While research on cancer development is traditionally focusing mainly on the neoplastic cell per se, nowadays the role of tumor stroma in this process is indisputable. The stroma - mainly composed of extracellular matrix (ECM) - is a source of mediators and signals originating from heterotypic cell-cell and cell-matrix interactions that steer the progression of the disease in a context- and a cancer type-dependent manner. With advancing age the stroma exhibits alterations, important being the accumulation of senescent cells. Senescence is often triggered by exogenous stresses, including genotoxic anticancer treatment modalities (such as chemotherapy or radiotherapy) and is manifested as an inhibition of cell proliferation, ascribing to cellular senescence the role of a potent antitumor barrier. On the other hand, senescent cells, through their specific senescence-associated secretory phenotype (SASP) - comprising cytokines, growth factors, ECM components and ECM-degrading enzymes - can establish an immunosuppressive, inflammatory and catabolic microenvironment that may stimulate tumor growth and metastasis. Given that the persistent presence of senescent cells could prove detrimental for tissue homeostasis, inclusion of a senotherapeutic arm in novel anticancer approaches seems compulsory.

传统上，癌症发展研究主要集中在肿瘤细胞本身上如今，肿瘤基质在这一过程中的作用是无可争议的。基质主要由细胞外基质（ECM）组成，是中介物和信号的来源，其源于异型细胞-细胞和细胞-基质的相互作用，以与环境和癌症类型相关的方式指导疾病的发展。随着年龄的增长，基质表现出改变，重要的是衰老细胞的积累。衰老通常由外源性应激触发，包括遗传毒性抗癌治疗方式（例如化学疗法或放射疗法），并表现为对细胞增殖的抑制，这归因于细胞衰老是有效抗肿瘤屏障的作用。另一方面，衰老细胞通过其特定的衰老相关分泌表型（SASP）-包括细胞因子，生长因子，ECM成分和ECM降解酶-可以建立免疫抑制，炎症和分解代谢的微环境，可能刺激肿瘤的生长和转移。考虑到衰老细胞的持续存在可能对组织动态平衡有害，因此在新的抗癌方法中纳入一个治疗臂似乎是强制性的。