In a recent study published in the Journal of Cancer Research and Clinical Oncology, researchers from The First Affiliated Hospital of Guangxi Medical University and The First People’s Hospital of Qinzhou (China) investigated the expression pattern, molecular mechanisms and clinical relevance of GALNT1 in breast cancer.
Intercellular communication between tumor cells and cancer-associated fibroblasts (CAFs) plays a key role in tumorigenesis and progression, and CAFs generate an extracellular matrix that provides a repository for factors that promote cancer progression. Alpha Beta Therapeutics Inc. researchers aimed to investigate the mechanisms by which CAFs facilitate tumor initiation and tumorigenesis of pancreatic cancer.
Targeted protein degradation has gained attention in recent years due to its potential to hit proteins that are difficult to engage with conventional small molecules. Pin1 is an enzyme associated with tumor formation overexpressed in pancreatic cancer cells or cancer-associated fibroblasts in particular.
Early steps in cancer development are closely linked to fibroblast senescence and their transformation into tumor-promoting cancer-associated fibroblasts (CAFs).
The fibroblast activation protein (FAP) is a known biomarker expressed on the surface of cancer-associated fibroblasts (CAF), as well as an important target that distinguishes normal fibroblasts from CAF. Researchers from National Yang-Ming University recently reported the discovery and preclinical evaluation of a novel PET tracer, [18F]FEQGP, being developed for the detection of FAB expression in CAF imaging.
Heterogeneity, in both tumors and their microenvironment, limits the success of current cancer treatments. But it also provides opportunities. Heterogeneities “are not barriers to therapy, they are vulnerabilities to be exploited,” was how David DeNardo described his take at the 2023 annual meeting of the American Association for Cancer Research (AACR) on Sunday.
The Institute of Cancer Research (ICR) in London is shifting the focus of drug discovery from molecular targets in cancer cells to take in the whole ecosystem supporting tumor growth, evolution and the development of resistance. The aim is to exploit new understanding of the way cancers evolve within the ecosystem of the body, the interaction between cancer cells and the immune system, and the reliance of a tumor on the tissue and growth signals that surround it. Manipulating this environment could make cancer cells become “extinct,” ICR researchers say.
Cancer-associated fibroblasts (CAF) expressing the LRRC15 protein (leucine-rich repeat-containing protein 15) could be responsible for the suppression of antitumor immunity, according to a study using mouse models of pancreatic cancer. Scientists from Roche Holding AG subsidiary Genentech Inc. demonstrated in vivo that TGF-β type 2 receptor signaling in healthy universal fibroblasts produces cancer-associated LRRC15+ myofibroblasts.
