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An international study led by scientists from the Crick Institute in London and the Hebrew University of Jerusalem has revealed the survival mechanism siftage in cancer cells, and even after aggressive treatment, the disease can erupt again. In a paper published in Science (LINK
, researchers describe the mechanism by which cancer tumor cells become cancer stem cells that sustain long-term growth.
as cancer develops, the resulting cells are not biologically uniform in their biological properties and contribute differently to tumor development.
only a small percentage of cancer cells can form new tumors or metastasis, known as "cancer stem cells." this difference
tumor cells poses a major challenge in understanding the nature of tumors, their sensitivity to drugs, and planning for effective treatment of all tumor cells. Professor Eran Meshorer, director of the Stem Cell and Epigenetics Laboratory at the
Institute for Life Sciences, said: "Many chemotherapy drugs leave a small amount of cancer stem cells, causing the disease to re-emerge in a few years.
therefore, it is important to identify cancer stem cells in tumors and to characterize differences between different tumor cells as a basis for detection of weaknesses in disease development".
cancer stem cells are not limited to the tumor itself, they can re-engage in a healthy environment and stimulate the disease.
to study the characteristics of these unique cells, Professor Meshorer and PhD student Alva Biran from the Hebrew University worked with Drpaula Scaffidi and Dr Christina Morales Torres from the Crick Institute in London. The
International Research Group also includes Dr. Ayelet Hashahar Cohen of the Hebrew University, Dr. Rotem Ben-Hamo and Professor Sol Efroni of Bar-Ilan University, and Dr. Tom Misteli of the NIH National Cancer Institute.
team found that in many cancer types, those cancer stem cells lost one of their DNA-packed proteins, H1.0.
is expressed by the H1.0 gene by binding to DNA. Professor
Explained: "We found that the disappearance of H1.0 is critical to the ability of cancer cells to remain active, and in order to understand the mechanism of action, we mapped the interaction sinthing with DNA and found that it binds to the regulatory region of the gene, which inhibits the spread of cancer cells when H1.0 levels rise."
the study is based on epigenetics-- a scientific field that investigates DNA expression by switching genes on and off.
to identify cancer stem cells from other cells in the tumor, the team studied epigenetic mechanisms that distinguish the least selected cells, have infinite division properties and growth potential, and more sorted cells that lack this ability.
results show an inverse relationship between H1.0 and cancer cell division: as H1.0 levels decline, the greater the potential for uncontrolled division of cells, whereas high levels of proteins prevent this process, we find that the disappearance of the protein H1.0 is a characteristic of cancer stem cells and that it is necessary to maintain the ability and growth potential of division.
discovery could open the door to a medical intervention for cancer stem cells aimed at restoring high levels of H1.0 in all cancer cells and blocking the differentiation of cancer cells.
While further research requires an understanding of the effectiveness of H1.0 proteins in preventing the growth and spread of cancer, this study significantly expresses the mechanisms of cancer stem cells and relatively new epigenetic methods of cancer research.
Source: Decoding Medicine.