In a turn-around of sorts, it may be comforting to know that cancers can become addicted, too. Cancer cells have many different genetic changes, as well as changes in the expression of genes that are not due to mutations called epigenetic changes. Although cancer cells do have many differences from normal cells, they are still very similar to normal cells, making it very difficult to find treatments for cancers that don’t have serious side-effects.

Scientists, however, are beginning to identify genes that appear to be “Achilles heels” for cancers. It turns out that in many cases, reversing a defect in just one gene can have a profound effect on the growth of a cancer. Genes that promote cancer when mutated are called oncogenes, so this dependence on a particular genetic change in a cancer is called “oncogene addiction.” Often, treating these changes can be accomplished with little effect on normal cells, because the biology of cancer cells and normal cells has different wiring. So, a cancer cell may need to express a particular protein to keep dividing, while a normal cell might have other ways to keep going.

For instance, HER-2 is a receptor that is expressed on the surface of many breast cancers. HER-2 expressing cancers are often dependant on HER-2 to keep growing. This dependence is exploited in breast cancer treatments by an antibody drug, called Herceptin, which binds and inhibits HER-2.

Just as you can bring a cigarette smoker to their knees by taking away nicotine, so some cancers are tamed by taking away their favorite oncogene. Unfortunately, just like cigarette smokers who turn to other ways to cope, like caffeine or (more healthily) exercise, cancer cells can also escape their addictions, but that is another story…

MLL is not a nasty leukemia-causing protein. In fact, it is just the opposite. Cell division is somewhat like moving into a new apartment – all the DNA is still neatly packaged into moving boxes. By labeling genes immediately after division, MLL helps avoid potential errors in the operation of new cell.  Comparing cell division to Moving Day – all the DNA is still neatly packaged into moving boxes – it may become clear that labeling genes that are needed immediately may be a helpful trait to avoid hick-ups in a new cell’s operation. Just like labeling the moving box with the shampoo and the slippers might allow us to function efficiently at the evening of Moving Day. Just saying…

Elucidating MLL’s function adds to our knowledge about how information is being passed from one generation to the next. Mechanisms such as this operate on top of the genetic code and belong to a cell’s arsenal of epigenetics tricks. MLL confers information by sitting on genes that need to be activated, making sure the cell finds them quickly.

Mutated forms of MLL, however, can cause leukemia (among a slew of other troubles). Check out the story about another gene involved in chronic myeloid leukemia in Genes and Medicine at http://www.dnai.org/d/index.html.