Anti-EGF monoclonal antibody, clone 5F22

Inflammatory bowel diseases (IBDs), such as Crohn's disease and ulcerative colitis, are chronic inflammatory disorders of the gastrointestinal tract. Although IBDs increase the risk of colitis-associated colon cancer, the underlying mechanisms are not fully understood. Extracellular vesicles (EVs) are lipid-bound sacs that transport proteins, RNA, and lipids between cells and are key mediators of cellular communication in both physiological and pathological settings. EVs have been implicated in many cancer hallmarks, including uncontrolled tumor growth and metastasis. In this study, we investigated the effects of colon-derived EVs on the proliferation of fibroblasts. We used comparative proteomics to characterize protein profiles of colorectal EVs isolated from healthy mice (Con-EVs) and those with dextran sulfate sodium-induced colitis (IBD-EVs). The results showed that 109 proteins were upregulated in IBD-EVs. Notably, expression of epidermal growth factor receptor (EGFR), which plays important roles in cell proliferation and development, was increased in IBD-EVs. We then examined the effect of EVs on murine NIH3T3 fibroblasts and found that IBD-EVs significantly promoted cell proliferation in EGFR- and ERK-dependent manner. Our findings suggest that inflamed colon-derived EVs promote tumor development thorough activation of fibroblasts.

Background Epidermal growth factor receptor inhibitors (EGFRI) used in cancer chemotherapy cause acneiform folliculitis in 70%-100% of patients in a dose-dependent manner. Acneiform folliculitis is considered to be caused by an inflammatory process due to follicular hyperkeratosis and subsequently a set of changes both in epidermis and hair follicles as a result of epidermal growth factor receptor (EGFR) blockade. Both acne vulgaris and acneiform folliculitis due to EGFRIs show similar changes in the pilosebaceous unit. Furthermore, in both groups of patients, topical application of recombinant human epidermal growth factor (EGF) has been reported to improve the disease. Aims In this study, it was aimed to investigate the role of EGF and EGFR amount, expression, and EGFR gene polymorphisms in the etiopathogenesis of acne vulgaris. Patients/Methods 156 acne vulgaris patients, within 18-25 years of age, who had 15 or more inflammatory acne lesions on dermatologic evaluation were included in this study. The absence of any known systemic or genetic disease or cancer and any systemic or topical treatment for the last 1 month were prerequisites. In the control group, 154 volunteers in the same age range who were examined at the outpatient clinic with diagnoses of melanocytic nevus, ephelid, cherry angioma, and callus and who had no more than 3 inflammatory acne lesions were recruited. The amounts of EGF and EGFR were determined by sandwich ELISA, expressions of EGF and EGFR by reverse transcriptase polymerase chain reaction; EGFR polymorphisms were examined by restriction enzyme digestion, Sanger, and high-resolution melting methods. Results The patient and control groups were compared in terms of EGFR gene polymorphisms in addition to the amount and expressions of EGF and EGFR. The amount of EGF in the serum was found to be significantly higher in the acne group. (P = .0012). There was no significant difference in other parameters studied. Conclusion The results of our study showed a significant increase in the amount of EGF in the acne group. Though EGF may be incriminated in the etiopathogenesis of AV, the most likely explanation about its role may be controlling inflammation from the very first stage.