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The WASP protein in patient T cells could have been transcribed primarily from a single allele if most somatic mutations persisted in cells and were only occasionally transcribed.
Most somatic mutations in cancers are thought to be "passenger" events that do not contribute to cancer development.
Most somatic mutations in cancer cells arise due to genomic instability and do not contribute to tumorigenesis.
Most somatic mutations of the EGFR gene observed in NSCLC involve the tyrosine kinase coding domain (exons 18 21).
Although there exist well-described mutations in certain codons of key genes that drive oncogenesis, most somatic mutations in cancer are neutral with respect to overall cell fitness.
Despite the fact that there was no particular hot spot identified, most somatic mutations were localized in exons 4 8 of TP53.
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Most somatic TP53 mutations occur in patients with the triple negative (TN) or human epithelial growth factor receptor 2 (HER2) subtypes (TN: tumors without expression of the estrogen and progesterone receptors and lacking overexpression of HER2 (ErbB2); HER2: tumor with overexpression of HER2 [ 16].
The most frequent somatic mutations and Ig gene joints were then introduced into an engineered single-chain Fv (scFv) that expressed the germline-encoded VH and VL amino acid sequences.
FLT3-ITD mutations are among the most common somatic mutations in AML occurring in 20 35% of adult [4] [10] and ∼5 15% of pediatric [11] [13] AML.
Like most oncogenes, somatic mutations of BRAF are thought to be heterozygous in tumors.
Recent whole genome analysis demonstrated that TP53 gene mutation is one of the most frequent somatic mutations in breast cancer.
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