Evaluation of Prognostic Immune Signatures in Patients with Breast, Colorectal and Pancreatic Cancer Receiving Chemotherapy

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

“…Furthermore, Vogl et al [94] revealed that the levels of CD97, CD274, and CD276 assessed by ELISA could serve as readily measurable prognostic or predictive markers in patients with advanced disease or metastatic breast, colon, or pancreatic cancer, being at baseline before cytotoxic treatment, and during the course of the chemotherapy, as well.…”

“…Consequently, it has been demonstrated that CD97 levels expressed considerable variability during the course of chemotherapy [94]. No correlations were found between CD97 expression, clinical infection, or C-Reactive Protein level, being hypothesized that infection could activate CD97 through upregulation of its ligand, CD55.…”

“…However, CD97 levels are prognostic for overall survival, and thus they predefine the disease's aggressiveness. Chemotherapy also affects certain cancer cell clusters which express the membranous form of the molecule CD97 [94].…”

To Detach, Migrate, Adhere, and Metastasize: CD97/ADGRE5 in Cancer

“…Overall, sCD97 detection is related to malignant tumors and/or inflammation (Table S4). Inconsistent results on the detection of circulating sCD97 in patients with solid tumors [67,68] may be caused by the applied self-made ELISAs, which are not well-validated; spike-and-recovery and linearity-of-dilution experiments have not been performed when applying the various body fluids.…”

Ανακάλυψη Νέων Μεμβρανικών Υποδοχέων Και Πρωτεϊνών Ως Φαρμακευτικών Στόχων Για Τη Θεραπεία Του Καρκίνου Του Μαστού

“…CD97 is the most broadly expressed member of the epidermal growth factor seven-span transmembrane (EGF-TM7) subfamily of adhesion GPCRs, that is involved in cell proliferation, differentiation, and apoptosis (50). CD97 has been demonstrated to confer an invasive phenotype and its interaction with its ligand, CD55, has been shown to contribute to tumorigenesis through cell adhesion, migration, and angiogenesis through Gprotein dependent or G-protein-independent signaling (50,51). The receptor tyrosine kinase AXL has been demonstrated to be preferentially upregulated in TNBC and its high expression levels has been associated with reduced RFS and OS in TNBC patients treated with anthracycline-taxane-based adjuvant chemotherapy (52,53).…”