In terms of midkine signalling, a study in could be interesting. neuroblastoma patients, the further refinement of the RNA aptamer or antibody as tools and the elucidation of midkine signalling are immediate issues that need to be resolved. Regarding the latter, although it has been shown that Notch2 functions as a receptor in neuroblastoma cells, it is likely that other receptors (e.g. anaplastic lymphoma kinase) are also involved in midkine signalling. Linked Articles This article is usually a part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4 (Kadomatsu amplification, low expression, diploidy, stage 3 and 4 disease, and over 18 months aged at diagnosis. In addition, there is a striking correlation between a high plasma midkine level itself and poor prognosis (Ikematsu hepatocellular carcinoma modelDai hepatocellular carcinoma modelDai hepatocellular carcinoma modelDai data utilizing animal models is needed. Recently, the involvement of midkine in neuroblastoma, one of the most malignant paediatric solid tumours known, was revealed for the first time in a study using a mouse model (Kishida gene initially plays a role in the normal development of sympathetic neurons (Nakagawara and Ohira, 2004), but the ectopic expression of at a particular stage of development is usually thought to be a trigger for oncogenesis, and Rabbit Polyclonal to HNRNPUL2 as a result, the neuroblasts in which human is usually ectopically expressed remain in an undifferentiated state and proliferate transgenic (Tg) mice in which the human gene was introduced under the control of a rat tyrosine hydroxylase (TH) promoter have been developed as an animal model for neuroblastoma, (Weiss Tg mice spontaneously develop tumours from the superior mesenteric ganglion (SMG), one of the sympathetic ganglia. The SMG lies on the superior mesenteric artery between the left and right kidneys, and its size is usually less than 1?mm in diameter. Although the most frequent origin of human neuroblastoma is the adrenal grand, the dominant origin in Tg mice is the SMG. D-(-)-Quinic acid These tumours are pathologically similar to human neuroblastoma with respect to both histology (Weiss Tg mice undifferentiated neuroblasts are accumulated in the SMG (Hansford Tg mice, midkine was highly expressed in both those precancerous SMG and later terminal tumour tissues (Kishida Tg mice, (the mouse gene name of midkine)-knockout mice were crossed with Tg mice. As a result, it was found that the genetic ablation of resulted in suppressed tumourigenesis (lower tumour incidence and delayed growth) of Tg mice (Kishida level, and the results demonstrate that midkine has certain properties that promote the tumourigenesis of neuroblastoma. It should be noted that this mechanism of action of midkine has not been fully elucidated. In terms of the initiation of midkine signalling, several receptor candidates, including anaplastic lymphoma kinase (ALK; Stoica Tg mice (Kishida results suggest that a midkine-Notch2-HES1 signalling pathway is usually involved in neuroblastoma. The same pathway was previously implicated in pancreatic ductal adenocarcinoma (PDAC) (Gng?r model of human hepatocellular carcinoma in mice suppressed the tumours to some extent (Dai effect was not outstanding, the D-(-)-Quinic acid fact that systemic administration of this monoclonal antibody evoked D-(-)-Quinic acid a slight but clear effect suggests that it has potential for clinical application in the future. However, the use of an effective monoclonal antibody against midkine for neuroblastoma therapy will have to await further studies. As D-(-)-Quinic acid described above, the involvement of midkine in the tumourigenesis of in Tg mice (Kishida were simultaneously attenuated in the RNA aptamer-treated tumours (Kishida.