A study by the Cancer Research Institute 'Dana Farber' launches the hypothesis that cancer stem cells - a small number of cells in a self-regenerating tumor - are responsible for the development and recurrence of cancer, and eliminating these cells would could cure the disease.
The researchers revealed in the March issue of the publication 'Cancer cell' that they identified two groups of cancer cells, genetically distinct, in breast cancer tumors. One of these groups contains cells that scientists believe are stem cells, found in breast cancer. "If the cells that cause breast cancer come from a single cancer cell, the disease could be treated with only one drug," says Dr. Kornelia Polyak, lead author of the study.
"However, our findings suggest that tumor cells come from a stem cell, similar to stem cells, which then have a genetic deviation, so both types of cells should be treated." The results show that both cell types and probably others are involved in the development of breast cancer. While analyzing the genetics of each cell type, the researchers found that the so-called 'cancer stem cells' were driven on a molecularly activated pathway, which makes them resemble normal stem cells. Women suffering from breast tumors, formed from the so-called 'cancer cells' are at higher risk of cancer recurrence.
Looking at the optimistic side of things, the abnormally activated pathway of these cells, also known as TGF-Beta1, can be blocked with the experimental drugs being tested now, says Polyak, who is also a professor at Harvard Medical School. These inhibitors, combined with other drugs, can improve the prospects of treating cancer caused by these cells.
Considering the cancers encountered so far, this disease arises from the development of normal cells, which undergo mutations and form a complex cancer cell tumor.
Lately, there has been an increased interest in alternative explanations for the occurrence of cancer - more and more people believe that tumors are caused by a single stem cell that suffers from a deviation, for example, in breast tissue, and results in a group of cancer cells. genetically identical. Furthermore, more pathways and genes needed for normal stem cell function are activated in cancer cells and play an essential role in tumor development. According to the theory regarding cancer stem cells, the few self-regenerating cells of this kind are difficult to destroy, and their resistance may explain why they reappear after being treated.
In 2003, the researchers realized what it is about stem cells found in patients' tumors. A distinct molecule, or marker, from the cell surface, also known as CD44 +, was identical to the marker in normal breast tissue cells. When CD44 + was injected into a guinea pig with a deficient immune system, they demonstrated the ability to initiate cancerous tumors. The researchers also found that certain cells were tightly bound to the CD24 + marker and are supposed to come from CD44 + cells.
Dr. Polyak and Dr. Michail Shipitsin used gene activity analysis to establish the relationship between the two cell types. They performed a genetic inventory consisting of CD24 + and CD44 + purified cells from healthy breast epithelium, chest fluid and invasive tumor samples collected from breast cancer patients. The findings show that CD24 + cells were very similar to CD44 + cells, but not always genetically identical.
These could have been identical if the CD44 + cells had been true stem cells and CD24 + had come from them. Even though CD44 + cells appear to contain more stem cells as markers, the genetic difference between CD24 + and CD44 + in a tumor casts doubt on the validity of the hypothesis that stem cells cause breast cancer and warns the involvement of clonal evolution in intra-heterogeneity. tumor, write the authors. The team led by Polyak discovered that, in fact, CD44 + cells were those driven by the TFG-Beta 1 active pathway, and not those of the CD24 + type.
For this reason, they stated that 'tumors composed mostly of CD44 + may manifest clinically worse than tumors composed of CD24 + cells, and these patients may benefit from therapy targeting the TFG-Beta 1 pathway' .
16 March 2007