasis risk [3][14][15]. Group 1: Research Findings - Influenza and SARS-CoV-2 infections can cause dormant DCC in the lungs to awaken, leading to rapid proliferation and metastasis [3][4]. - The research indicates that the presence of interleukin-6 (IL-6) is crucial for the reactivation of DCC, as its levels increase following viral infection [9][12]. - CD4+ T cells play a necessary role in maintaining the awakened state of DCC, although they are not required to initiate this process [12][14]. Group 2: Clinical Implications - The study found that cancer patients infected with SARS-CoV-2 have a significantly higher risk of cancer-related death and lung metastasis compared to those who are not infected [14][15]. - The findings suggest a potential link between respiratory infections and the recurrence of metastatic cancer, emphasizing the need for further exploration in this area [4][15]. Group 3: Mechanisms of Action - The research demonstrated that CD4+ T cells limit the ability of CD8+ T cells to control DCC growth, indicating a complex interplay between different immune cell types in the context of viral infections and cancer [12][14]. - The study also explored the role of inflammation caused by respiratory infections in influencing dormant cancer cells, which had not been a primary focus in previous research [7][8].

Core Viewpoint - The research highlights a novel biological signaling axis between nerves and cancer cells, revealing that cancer cells can hijack mitochondria from neurons to enhance their metastatic capabilities, thus providing new therapeutic targets for cancer treatment [4][5][6]. Group 1: Research Findings - The study published in Nature identifies that cancer cells utilize tubular structures to steal mitochondria from neurons, which helps them withstand stress during metastasis [4][5]. - The research team observed a universal phenomenon of mitochondrial transfer between neurons and cancer cells, confirming that cancer cells with stolen mitochondria generate more energy [11][12]. - Experiments showed that cancer cells that had acquired mitochondria from neurons had a significantly higher survival rate when subjected to stress conditions, indicating the importance of mitochondrial transfer in cancer metastasis [12]. Group 2: Implications for Cancer Treatment - The findings suggest a need for further investigation into the mechanisms of nerve-cancer cell mitochondrial transfer and the development of targeted therapies to prevent cancer metastasis [15]. - The research provides a compelling metabolic explanation for the observed dependency of cancer cells on the nervous system, which could apply to a broader range of cancers [15].