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  1. 1941
    “…Previous reports have suggested a functional role for cancer-associated fibroblasts (CAFs) or senescent TC cells in the progression of PTC. In this study, we investigated the presence of CAFs and senescent cells in proprietary human TCs including PTC, PDTC, and ATC. …”
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  2. 1942
  3. 1943
    “…Our results demonstrate that the absence of FAP senescence after exercise leads to muscle degeneration with FAP accumulation. …”
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  4. 1944
    “…For NK cells, it is unclear if exhaustion, anergy, and senescence entail separate and distinct entities of dysfunction, though all are typically characterized by decreased effector function or proliferation. …”
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  5. 1945
    “…Cyclic cGMP-AMP synthase (cGAS) is a pattern recognition cytosolic DNA sensor that is essential for cellular senescence. cGAS promotes inflammatory senescence-associated secretory phenotype (SASP) through recognizing cytoplasmic chromatin during senescence. cGAS-mediated inflammation is essential for the antitumor effects of immune checkpoint blockade. …”
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  6. 1946
  7. 1947
    “…Telomere shortening rates must be regulated to prevent premature replicative senescence. TERRA R‐loops become stabilized at critically short telomeres to promote their elongation through homology‐directed repair (HDR), thereby counteracting senescence onset. …”
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  8. 1948
  9. 1949
  10. 1950
  11. 1951
    “…Lesions with driver mutations, including atypical nevi and seborrheic keratoses, are very common in dermatology, and are prone to senescence. The molecular events that prevent senescent lesions from becoming malignant are not well understood. …”
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  12. 1952
    “…In this study, we examined the influence of replicative senescence on the angiogenic potential of adipose-derived MSCs (ASCs). …”
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  13. 1953
    “…PML inhibition led to a remarkable growth arrest combined with features of senescence in vitro and in vivo. Mechanistically, the growth arrest and senescence were associated to a decrease in MYC and PIM1 kinase levels, with the subsequent accumulation of CDKN1B (p27), a trigger of senescence. …”
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  14. 1954
    “…We confirmed UVB-induced senescence with increased senescence-associated β-galactosidase positivity and changed expression of several senescence markers, including p21, p53 and Lamin B1. …”
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  15. 1955
  16. 1956
    “…Here, we show that MK2 inhibition strongly attenuated glioblastoma cell proliferation through p53(wt) stabilization and senescence. The senescence-inducing efficacy of MK2 inhibition was particularly strong when cells were co-treated with the standard-of-care temozolomide. …”
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  17. 1957
  18. 1958
    “…Using young to old‐aged human dermal fibroblasts, we observed a dysfunction of the mitotic machinery arising with age that mildly perturbs chromosome segregation fidelity and contributes to the generation of fully senescent cells. Here, we investigated mitotic mechanisms that contribute to age‐associated CIN. …”
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  19. 1959
    “…While oncogene-induced senescence (OIS) driven by excessive RAS/ERK signaling has been well studied, little is known about the mechanisms underpinning the AKT-induced senescence (AIS) response. …”
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  20. 1960
    “…Here, we review the current knowledge of the phenotypic and functional characteristics of senescent MSCs, molecular mechanisms underlying MSCs aging, and strategies to rejuvenate senescent MSCs, which can broaden their range of therapeutic applications.…”
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