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Ameloblastoma is a benign tumor of the odontogenic epithelium with several histological subtypes. All subtypes of ameloblastoma contain abundant stroma; the tumor cells invade collectively into the surrounding tissues without losing intratumor cell attachments. However, the molecular mechanisms mediating ameloblastoma invasion remain unclear. Here, we evaluated the functional significance of the interactions between ameloblastoma tumor cells and stromal fibroblasts on collective cellular invasion using a three‐dimensional cultivation method, double‐layered collagen gel hemisphere ( DL ‐ CGH ) culture. The AM ‐1 plexiform and AM ‐3 follicular human ameloblastoma cell lines and HFF ‐2 human fibroblasts were labeled with GFP and DsRed, respectively. Collective cellular invasion of ameloblastoma cells was assessed in the presence or absence of fibroblasts. Notably, without fibroblasts, AM ‐1 cells formed sharp, plexiform‐like invasive processes, whereas AM ‐3 cells formed a series of blunt processes often observed during collective migration. In comparison, under the cocultures with HFF ‐2 fibroblasts, AM ‐3 cells formed tuft‐like invasive processes and collectively invaded into outer layer more than that observed with AM ‐1 cells. Moreover, HFF ‐2 fibroblasts localized to the tips of the invasive tumor processes. These findings suggest that tumor‐associated cells assist tumor cell invasion. Microscopic analysis of sectioned three‐dimensional cultures revealed that AM ‐3/ HFF ‐2 hemispheres were histologically similar to follicular ameloblastoma tumor samples. Therefore, our findings suggest that ameloblastoma subtypes exhibit distinct invasion patterns and that fibroblasts promote collective tumor invasion in follicular ameloblastoma.

Ameloblastoma is benign odontogenic tumours that mainly occur in the jawbone. This tumour induces aggressive invasion into the surrounding bone and has a high recurrence rate after surgery. Therefore, mandibular resection is performed in many patients with this tumour, causing aesthetic and functional problems. It is necessary to develop a novel treatment strategy for ameloblastoma, but there are currently no innovative treatments. Although our understanding of the molecular biological mechanisms of ameloblastoma is still insufficient, there have been many recent reports of new molecular biological findings on ameloblastoma. Therefore, bioactive factors that have potential for novel therapeutic methods, such as molecular targeted therapy, have been discovered in ameloblastoma. In this review, we summarize the molecular biological findings of ameloblastoma reported over several decades, focusing on factors involved in invasion into surrounding tissues and disease-specific gene mutations. We also mention the effect of the interaction between tumour cells and stromal components in ameloblastoma on tumour development. Scientific field of dental Science: Oral surgery, Odontogenic tumor, Ameloblastoma.

Glioblastoma is characterized by marked invasiveness, but little is known about the mechanism of invasion in glioblastoma cells. Wnts are secreted ligands that regulate cell proliferation, differentiation, motility and fate at various developmental stages. In adults, misregulation of the Wnt pathway is associated with several diseases. Recently, we reported that Wnt-5a was overexpressed and correlated with cell motility and infiltrative activity through the regulation of matrix metalloproteinase (MMP)-2 in glioma-derived cells. Although several receptors for Wnt-5a were identified, the receptors of Wnt-5a that mediate cellular responses of glioma were not clearly identified. Knockdown of receptor-like tyrosine kinase (Ryk) but not that of Ror2 suppressed the activity of MMP-2 and Wnt-5a-dependent invasive activity in glioma cells. These results suggest that Ryk is important for the Wnt-5a-dependent induction of MMP-2 and invasive activity in glioma-derived cells and that Ryk might have a novel patho-physiological function in adult cancer invasion. Furthermore, not only the expression of Wnt-5a but also that of Frizzled (Fz)-2 and Ryk was correlated with the WHO histological grade in 38 human glioma tissues. Taking these findings together, Fz-2 and Ryk could be therapeutic or pharmacological target molecules for the control of Wnt-5a-dependent invasion of human glioma in the near future.

These findings indicate that PNAM for infants with UCLP enhanced symmetry in the maxillary alveolar arch and nasolabial form. In addition, the posterior movement of the anterior points of the maxillary alveolar arch was correlated with the improvement of columella deformation.

Objective : To elucidate the various effects on maxillary growth following different procedures for vestibular expansion at the time of primary lip repair for unilateral cleft lip and palate (UCLP). Participants : Thirty patients with complete UCLP who underwent primary lip repair using a triangular-flap technique with nasal vestibular expansion (NVE; the NVE group) and 30 patients who underwent the same lip repair with closure of the nasal floor (non-NVE group) were enrolled in this study. Interventions : Serial dental casts on lip and palatal repair were scanned with a laser scanner. The three-dimensional coordinates of seven anatomical landmarks and their growth changes, the curvature radius rate between major/minor segments, and the collapse rates were compared between the two groups. Results : At the time of lip repair, the incisal point was located slightly anteriorly in the non-NVE group. At the time of palatal repair, the cleft edge of the alveolar process in the minor segment was located significantly anteriorly and laterally in the NVE group, showing the significantly forward change of the minor segment. The minor segment collapsed in the non-NVE group. The collapse rate of the NVE group (3.3%) was significantly lower than that of the non-NVE group (40.0%). Conclusions : NVE following simultaneous advancement of nasolabial components on the affected side at the time of primary lip repair for UCLP facilitates the forward molding of the maxilla, resulting in a more symmetrical alveolar arch form.