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The high interaction regions may drive breast cancer development and progression.
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Aberrant FGFR pathway amplification may drive some breast cancers.
Our studies suggest that nuclear bFGF may drive TN breast cancer resistance in a manner independent of angiogenesis.
We propose that PR acts as a sensor for activated mitogenic protein kinases (that is, MAPKs and CDK2) frequently elevated in human breast cancer; under the influence of elevated Ser294 phosphorylation, genes that are sensitive to (that is, normally repressed by) PR SUMOylation may instead cooperate to drive breast cancer cell proliferation and pro-survival signaling.
The chromosomal instability associated with unchecked telomere dysfunction can drive breast carcinogenesis in vivo in telomerase-deficient mice, suggesting that telomere-based crisis in humans may similarly enhance rates of epithelial tumorigenesis.
Experiments in telomerase-deficient mice have shown that such unchecked telomere dysfunction can drive breast carcinogenesis.
Thus, we hypothesized that PI4KIII β may drive filopodia formation in breast cancer cells, potentially enhancing their invasivenes.
These 2 studies indicate that low BECN1 expression may drive particular lung and breast cancer subsets toward squamous, rather than adenocarcinoma, histologies, thus also raising the possibility of concurrent EGFR activation.
By this mechanism, IL-6 may drive the basal-like (hormone receptor negative) breast cancer phenotype (76).
In addition, the sequencing of breast cancer patient genomes suggests that infrequent mutations may drive tumor progression through known signaling pathways, such as the Raf MEK1/2 ERK1/2 cascade [ 5].
It is implied that oestrogen may drive cellular responses that are growth factor dependent via GPR30 in ER-negative breast tumours [ 10].
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