Title : Increased growth-inhibitory and cytotoxic activity of arsenic trioxide in head and neck carcinoma cells with functional p53 deficiency and resistance to EGFR blockade.

Pub. Date : 2014

PMID : 24927258






9 Functional Relationships(s)
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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