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New research published in the Journal of Experimental Medicine, reveals a new mechanism that fuels tumor growth in bad cancer and can have a negative impact on a person's prospects. However, the results could also help scientists develop personalized treatments specifically targeting bad cancer tumors.
Neta Erez, a senior lecturer in the pathology department of the Sackler School of Medicine at Tel Aviv University in Israel, is the first author of the new paper detailing a new mechanism of tumor growth in bad cancer.
As noted by scientists in their study, bad cancer is still "one of the leading causes of cancer deaths among women in the western world," despite intense research efforts by the medical community and women. public awareness campaigns.
In the United States, bad cancer remains the most common cause of cancer deathsebqbyetqxcceztucxftwdudrfxcaxuvrxxbszz in women of all races and ethnicities.
The new research by Professor Erez and his colleagues reveals a mechanism that could explain why some people have worse prospects than others after being diagnosed with cancer. The authors explain that this mechanism involves fibroblasts, cells that allow tumor growth, even if they are not cancerous.
In the case of bad cancer, these fibroblasts help cancer cells to proliferate by stimulating inflammation and helping to form blood vessels that provide oxygen-rich blood and nutrients to growing tumors.
Until now, scientists thought that most of these cells came solely from the surrounding bad tissue, but new research by Professor Erez and his colleagues shows that many of these fibroblasts actually come from bone marrow cells.
Results reproduced in bad tumors in humans
The researchers studied a mouse model of bad cancer and found that a significant proportion of "cancer-badociated fibroblasts" came from so-called mesenchymal stromal cells, that is, bone marrow cells. "spindle shaped" able to differentiate into other cells. cells, such as those that form bone, muscle, cartilage or connective tissue.
However, in the case of bad cancer, Professor Erez and his team discovered that tumors could "recruit" these mesenchymal stromal cells into the bone marrow and differentiate them into fibroblasts, which, in turn, promoted the growth of you die.
The new research has revealed additional nuances. For example, it has been found that, unlike other cancer-badociated fibroblasts, those derived from bone marrow cells do not have a signaling protein called PDGFRα.
However, the cells compensate for this lack by excessively producing a protein called clusterin. This protein helps tumors produce more blood vessels and multiply much faster than those fed exclusively with fibroblasts from nearby bad tissues.
Importantly, scientists have reproduced their findings in human bad cancer tissues. They found that human bad cancer tumors also had PDGFRα-deprived fibroblasts, which led researchers to believe that these fibroblasts could also be derived from bone marrow cells.
Finally, bad cancer tumors with lower levels of signaling protein, PDGFRα, were more likely to die of cancer.
The authors conclude that the results "may have important implications for patient stratification and precision treatment".
Professor Erez also comments: "Our study shows that recruitment of bone marrow-derived fibroblasts is important for promoting tumor growth, probably by improving the formation of blood vessels."
"Understanding the function of these cancer-badociated fibroblasts could be the basis for the development of novel therapeutic manipulations targeting bone marrow-derived fibroblasts as well as the cancer cells themselves."
-Teacher. Neta Erez
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