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Hes1 transgenic mice develop thymic lymphomas at about 20 weeks of age with a low penetrance.
It is of some interest that p53 knockout mice develop thymic lymphomas.
24 Most irradiated Mlh1−/− mice develop thymic lymphomas before colon tumors arise, which makes it difficult to quantitatively assess the role of Mlh1 deficiency in colon carcinogenesis.
Mice develop thymic and lymphocytic lymphomas, Zymbal gland, lung and ovarian tumors, and myelogenous leukemias from chronic exposure to benzene (Cronkite et al., 1984, 1989; Farris et al., 1993).
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First, we observed that P1A Tg mice developed thymic leukemia after 7 months of age, particularly in immunocompromised mice.
We observed that immunodeficient host P1A transgenic mice developed thymic tumors after 7 months of age and had shorter survival rates compared to control groups.
Thus, p53−/− mice developed thymic lymphomas (66%), high-grade sarcomas (26%), B cell lymphomas (8%), as well as occasional adenocarcinomas (4%), teratocarcinomas (4%), mesothelioma, and medulloblastoma (Fig. 1D and Table 1).
Wild-type (wt) mice developed thymic lymphomas with a median survival of 181 days (d).
Almost one-third (28.6%) of ku70 −/− mice developed thymic tumors or disseminated lymphoma with splenomegaly and hepatomegaly (Table 1 and Supplementary Figure S1).
p53 knockout mice predominately develop thymic lymphomas, which are believed to result from failure of p53-induced apoptosis or cell cycle arrest, for which Puma and p21 are thought to be the most important transcriptional targets, respectively (Lane & Levine, 2010).
Somewhat surprisingly, Egle and Strasser independently presented that Puma/ p21 double-knockout as well as Puma/ Noxa double-knockout mice do not develop thymic lymphomas or any other cancers for that matter, which would be predicted if these are the most relevant targets for p53-mediated tumour suppression.
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