New research at Washington University could redefine cancer treatment.

Researchers at the School of Medicine recently discovered the secrets of an enzyme that may lead to new, more effective ways of treating and curing cancer patients.

In a groundbreaking report recently published in the Journal Molecular and Cellular Biology, the researchers report that the enzyme MOF contributes to the development of tumors and may be susceptible to radiation treatment.

The discovery dramatically alters the perception of the scientific community regarding the enzyme and opens new avenues for pursuing potential cancer treatments.

“We have challenged one of the greatest dogmas in cancer field,” said Dr. Tej Pandita, a professor of radiation oncology and genetics. “Depletion of MOF results in cell growth inhibition. Over-expression of MOF results in enhanced oncogenic transformation and tumor growth.”

MOF provides critical instructions for cellular structure and dictates the activity level of genes within DNA strands throughout the body, and cells without MOF cannot survive.

The researchers state in their study that they first became interested in the enzyme because of its various proven critical effects.

“Recent studies have shown that depletion of [MOF] in human cell lines leads to genomic instability, spontaneous chromosomal aberrations, cell cycle defects, [and] altered nuclear morphology,” read the study.

Past studies had also indicated that a lack of a tag created by MOF is typical of cancer cells. However, the researchers at the School of Medicine reviewed hundreds of tumors and found that they contained relatively high levels of MOF.

After increasing the amount of MOF in tumor samples in mice, the tumors grew faster.

“Tumor cells with higher levels of MOF had faster initial growth as well as immediate regrowth of tumors post-irradiation exposure,” stated the study.

The researchers discovered that cells with less of the enzyme are more susceptible to radiation. Pandita hopes that finding MOF inhibitors will enhance treatment options for cancer patients.

“It could be the Achilles’ heel of cancerous growth,” said Pandita. “[This research] is exciting as it opens areas which can be used for therapeutic purposes.”

The researchers now plan to identify the other components of cells that MOF influences. Pandita hopes to use the research to make cancerous cells more vulnerable to radiation therapy.

“If we affect MOF in tumor cells, they will be weakened and unable to recover after radiation exposure,” said Pandita.

The study is also the first extensive report to demonstrate that MOF is necessary for cell proliferation during embryonic development. Though the researchers note that the precise role of the enzyme in embryogenesis is unclear, they did discover that stem cells in the embryos of laboratory mice grew faster with high amounts of MOF.

Because both stem cells and cancer cells develop faster when more MOF is present, the researchers note the possibility that cancer cells are in fact malfunctioning stem cells.

“Evidence is accumulating to suggest that cancer cells could be considered aberrant stem cells,” said Pandita.

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