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Mounting evidence now connects several neurological disorders with CAMs, as many mutations or aberrant expressions of CAMs are associated with neurological disorders.
Although it is well-established that the pathogenesis of PDAs follows stepwise stages that display increasing cellular atypia and accumulate clonal mutations or aberrant expression of oncogenes or tumor suppressor genes such as K-Ras, p16, p53, and DPC4/SMAD4 [2], drugs that target these molecular abnormalities have not yet translated into improved clinical responses [3].
However, these genes are rarely inactivated by mutations or aberrant promoter methylation.
Tyrosine kinase inhibitors (TKIs) have been used to treat the cancer harboring EGFR mutations or aberrant activation of EGFR.
However, during tumorigenesis there is often constitutive activation of PTKs due to activating mutations or aberrant growth factor or cytokine signaling.
Mutations or aberrant expression of canonical Wnt pathway components, have been identified to promote deregulation of β-catenin-responsive genes affecting cell differentiation and apoptosis, and are thus responsible of tumor initiation and progression.
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Mutation or aberrant inhibition of the TSC complex is common in various human tumor syndromes and cancers.
Mutation or aberrant gene expression may therefore result.
Mutation or aberrant BUB1 expression is associated with chromosomal instability, aneuploidy, and human cancer [ 43].
TAA comprise a range of self‐derived proteins rendered immunogenic in tumors either by mutation or aberrant expression.
Taken together, these results suggest that limited or no presence of functional Smad4, TβR-I or TβR-II, due to mutation or aberrant expression, may contribute to loss of TGF-β growth inhibition in a small percentage of breast carcinomas.
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