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Human prostate cancer is a complex heterogeneous disease characterized by the activation of multiple pathways contributing to its progression.
Co-expression of survivin and cyclo-oxygenase-2 may suggest multiple pathways contributing to the inhibition of apoptosis in gastric cancer.
Multiple pathways contributing to colorectal cancers were well established including adenoma-carcinoma sequence, inflammatory bowel disease-dysplasia-cancer, hyperplastic polyposis-intraepithelial neoplasia (IEN -cancer or juvenIEN -canceris-IEN-cancer as well as direct malignant transformation from normal mucosa (de novo) [ 1].
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Multiple pathways contribute to tumor angiogenesis including vascular endothelial growth factor (VEGF), fibroblast growth factor, and platelet-derived growth factor [2]. Based on the central role of VEGF in tumor angiogenesis and growth, it has emerged as a promising therapeutic target for angiogenesis inhibition [3].
A few studies have proposed that multiple pathways contribute significantly to total human PCB exposure.
Given that multiple pathways contribute to tumor growth, it is conceivable that anti-tumor activity may be increased by agents targeting multiple pathways [ 26- 28].
This residual risk can be attributed to the fact that multiple pathways contribute to platelet activation, and aspirin and P2Y12 ADP receptor antagonists each inhibit only one of these pathways (the thromboxane A2 and ADP pathways, respectively).
The goals of this research, therefore, were to assemble, characterize, and annotate the fruit transcriptome of M. dubia in order to reconstruct metabolic pathways and determine if multiple pathways contribute to AsA biosynthesis.
These data suggest that immune dysregulation involving multiple pathways contributes to SLE pathogenesis.
The complementary mechanisms of action of an angiotensin receptor blocker, calcium channel blocker, and diuretic result in each agent targeting a separate pathway and provide coverage for multiple different pathways contributing to hypertension [ 14, 25, 35].
Taken together in these experiments we show that Hsp70s, in particular Hsc70, are involved in multiple oncogenic pathways contributing to MM survival and targeting the Hsp70s for therapy could be useful clinically.
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