Received truth turned on end in cancer research


This release is also avaialable in Swedish.

It has long been the accepted view of cancer researchers that there is a difference between the mechanism behind the development of leukemias, on the one hand, and solid tumors like breast cancer, prostate cancer, gastrointestinal cancer, etc, on the other. A research team at the Section for Clinical Genetics at Lund University is now claiming just the opposite: the same mechanism gives rise to all non-hereditary forms of cancer. These findings are being published in Nature Genetics.

A well-known mechanism for the development of cancer is that the chromosomes in a cell break apart and then recombine in an incorrect way. At the points of fissure, gene fragments are exposed that can recombine with so-called fusion genes, yielding fusion proteins. Leukemias-­blood cancer­-normally develop from cells that contain such fusion proteins. It is not known how this occurs in detail, but in some way the fusion proteins prompt formerly normal cells to transform into cancer cells. On the other hand, solid tumors, which make up the majority of all cancer cases, have been seen as developing as a result of certain cells losing the inhibiting mechanism in the form of so-called tumor suppressor genes that keep tumors from arising.

"This is no doubt correct in regard to hereditary cancer. But hereditary cancer accounts for only 5-10 percent of all cancer cases. We now maintain that all of the others have the same developmental mechanisms. In non-hereditary cancer forms it is the occurrence of fusion genes and not the lack of tumor suppressor genes that is essential," says Professor Felix Mitelman.

Mitelman and his associates Bertil Johansson and Fredrik Mertens have gathered information about aberrant chromosomes in cancer for years. In 1997 Nature Genetics devoted an entire issue to the large material the Lund team had compiled, something that has only happened on one other occasion (when the human genome was presented). This material is now available as a large and constantly growing database in the so-called Cancer Genome Anatomy Project at the US National Cancer Institute, called the Mitelman Database of Chromosome Aberrations in Cancer.

In leukemia cells it is rather easy to find fusion genes and fusion proteins. For technical reasons, this is much more difficult in solid tumors.

"And if you haven't seen them, you assume that they're not there. But what has been lacking is appropriate methods of examination," claims Felix Mitelman.

The research team has found that the number of fusion genes in solid tumors stands in the same proportion to the number of patient cases examined with leukemias. This shows that the same mechanisms are involved: the chance of this match being coincidental is less than 0.0001.

The good thing about this discovery is that it should lead to more effective treatment of the major cancer forms. For one type of leukemia, at any rate, there is a medicine that specifically targets the active fusion protein, and it is both effective and mild.

The downside is that there are probably a very great number of different fusion genes behind the major forms of cancer. Each transformation of genes is found in just a few patients.

"Small groups of patients are not of interest to pharmaceutical companies. On the other hand, it may be that several fusion proteins have common traits that make it possible to use the same drug to combat them," hopes Felix Mitelman.

The fact that his research team have now turned on end an established truth does not mean that other ongoing research on the significance of genetic factors in the emergence of cancer has also been overturned, he emphasizes. Much of this research is about the long road from the first cancer cell to a full-blown tumor, and in this process tumor suppressor genes are probably of great importance. What the Lund team has done is to provide a revolutionary new picture of how this very first cancer cell arises.

Source: Eurekalert & others

Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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