Cancer, we are told, is a disease of the genes. It originates in mutations in the DNA. But a paper published by a Weizmann Institute group in Cell Reports flips that idea sideways by about 90 degrees: For at least some types of the disease, the healthy, non-mutated version of a gene is no less of a driving force behind the development of cancer than its mutated form.
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Surprising Behavior of Transcription Factors Challenges Theories of Gene Regulation
How cells develop and the diseases that arise when development goes wrong have been a decades-long research focus in the laboratory of Distinguished Professor of Biology Ellen Rothenberg. In particular, the lab studies the development of immune cells known as T cells, which act as “intelligence agents”-they circulate throughout the body, detect threats, and determine what kind of response the immune system should make. However, when the many stages of T cell development do not occur perfectly, leukemia occurs.
“Many of the genes that we study in normal developing T cells are the same genes that, when regulated incorrectly, lead to the cells becoming T-cell leukemia,” says Rothenberg. “Understanding the precision of this process is really important. There’s also an interesting aspect of irreversibility: Some of the genes we study only have activity at a specific time period in