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We found that 24 h after exposure to a single dose of UVB, the skin of Cbl-b−/− mice developed fewer SBCs and DNA dimers (Fig. 1c h).
However, after 24 h, the skin of Cbl-b−/− mice developed fewer SBCs compared to WT mice (i.e., 20 vs. 33 SBCs per microscopic field) (Fig. 1d, e).
In addition, it has been demonstrated that Cbl-b-deficient mice developed fewer UVB-induced skin malignancies by spontaneously rejecting tumor cells in a CD8+ T-cell and NK-cell dependent manner4,6,7.
The mice developed fewer and smaller colon tumors compared with control mice.
In a recent study, it was reported that while Il1r1−/− and Casp1−/− mice developed fewer tumors and had delayed tumor incidence compared to WT mice in a chemical-induced skin cancer model, Asc−/− mice had no discernible phenotype when compared to WT animals.
Despite the antioxidative function of Nrf2, we observed that ApoE−/− Nrf2−/− mice developed fewer plaques than ApoE−/− controls.
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Castrated male mice develop fewer liver tumors than intact males, whereas ovariectomized females develop more liver tumors than their intact counterparts (7, 9– 11).
Similar to our findings, another group also reported Smad3+/- mice develop fewer tumors than the wild-type mice during chemically induced skin carcinogenesis [ 25].
There might be an age component as p53+/− mice live longer than p53−/− mice, develop fewer lymphomas, and have a more complex tumor spectrum, although loss of the wild-type allele was common in p53+/− tumors, unlike our Δ122p53/mΔpro tumors.
However, as discussed earlier, the observation by Brouxhon et al. [ 46] that while EP2 null mice develop fewer tumors than wild-type mice, the tumors that do arise are more aggressive.
Animals with reduced KIT expression (e.g the W/W V mutant mouse) develop few ICC at the level of the myenteric plexus (IC-MY) in the small intestine [ 2, 3], and lose intramuscular ICC (IC-IM) in the stomach [ 4].
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