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Down Regulating Mutant p53 Protein
In breast cancer cell lines quercetin was able to minimize the expression of mutant p53 protein to insignificant levels. By minimizing the expression of p53 the cells were stopped at the G2-M cell cycle check point.

G1 Phase Arrest
Cellular proliferation has many sites of control, one if which is the G1 cell cycle checkpoint. In human leukemic T-cells quercetin was able to stop the cells at the G1 checkpoint. Not only was this stop at the G1 checkpoint seen in leukemic t cells but it was also seen in gastric cancer cells treated with quercetin. However when the gastric cell line had the quercetin removed the cells were able to continue through the cell cycle.

Tyrosine Kinase Inhibition
Tyrosine kinases are involved with the transduction of growth factor signals to the nucleus. Patients that had advanced cancers were given quercetin intravenously suppressing the activity of lymphocyte tyrosine kinase in some patients for as long as 16 hours. Furthermore, in vitro studies have had similar results in non-malignant cells and in rat mammary tumor cells. It is possible that in oncogenesis tyrosine kinase expression has some contribution to the ability of cells to bypass the normal regulatory growth control. Drugs that target tyrosine kinase activity are thought to be possible antitumor agents that do not have the regular cytotoxic effects that are seen in chemotherapy. Quercetin was the first such compound to be tested in a human phase I trial.

Inhibition of Heat Shock Proteins
Quercetin is able to inhibit production of heat shock proteins in many malignant cell lines such as breast cancer, leukemia, and colon cancer. Heat shock proteins allow tumor cells to bypass normal mechanisms of cell cycle arrest by forming a complex with mutant p53 and allows for an increased survival rate of cancer cells under different bodily stresses such as low circulation and high fever.

Inhibition of Expression of Ras Proteins
Quercetin inhibits the p21-ras oncogene from being expressed in cultured colon cancer lines. Mutations in Ras do not allow cellular GTP-ase to function properly by repeatedly activating the signal for DNA replication. Mutations of Ras proto-oncogenes are found in more than 50% of colon cancers and in other cancers as well.

Radiotherapy
An in vitro study showed a small improvement of the cytotoxic effect of radiation on rat hepatoma cells when quercetin was added. In a human study quercetin was given to the patient orally and topically to reduce skin damage during radiotherapy in patients who had head and neck cancers.

Chemotherapy
Quercetin showed improvements on the efficiency of cisplatin treatment both in vivo and in vitro. In mice with human tumor xenografts, an intraperitoneal treatment with quercetin and cisplatin greatly reduced tumor growth while treating the xenografts with solely quercetin or solely cisplatin did not work as well as when they were used together. Another in vitro study using human ovarian and endometrial cancer cell lines showed that adding quercetin to cisplatin caused an increased cytotoxic effect of cisplatin. Quercetin was able to protect normal renal tubular cells from cisplatin toxicity. Another in vitro study with human leukemia cell lines showed quercetin working with busulphan against these cells. Adriamycin treatment with quercetin showed a dose-dependent increase in cytotoxicity. Quercetin has also been shown in vitro to increase the cytotoxic effect of cyclophosphamide and a decreased resistance to gemcitabine and topotecan.

In vivo Studies
There has only been one phase of a quercetin trial in advanced cancer patients who had stopped responding to chemotherapy. The results from this trial however did not meet the World Health Organization definition of a tumor response. In a study that used rodents, it was confirmed that quercetin that is administered orally is turned into quercetin conjugates before it enters the plasma and starts accumulating.