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These cells are more aggressive, basal like, with mesenchymal characteristics, and with most of the cells being similar, detection of differentially expressed markers is less likely.
E74-like factor 5 (Elf5) has now been identified as a marker of oestrogen receptor status, and high expression correlates with more aggressive basal cancers and resistance to anti-oestrogens.
From a literature search, there is evidence that some phosphoproteins have the potential to qualify as phosphopeptide plasma biomarker candidates for the more aggressive basal and also the luminal-type breast cancers [ 26].
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Amongst breast cancer subtypes we found that the stroma at the invasive region of the more aggressive Basal-like and Her2 tumor subtypes was the most heterogeneous and the stiffest when compared to the less aggressive luminal A and B subtypes.
Moreover, the CD44+/CD24- phenotype was found to correlate with the more aggressive basal-like subtype of breast cancer [ 10].
Higher levels of glycine have also been detected in pre-clinical studies of the more aggressive basal-like breast cancer model compared to the luminal-like model [ 43].
In the more aggressive basal-like tumor, GPC concentrations were higher than PCho concentrations, whereas this pattern was reversed in the luminal-like model.
In our study, TNBC has significantly higher Choline levels compared to TPBC, and this is in accordance with previous findings where higher Choline levels were detected in the more aggressive basal-like xenografts and TNBC patients as compared to the less aggressive luminal-like xenografts and ERpos/PgRpos breast cancer patients [ 12].
It has been previously observed that low dicer expression and high ago2 expression in breast cancer is associated with the more aggressive basal-like, HER2+ and luminal B subtypes (Blenkiron et al, 2007), which are known to be overrepresented in IBC (Van Laere et al, 2006).
It is more aggressive than basal cell cancer, the most common form of skin cancer, and it is more likely than basal cell cancer to spread.
An initial study by Zhao et al. [ 5] showed that miR-221/222 directly targeted ERα and that their overexpression in breast cancer contributed to progression of the more aggressive ER-negative basal phenotype in a subset of breast cancers.
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