Although the survival rate of the pancreatic cancer has increased, it is still the most lethal. Only 12% of patients survive five years, mainly because when it is discovered it is too late and it is in an advanced stage. Hence, the research focuses on finding out what causes the cells become cancerous, in search of therapies in earlier stages.
One of the preclinical studies that has given more results hopeful has been the one developed by the Spanish doctor Direna Alonso-Curbelomember of the Biomedical Research Institute (IRB Barcelona), along with researchers from the Memorial Sloan Ketterin Cancer Center (MSKCC) in NYwhich has been published this Thursday in ‘Science’.
The investigation reveals that the DNA mutationswhich are causes already studied in cancer, specifically the mutation of the KRAS oncogene It is frequent in tumors in the lung, colorectal and pancreas, they only explain a part of the development of the disease. Other external factors have to appear, such as a tissue injury that causes inflammation, which modifies the identity of cells and their environment and favors the appearance and progression of tumors. In the pancreas, this “tissue injury” can be caused, for example, by a pancreatitisas explained by the Spanish scientist.
Researchers have combined models of mouse genetically modified with computational methods, in order to study the ability of cells to mutate and have discovered that in pancreatic cancer the cell modifications and the environment begin to occur rapidly, between 24 and 48 hours after the injury occurs, and occur in a predictable manner.
The communication
As a consequence, the ability of some cells -with the mutant KRAS oncogene- to communicate and interacting with other cells in its environment is greatly increased. “Precancerous cells acquire the ability to send and receive many more signals than a normal cell,” explains Dr. Dana Pe’er, one of the lead authors of the study. “And we saw that this is not random: it is structured. You see the same patterns over and over again when you do the experiments on different mice.”
The study is characterized by the use of computational innovation. “We had to invent a series of new methods to answer questions not often asked about plasticity, cell-to-cell communication, and tumor progression,” adds Dr. Pe’er.
new roadmap
The advance also represents the culmination of a line of research initiated by the Spanish scientist Alonso-Curbelo, which details epigenetic mechanisms, that is, changes that activate or inactivate genes without changing the DNA, through which the inflammation favors the initiation of cancer.
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Taken together, the research “provides an new roadmap that may help develop strategies to detect or even prevent pancreatic tumors before they reach advanced stages,” according to Dr. Lowe, a member of Memorial Sloan Kettering Cancer Center. “Understanding how networks of communication between cells drive initiation is promising for the development of therapies that block or slow early progression and potentially even more advanced disease,” he adds.
The publication of the research takes place the day after the first results of a clinical trial with 16 volunteers have shown that a experimental messenger RNA vaccine potentially delays relapse in patients with pancreatic cancer.