Progress in molecular targeting therapy for gastrointestinal stromal tumors / 中国肿瘤生物治疗杂志

@#Gastrointestinal stromal tumors (GISTs) are the most common malignant tumor of abdominal soft tissue. It originates from Cahal (Cajal) interstitial cells or common precursor cells, and is driven by the mutated KIT gene or platelet-derived growth factor receptor alpha (PDGFRa) gene, all expressing type Ⅲ tyrosine kinase receptors. Imatinib mesylate, a tyrosine kinase receptor inhibitor, has been used for the standard treatment of advanced GIST, which has achieved remarkable results. Thus, GIST has become the most successful example of target therapy for solid tumors. In the context of the era of precision medicine, with the deepening in research of GISTs molecular biology，the molecular targeted treatment of GISTs has obtained a clear venation from the first-line, second-line and third-line of the advanced stage to the postoperative auxiliary and preoperative treatment, providing significant survival benefits for GISTs patients. This article systematically and comprehensively combed the preoperative and postoperative molecular targeting therapy from advanced GIST to early GIST, and analyzed the problems, proposed solutions and prospects for the future, aiming to provide reference for clinical application of molecular targeting drug therapy for GIST.

Effect of Retinoic Acid on the Expression of PDGF Receptors During Palatogenesis / 대한해부학회지

Although cleft lip and palate are one of the most common craniofacial malformation, little is still known about the mechanism of the palate formation. Retinoic acid (RA) is known a teratogen, and cleft palate is induced by retinoic acid administration in the secondary palate formation stage. Many growth factors and their receptors are involved in the formation of the secondary palate. Here, we investigated the expression of PDGFR-alpha, and PDGFR-beta during palatogenesis after retinoid acid administration in mice by RT-PCR and immunohistochemistry. At E15.5, the opposing palatal shelves fused with one another in the control group, but the palatal shelves were not elevated and cleft palate was induced in the RA-treated group. In RT-PCR, PDGFR-beta was downregulated during palatogenesis after RA administration. In immunohistochemical experiment, PDGFR-alpha and PDGFR-beta were reduced in RA-induced group. Taken together, we suggest that PDGF receptors may be molecules involved in palate formation.