Study clarifies the role of collagen during pancreatic cancer development
Contrary to long-held beliefs, Type I collagen produced by cancer-associated fibroblasts may not promote cancer development but instead plays a protective role in controlling pancreatic cancer progression, reports a new study from researchers at The University of Texas MD Anderson Cancer Center. This new understanding supports novel therapeutic approaches that bolster collagen rather than suppress it.
The study finds that collagen works in the tumor microenvironment to stop the production of immune signals, called chemokines, that lead to suppression of the anti-tumor immune response. When collagen is lost, chemokine levels increase, and the cancer is allowed to grow more rapidly. The research was published today in
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BENNINGTON â Maryam Zenali, MD, has joined Southwestern Vermont Medical Center Pathology and Dartmouth-Hitchcock Putnam Physicians, SVMC has announced.
Zenali earned her medical degree at the University of Texas Medical School and her bachelorâs degree in biology from the University of Houston. She completed her residency at the University of Texas Medical School and two fellowships â one in surgical pathology and a second in biomarker, combined with gastroenterology pathology, research â both at the University of Texas MD Anderson Cancer Center. She is board certified in surgical pathology and clinical pathology.
Most recently, Zenali worked as an anatomic pathologist within the Department of Pathology and Laboratory Medicine at the University of Vermont Medical Center.
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IMAGE: A model produced by scientists at Rice University shows the conformational changes caused by a mutation in the cancer-fighting p53 protein. At top left, the red box highlights the aggregation-prone. view more
Credit: Kolomeisky Research Group/Rice University
HOUSTON - (March 4, 2021) - A mutation that replaces a single amino acid in a potent tumor-suppressing protein turns it from saint to sinister. A new study by a coalition of Texas institutions shows why that is more damaging than previously known.
The ubiquitous p53 protein in its natural state, sometimes called the guardian of the genome, is a front-line protector against cancer. But the mutant form appears in 50% or more of human cancers and actively blocks cancer suppressors.
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Researchers at Baylor College of Medicine show that analysis of the proteomics, or all the protein data, from aggressive human cancers is a useful approach to identify potential novel therapeutic targets. They report in the journal
Oncogene, the identification of proteomic signatures that are associated with clinical measures of aggressive disease for each of the seven cancer types studied. Some signatures were shared between different types of cancer and included cellular pathways of altered metabolism. Importantly, experimental results provided proof-of-concept that their proteomics analysis approach is a valuable strategy to identify potential therapeutic targets. There are two notable aspects of this study. One is that we explored the proteomic landscape of cancer looking for proteins that were expressed in association with aggressive forms of cancer, said co-corresponding author Dr. Chad Creighton, professor of medicine and co-director of Cancer Bioinformatics