History: Targeted malignancy therapy is a new approach for the Magnolol treatment Magnolol of cancer. EGFR and VEGFR inhibition were selected. Finally 13 content articles met the criteria. Results are discussed and possible pathogenetic mechanisms for the complications of targeted malignancy therapy regimens are offered. Results: It appears that the most severe side-effect is definitely mucositis/stomatitis that may affect the whole gastrointestinal tract. It hardly ever results in treatment discontinuation. Reduced saliva secretion xerostomia and dysphagia can be severe with some regimens and interfere with food uptake. Osteonecrosis wound healing impairment spontaneous gingival bleeding and dysgeusia were also reported. Conclusions: Considering these data it is obvious that symptoms related to malignancy treatment should be considered in the context of the alternative management of individuals. Oral complications should not be overlooked but recorded during physical exam because they may significantly impair daily activities and individuals’ quality of life. Keywords: bevacizumab cetuximab oral complications molecularly targeted medicines EGFR VEGFR Intro The first to describe a concept of selective uptake of molecules by cells was Ehrlich in the 19th century. He explained the side-chain theory that created the basis for the understanding of the effects of serum and the coupling between an antigen and an antibody that built the Colec10 basis for the discovery of monoclonal antibodies and targeted malignancy therapy. Molecularly targeted medicines interact with a specific target mostly a protein inside a selective way. This protein is definitely a growth element a growth element receptor a signaling molecule a cell cycle protein an apoptosis mediator a molecule implicated in malignancy cell dispersal and angiogenesis1. Side effects of molecularly targeted medicines differ on the severity of reported symptoms compared to classical chemotherapy providers because they hardly ever cause alopecia nausea and vomiting. Reports concerning oral complications are sparse and the most frequently reported sign in medical control tests is definitely mucositis/stomatitis. The aim of this review of the literature is definitely twofold: 1. to present the oral complications of targeted malignancy therapy in particular those that are the result of treatments that target EGFR and VEGFR 2 to analyze the possible pathogenetical mechanisms. Molecularly targeted medicines This general term includes two main categories of molecules monoclonal antibodies and tyrosine kinase inhibitors. Tyrosine kinase inhibitors connect to the cytoplasmic part of membrane receptors. They may be small molecules Magnolol given per os once daily. Because of their small size they provide enhanced bioavailability. On the contrary monoclonal antibodies take action within the extracellular website part. They are large molecules given by intravenous route once a week and show decreased bioavailability in certain compartments like the CNS. Because of their size they do not normally pass the basal membrane Magnolol therefore they are hardly ever related to symptoms from your gastrointestinal tract. They connect to a certain epitope of an antigen/protein. Receptors: action and side-effects 1 EGFR EGF receptors are membrane receptors with tyrosine kinase activity. Like all receptors of this family they need ATP for the phosphorylation of their cytoplasmic domain that possesses enzymatic activity. They play a major role in cancer progression because they inhibit apoptosis enhance cell cycle progression angiogenesis cancer cell motility and metastasis malignant transformation and lead to cancer phenotype2 3 The overexpression of EGFR in various cancer types especially in the head and neck cancer in which an overexpression is present in 42%-98% of the cases is related to an increased transcriptional activity and anticipates a bad outcome2 3 EGFR inhibition and oral complications Two different ways of EGFR-molecularly targeted drug interaction offer a more effective inhibition. The first involves the connection of the drug to the extracellular domain of the receptor that inhibits the connection of the ligand. The second targets the intracellular portion that has tyrosine kinase activity and exerts its action by restricting ATP binding or binding to the active site of the enzyme3 4 Thus both monoclonal antibodies and tyrosine kinase inhibitors can effectively inactivate.