Sentence examples for multiple cancer phenotypes from inspiring English sources

Excessive insulin action associated with insulin resistance is thought to progress these multiple cancer phenotypes.

Altered AKAP activity is implicated in many pathological processes including cardiovascular disorders, immune diseases, and multiple cancer phenotypes.

The hypomethylation and/or transposition of LINE-1 elements during carcinogenesis have been suggested to alter the transcriptome [ 12] and to play a role in the acquisition of multiple cancer phenotypes including invasion and metastasis.

Once activated, these signaling pathways may stimulate multiple cancer phenotypes including proliferation, protection from apoptotic stimuli, invasion, and metastasis, potentially enhancing promotion and progression of many types of cancer cells.

In addition, identifying individual miRNAs that regulate multiple cancer cell phenotypes such as anoikis resistance and metastasis will allow the development of a more potent miRNA based drug.

The altered expression of one miRNA can regulate the expression of multiple target genes and modulate multiple cancer cell phenotypes, such as motility, invasion, resistance to anoikis and metastatic colonization.

The Wnt pathway can modulate multiple breast cancer phenotypes including proliferation (9-11), migration (6) and stem cell fitness (12).

In this manuscript we explore the interrelation of different stress phenotypes in multiple cancer types and ask if these phenotypes could be used to explain prognostic differences among tumor samples.

BI-69A11 can suppress wound healing, angiogenesis (CAM assay), tumour cell invasion (Boyden chamber assay) and tumourigenesis in vivo in an animal model indicating multiple targets for inhibiting cancer phenotypes that are regulated by Akt pathway activation.

Previously, NHE1-mediated intracellular alkalinization has been proposed to play a role in cancer cell growth because it has been shown that an increased pHi of tumor cells is associated with increased in vivo tumor growth, DNA synthesis, and cell-cycle progression, suggesting that an overexpression of NHE1 contributes to the transformed phenotype of multiple cancer cells.

Using SLEA we are able to find relationships between stress phenotype pathways across multiple cancer types.