众所周知，衰老与癌症有关，同样，癌症幸存者也会加速衰老。随着老年人和癌症幸存者数量的持续增长，引起了全社会的更多关注。因此，揭示组织衰老的分子机制对于开发有效的疗法来对抗癌症幸存者和癌症患者的衰老和癌症疾病至关重要。事实上，细胞衰老是一种关键反应，或者是抑制正常细胞向癌细胞转变的天然屏障，然而，维持干细胞生态位的生理所需的缺氧会因衰老而增加，并抑制组织的衰老。有趣的是，缺氧或缺氧可以延长人类的寿命并减缓衰老过程，但缺氧也可以促进血管生成，从而促进癌症进展。此外，癌症治疗被认为是导致细胞衰老的主要原因之一，随后加速衰老。最近的一些临床试验评估了消除衰老细胞的抑制剂。然而，一些衰老机制通常也会阻止癌细胞的生长和进展，这可能需要谨慎的策略才能获得更好的临床结果。在这里，我们描述了癌症患者和癌症幸存者中 DNA 损伤和缺氧信号通路串扰中衰老和癌症的分子调节。我们还更新了几种可能对逆转癌症治疗相关的衰老过程至关重要的治疗策略。版权所有 © 2024。由 Elsevier Ltd 出版。

It is well documented that aging is associated with cancer, and likewise, cancer survivors display accelerated aging. As the number of aging individuals and cancer survivors continues to grow, it raises additional concerns across society. Therefore, unraveling the molecular mechanisms of aging in tissues is essential to developing effective therapies to fight the aging and cancer diseases in cancer survivors and cancer patients. Indeed, cellular senescence is a critical response, or a natural barrier to suppress the transition of normal cells into cancer cells, however, hypoxia which is physiologically required to maintain the stem cell niche, is increased by aging and inhibits senescence in tissues. Interestingly, oxygen restriction or hypoxia increases longevity and slows the aging process in humans, but hypoxia can also drive angiogenesis to facilitate cancer progression. In addition, cancer treatment is considered as one of the major reasons that drive cellular senescence, subsequently followed by accelerated aging. Several clinical trials have recently evaluated inhibitors to eliminate senescent cells. However, some mechanisms of aging typically can also block cancer cell growth and progression, which might require careful strategy for better clinical outcomes. Here we describe the molecular regulation of aging and cancer in crosstalk with DNA damage and hypoxia signaling pathways in cancer patients and cancer survivors. We also update several therapeutic strategies that might be critical in reversing the cancer treatment-associated aging process.Copyright © 2024. Published by Elsevier Ltd.