Skip to main content
Fig. 5 | Journal of Hematology & Oncology

Fig. 5

From: Aging microenvironment and antitumor immunity for geriatric oncology: the landscape and future implications

Fig. 5

Potential risk factors for stromal cell senescence. Senescence can be induced in stromal cells with different signals from different avenues. Cancer cells can release cytokines and growth factors (IL-1α, TGF-β, CXCL1) that induce stromal cell senescence directly. Cancer cells can alternate TME via regulating metabolism, environmental stress, physical forces, and matrix disruption to indirectly induce stromal cell senescence. Different types of cancer therapy (i.e., chemotherapy, radiotherapy, immunotherapy, and personalized therapy) may have the possibility to induce paracrine senescence of cancer cell senescence and induce stromal cell senescence via DNA damage signal. Immune cell may emit diverse immune inflammatory factors to promote stromal cell senescence. Microbiota in the gut or TME can also cause stromal senescence by generating toxins and metabolites. The common cancer risk factors including alcohol, smoking, radiation, and genetic disease are associated with DNA damage signal to induce stromal senescence. Furthermore, other age-associated damage signals may arouse stromal senescence. TME, tumor microenvironment; CAFs, cancer-associated fibroblast (Mainly from https://doi.org/10.1016/j.trecan.2022.09.002)

Back to article page