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The risk factors relating to malignant formation of OPMDs were not well defined in previous studies.
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These events include CDKN2A deletion and MYC amplification in immortalization, HRAS activation in transformation, PIK3CA activation in the formation of malignant tumors, and RUNX1 deletion associated with poorly-differentiated malignant tumors.
These genetic changes include CDKN2A deletion and MYC amplification in immortalization, HRAS activation in transformation, PIK3CA activation in the formation of malignant tumors, and RUNX1 deletion associated with poorly-differentiated malignant tumors.
The involvement of non-malignant TSCs in the formation of the tumor vasculature suggested that normal and malignant tissues share the cellular mechanism of vasculature formation.
This led us to question whether recurrent vulvovaginal candidosis in the cancer patient is involved in the formation of malignant tumors of the genital tract.
Knockdown of EphA2 in malignant melanoma cells impaired formation of the VM network [29].
We conclude that long-term uncontrolled hVEGF-A165 expression in only a limited number of target cells in adult mice can be associated with pathological changes, including possible formation of malignant tumors and uncontrolled bleeding in target tissues.
So, it is concluded that upregulation of Bcl-6 in myeloma cells may protect the cells from apoptosis and idiovariability and thereby facilitate the formation of malignant clones.
In the present study, we showed that downregulation of miR-100 might play critical roles in the formation of malignant phenotypes by posttranscriptionally regulating PLK1 expression.
14-3-3epsilon 14-3-3epsilon 14-3-3epsilon 14-3-3epsilonesses, including cell cycle contregulatesiferation, and apoptosis, and plays a significant role in neurogenesis and the formation of malignant tumours.
Although the incidence is not so high, introduction of either c-erbB-2 or mutant Ha-ras into immortalized cells results in formation of malignant tumours.
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