WASHINGTON, June 11 (Xinhua) -- The presence of normal p53, a tumor suppressor gene, instead of a mutated version, makes breast cancer chemotherapy with doxorubicin less effective, according to a study published Monday in the Journal Cancer Cell.

In this study, doxorubicin-treated p53 mutant tumor cells did not stop cell proliferation, leading to abnormal mitoses and cell death, whereas tumors with normal p53 arrested, avoiding mitotic catastrophe.

The scientists first examined the response to doxorubicin in mice with mammary tumors and the role of p53 in the chemotherapy process. When they analyzed the results, they found the mice that responded poorly to treatment had normal p53 genes, while the mice that responded best had mutated p53 genes. Using human breast tumor cell lines with normal p53, the researchers then replicated the mouse experiment with the same results.

"It's really important to understand the genetic defects a tumor cell has before we treat it," said lead author Guillermina Lozano, a professor at the Texas-based M.D. Anderson Cancer Center. "What we learned here is the complete opposite of what we expected. We thought tumors would respond better to treatment if the p53 gene were normal. But the opposite was true, and for a really interesting reason."

The tumor suppressor p53 is mutated or inactivated in the majority of cancers, and about one-third of breast cancers have mutations in the gene. It has long been thought that normal p53 results in a better chemotherapy response, but the evidence in breast cancer has been conflicting.

According to the U.S. National Cancer Institute, about 227,000 women in the United States are diagnosed with breast cancer each year.