Pub. Date : 2014
PMID : 24927258
9 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | Increased growth-inhibitory and cytotoxic activity of arsenic trioxide in head and neck carcinoma cells with functional p53 deficiency and resistance to EGFR blockade. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
2 | The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
3 | The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
4 | The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
5 | RESULTS: Functional rather than structural defects in the p53 gene predisposed tumor cells to increased sensitivity to ATO. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
6 | Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
7 | Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
8 | The inhibitory effect of ATO in p53-deficient tumor cells was mainly associated with DNA damage, G2/M arrest, upregulation of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptors and apoptosis. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
9 | CONCLUSIONS: Addition of ATO to treatment regimens for p53-deficient SCCHN and tumor recurrence after cetuximab-containing regimens might represent an attractive strategy in SCCHN. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |