2023-05-20 02:26:22
A study with Spanish participation identifies key factors for the development of the disease.
Pancreatic cancer is one of the deadliest tumors. The survival rate for pancreatic ductal adenocarcinoma, the most frequent form of the disease, stands at 8.6%, the lowest percentage of all common tumors, according to data from the Spanish Society of Medical Oncology.
Much is still unknown about this tumor, which is often diagnosed when it is already in advanced stages, although research is progressing. The latest noteworthy novelty is signed by a team with Spanish participation that has managed to reveal why the wick of this type of cancer begins. Details of the process are published in the latest issue of the magazine Science.
It has been known for some time that, in pancreatic tumors, as in other types of cancer, mutations in the KRAS oncogene are key. The team that is now publishing news about the disease, made up of researchers from the Memorial Sloan Kettering Cancer Center (MSKCC) in New York, and the researcher Direna Alonso-Curbelo, who now works at the Barcelona Institute for Research in Biomedicine (IRB), He also previously demonstrated the inducing role that external factors play in triggering the disease, such as tissue injury that causes inflammation. And now, scientists have shown that cellular identity, the ability of some cells to respond to the influence of oncogenes and inflammation, is also central to the process.
The interactions between genetic mutations and external factors, emphasize the researchers, modify the identity of some subpopulations of cells, transform them. And, as a consequence of this, the ability of these cells to communicate and interact with other cells in their environment is greatly increased, which contributes to the development of cancer.
high plasticity
Specifically, scientists have shown that there are diverse cell subpopulations in the pancreas that have high plasticity and are much more responsive to genetic and non-genetic factors that predispose to cancer. According to their data, these cells have, on the one hand, a different and specific epigenome; and, on the other, an increased capacity to be able to respond and send signals to their environment.
Driven by the influence of mutations and inflammation, these cells generate aberrant communication networks, triggering a feedback loop that leads to cancer development and progression.
“Our work is designed to deepen our knowledge of pancreatic cancer, but having identified and unmasked the characteristics of these cells with a greater propensity to change their identity, more plastic, can serve as a guide to find useful molecules against this type of cancer” , says Alonso-Curbelo.
In mouse models, the team showed that it was possible to block such aberrant communication and that these conversations between cells played a key role in the development of cancer. “Our analyzes showed that these expansive communication networks established in the early stages of pancreatic cancer are functionally relevant and direct pancreatic tumorigenesis in mice,” adds the researcher, who stresses that the work has been possible thanks to an interdisciplinary team.
computational methods
Thus, the research combined sophisticated genetically modified mouse models and advanced computational methods to map the various cellular states that lead to cancer and unravel the characteristics of individual pancreatic cell subpopulations at each stage of tumor progression.
The computational area of the research has been led by Cassandra Burdziak, PhD student in Dr. Pe’er’s lab, at MSKCC; while the experimental and conceptual part has been led by Alonso-Curbelo herself, who began the research during her stay at the New York institution.
The finding coincides in its publication with another article that appears this week in Nature where promising results have been shown from an experimental vaccine based on messenger RNA technology, the same one that was used in vaccines against covid-19, against the most aggressive pancreatic cancer.
The results of a phase I clinical trial conducted in 16 patients show that personalized vaccines are capable of inducing an immune response against cancer.
Early study results have shown that the vaccine induces substantial immune response and potentially delays relapse of patients in a form of cancer, since they were made with neoantigens identified in their own tumors. The treatment was administered in combination with chemotherapy and immunotherapy. Cristina G. Lucio
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