Key Gene Plays Crucial Role in Malignant Transformation

February 1, 1997
Oncology, ONCOLOGY Vol 11 No 2, Volume 11, Issue 2

A major gene essential for controlling the synthesis of hereditary material and cell proliferation is also critically involved in determining the extent of malignant growth of cancer cells, reports a study published in a recent issue of the Proceedings of

A major gene essential for controlling the synthesis of hereditary materialand cell proliferation is also critically involved in determining the extentof malignant growth of cancer cells, reports a study published in a recentissue of the Proceedings of the National Academy of Sciences.

According to the new study, early cancer cells interacting with theR2 gene became highly malignant, producing tumor-like colonies and metastatictumor growth.

The study, performed at the Manitoba Institute of Cell Biology (MICB)at the University of Manitoba in Winnipeg, Canada, confirms the R2 geneas a key determinant of malignancy, say researchers, and suggests the greattherapeutic potential of two new cancer-fighting treatments that specificallytarget this gene.

The developer of these treatments, Dr. Jim A. Wright, chief researcherin the MICB study, said he believed it constituted "a vital step forward"in the understanding of the specific genetic factors responsible for producingaggressive malignant tumor growth. "We believe our discoveries willnot only help us in improving our understanding of cancer progression,"he said, "but also in refining chemotherapy and gene therapy treatmentsthat directly modify gene expression and interfere with disease relatedmolecular pathways."

In cooperation with Dr. A. Young of GeneSense Technologies, a drug researchcompany in Winnipeg, Dr. Wright has developed two compounds designed toact against the R2 gene, minimizing its ability to promote tumor cell growth.These therapies, he said, are designed to keep abnormal cells at a precancerousstage or in a localized, slow-growing tumor where they can be more effectivelytreated.

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