Our repair functions stop doing their job well as part of senescence. Increasing the chance and speeding up the development of tumors.

Those repair functions working better than normal is one of the hallmark signs of cancer, specifically telomerase being reactivated. Senescence is anti cancer, not pro cancer. You know those HeLa cells that are immortal? Cancer cells. Having a time limit or replication limit on cells through senescence is a great way of limiting tumors.

The two barriers to proliferation—senescence and crisis/apoptosis—have been rationalized as crucial anticancer defenses that are hard-wired into our cells, being deployed to impede the outgrowth of clones of preneoplastic and frankly neoplastic cells. According to this thinking, most incipient neoplasias exhaust their endowment of replicative doublings and are stopped in their tracks by one or the other of these barriers. The eventual immortalization of rare variant cells that proceed to form tumors has been attributed to their ability to maintain telomeric DNA at lengths sufficient to avoid triggering senescence or apoptosis, achieved most commonly by upregulating expression of telomerase or, less frequently, via an alternative recombination-based telomere maintenance mechanism. Hence, telomere shortening has come to be viewed as a clocking device that determines the limited replicative potential of normal cells and thus one that must be overcome by cancer cells.

https://www.cell.com/cell/fulltext/S0092-8674(11)00127-9