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Mutation and activation strategies have been deployed at large scales in rice and other species.
There is a latent danger in insertion mutation and activation of oncogenes in human being using retroviral vector system [ 24].
During the progression of prostate cancer, various alterations of AR signaling have been identified including AR amplification, mutation, and activation by other signaling pathways.
The PI3K/Akt/mTOR pathway is activated in pancreatic cancer by overexpression or activation of EGFR and insulin-like growth factor (IgF1R), by PTEN loss or secondary to k-ras mutation and activation of the Ras/Raf/MEK pathway.
In CMT few studies have examined the expression of c-kit suggesting that c-kit mutation and activation may be involved in the pathogenesis of these tumors [ 25– 27].
Previously, mutation and activation of epidermal growth factor receptor (EGFR) have been determined in a variety of solid tumours, including breast, head and neck, non-small-cell lung, gastric, colorectal and pancreatic cancers and mostly associated with a poor prognosis [ 8, 9].
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Men with prostate cancer may be initially responsive to androgen receptor (AR) inhibitors, but in some patients, single-cell RNA-seq of individual CTCs detected heterogeneity in the expression of AR gene mutations and activation of non-canonical (β-catenin-independent) Wnt signaling, which may promote invasiveness and malignant progression, thereby contributing to treatment failure [77].
These genes and pathways include TP53, BRCA1/2, PIK3CA, and PTEN mutations and activation of PI3K/AKT and RAS/RAF/MEK signaling pathways.
In our study, we did not observe an association between PIK3CA mutations and activation of downstream proteins like mTOR and p70S6K.
Mutations and activation of these genes may drive carcinogenesis [ 39], and increased expression is associated with a poor prognosis in NSCLCs [ 40- 43].
Tumor progression is a complicated biological process that comes with enormous genetic and molecular changes, such as chromosome aberration, gene mutations, and activation or inhibition of transcriptional pathways.
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