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In light of these recent findings, and the fact that ILK activation and overexpression can promote oncogenic phenotypes in both cell-culture and transgenic mouse models [ 13], we have initiated in vivo experiments to determine whether ILK and Wnt signaling pathways interact to modulate tumor formation and progression.
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In ovarian cancer cells, 1a,25(OH)2D leads to G2/M cell cycle arrest through a p53-independent induction of GADD45, which modulates tumor formation [ 133].
Mutant p53 was also demonstrated to inhibit autophagy (113), a process shown to modulate breast tumor formation and development (114).
Functional study showed that miR-34a-HNF4G axis could modulate tumor cell viability, colony formation rate, and invasion.
Recent molecular studies have identified multiple factors that modulate tumor progression, invasion, and metastasis formation.
Very recently, using a very powerful spectrometric imaging system, Hu et al observed metabolic changes in a model of c-myc driven oncogenesis and they established that those metabolic changes preceded tumor formation and were modulated by inactivation of c-myc.
Genome-wide analyses have identified deregulated miRNA expression in human malignancies [ 149] and a potential dual role in tumor formation, highlighting that miRNAs can modulate oncogenic or tumor suppressor pathways, including p53, c-MYC, RAS, and BCR-ABL, while expression of miRNAs themselves can be regulated by oncogenes or tumor suppressors.
However, our loss and gain of function studies indicate that p190B has pro-tumorigenic actions and that it may facilitate tumor formation and progression in part by modulating Rac1 activity.
The oncogenic potential of cells can be modulated by adjacent cells in opposite directions, sometimes contributing to tumor formation [ 4, 27] and others impeding it [ 28, 29].
The finding that CXCR7 specifically scavenges CXCL12 suggests a critical function of the receptor in modulating the activity of the ubiquitously expressed CXCR4 in development and tumor formation.
We show that activation of NF-κB in macrophages in a mammary tumor tail vein metastasis model leads to a reduction in lung tumor formation with effects observed only when NF-κB is modulated prior to tumor cell introduction during the early seeding phase.
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