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p53 is mutated in over 50% of colorectal tumours, and the mutational status of this tumour suppressor has been shown to increase or decrease tumour sensitivity to a number of chemotherapeutic agents.
Many animal models of colorectal cancer are based on mutations in the Apc (adenomatous polyposis coli) gene, which is mutated in over 80% of colon cancers in humans (Fearnhead et al., 2001).
This model is of preclinical utility, as the APC gene is mutated in over 80% of human cancer and human germline APC mutations are a cause of familial adenomatous polyposis.
Recent whole-exome sequencing efforts have revealed that the genes encoding subunits of mSWI/SNF complexes are mutated in over 20% of cancers, spanning a wide range of tissue types.
p53 is an important tumor suppressor gene and is mutated in over 50% of human cancers.
For example, the BRAF oncogene is mutated in over 60% of melanomas (3).
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The immunoglobulin variable heavy chain (IgVH) gene profile is mutated in 80%% of cases, with over-represented use of VH3 26 and VH4 34.
TP53 is one of the genes most frequently mutated in cancer, with inactivating mutations present in over 50% of patients with solid tumors.
When the same gene was expressed in an Arabidopsis mutated in a DGAT gene, seeds with over 60% of these TAG molecules were obtained (Timothy Durrett, MSU, personal communication).
Indeed, this codon, rarely mutated in most cancers, accounts for over 2% of all breast cancer mutations.
KRAS is mutated in 10% 30% of lung carcinomas and over 95% of all activating mutations in KRAS are located in exon 1 (codons 12 and 13) [29], [29].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com