Prospects for targeted treatment of glazed cranial pharynx tumors

Study backgroundglazed cranial pharynx tumor (adamantinomatous craniopharynoma, ACP) is a type of benign heterogeneous brain tumor formed by rathke's pouch residue in the saddle or saddle areaTumor pathological composition is complex, including epithelial tissue cells, cystic structure and calcium depositionCurrently, the standard treatment for ACP is surgical addition to radiotherapy or without radiotherapyTumors can be soaked or damaged in adjacent tissues, and full removal is more difficult and can lead to severe neuroendocrine damageRecently, Astrid CHengartner of Pediatric Neurosurgery at the University of Colorado School of Medicine in Colorado, USA, and others conducted a literature review, focusing on advances in the study of aCP molecular properties and potential targeted therapiesThe article was published in Neurosal Focus in January 2020findingsan important pathological mechanism of ACP is the classic Wnt/beta-catenin pathway disorderThe Wnt pathway is a stem cell responsible for organ formation and adult growth during embryonic development, and beta-cateninis is an important protein in the Wnt pathway, encoded by the CTNNB1 geneThe ctNNB1 gene mutation can lead to the accumulation of beta-catenin, thereby enhancing the ability of tumor cells to migrate, while the accumulation of beta-catenin further causes the imbalance of the Wnt pathway, which aggravates the aggressiveness of tumor cellsWnt pathway or beta-catenin inhibition may be a promising treatment for ACP, but the potential off-target effect limits its useshow reinforcable solid tumor components on MRI imaging tablets, and more than 90% of ACP has cystic changesRapid production of cyst fluids can damage surrounding tissue, increase intracranial pressure and produce unpredictable reactions to treatmentIncreased levels of pro-inflammatory media in ACP cystic fluid and solid tumors support the role of inflammation in the pathogenesis of ACP, and some scholars have suggested that targeted inflammatory treatment can block its progressionIntracytotherapy to control the enlargement of cysts may help to locally inhibit tumor development Pro-inflammatory media and immunosuppressants have been converted to clinical treatment, including leukocyte interleukin 6 and IDO-1 inhibition conclusions preclinical studies have revealed that in healthy cells, fissigen-activated protein kinase/extracellular signal regulation kinase (MAPK/ERK) mediates a series of extracellular stimulation transduction of intracellular signals to regulate cell proliferation, survival, differentiation and movement In tumor cells, overactivity of the MAPK/ERK pathway causes tumor cells to grow, multiply and migrate uncontrolledly The high expression of epidermal growth factor receptor (EGFR) in ACP promotes the activation of the MAPK/ERK pathway, so the MAPK/ERK pathway and EGFR are jointly involved in the growth progression of ACP, which also provides a potential way to treat ACP In addition, studies have shown that the pathway imbalance of the programmatic cell death protein 1 and its ligand (PD-1/PD-L1) leads to the emergence of various therapeutic targets, PD-1 expression through the downstream activation of MAPK/ERK associated with tumor production PD-L1, may regulate tumor-related immune cell activity In addition, elevated PD-L1 is associated with EGFR activation in ACP, a target that can also be used as a clinical treatment strategy The results of the above-mentioned preclinical studies and clinical trials need to be translated into clinical targets to guide the treatment of ACP.