RESUMEN

Ki-67 is a marker of cell proliferation, used as an important diagnostic marker in the pathologic differentiation of various lesions. It is also relevant for developing targeted molecular therapies. We carried out a systematic review to assess the Ki-67 labeling index (LI) in odontogenic cysts and tumors. Databases were searched, including PubMed (MEDLINE), Scopus, CINHAL, PsycoInfo, the Cochrane Library, and Proquest. The meta-analysis was carried out based on the data of 608 lesions. When a 5% cut-off point was set, ki-67 LI of all benign odontogenic tumors dropped below this point. All the malignant tumors demonstrated an LI of over 15.3%; a significantly higher Ki-67 LI in malignant odontogenic lesions (17.59±2.80) was observed. Among benign tumors, the largest and the smallest Ki-67 LIs were seen in ameloblastoma (4.39±0.47) and adenomatoid odontogenic tumor (0.91±1.71). The mean values of Ki-67 LI in tumors and cysts were 4.23 (0.38) and 1.04 (0.07), respectively. Among odontogenic cysts, the highest Ki-67 LI was found in odontogenic keratocyst (OKC) (3.58±0.51), and the lowest in the radicular cyst (1.29±0.62%). Ki-67 LIs in all odontogenic cysts were <3%, except for OKC. This controversial lesion seems to have a profile more similar to a tumor, and a treatment plan similar to tumors might be suggested. We found that odontogenic lesions have diverse proliferative activities that help differentiate between various lesions and suggest therapeutic plans.

RESUMEN

Based on Akt1 and Jak1 key roles in apoptosis and proliferation of many cancers, the aim of this study was to find a new gene therapy strategy by silencing of these main anti-apoptotic genes for HNSCC treatment. Cancerous HN5 and normal HUVEC cell lines were treated with Akt1 and Jak1 siRNAs alone or with each other combined with/without cisplatin. The MTS, flow cytometry, 4',6-diamidino-2-phenylindole staining, real-time PCR and ELISA methods were utilized in this study. The highest percentage of apoptosis was observed in the treatment of Jak1 siRNA/cisplatin group in cancerous HN5 cells (96.5%) where this treatment showed 12.84% apoptosis in normal HUVEC cell line. Cell viability reduced significantly to 64.57% after treatment with Akt1 siRNA in HN5 treated group. Knocking down Akt1 and Jak1 genes using siRNAs could increase levels of apoptosis and reduce proliferation rate in HNSCC indicating the powerful effects of these genes siRNAs with or without chemotherapeutic agents in HNSCC treatment. In conclusion, the combination of siRNA-mediated gene-silencing strategy can be considered as a valuable and safe approach for sensitizing cancer cells to chemotherapeutic agents thus proposed further studies regarding this issue to approve some siRNA based therapeutics for using in clinic.

Asunto(s)

Apoptosis/genética , Proliferación Celular/genética , Neoplasias de Cabeza y Cuello/genética , Janus Quinasa 1/genética , Proteínas Proto-Oncogénicas c-akt/genética , ARN Interferente Pequeño/genética , Carcinoma de Células Escamosas de Cabeza y Cuello/genética , Apoptosis/efectos de los fármacos , Línea Celular , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Supervivencia Celular/genética , Cisplatino/farmacología , Técnicas de Silenciamiento del Gen/métodos , Silenciador del Gen/efectos de los fármacos , Silenciador del Gen/fisiología , Neoplasias de Cabeza y Cuello/tratamiento farmacológico , Células Endoteliales de la Vena Umbilical Humana , Humanos , Carcinoma de Células Escamosas de Cabeza y Cuello/tratamiento farmacológico

RESUMEN

STATEMENT OF THE PROBLEM: Macrophages are the target of attention in numerous diseases. Many studies reported them as the regulators of the growth, dissemination, and clinical behavior of various lesions. There are relatively scarce data regarding the role of macrophages in oral lesions, particularly odontogenic lesions. PURPOSE: This study investigated the macrophage density in odontogenic lesions of diverse biologic performance. MATERIALS AND METHOD: In this comparative analytical study, 60 cases of odontogenic lesions including ameloblastoma, keratocystic odontogenic tumor, dentigerous cyst, and radicular cyst were immunohistochemically stained with anti-CD68 antibody. One-way ANOVA and Tukey's HSD test were used for statistical analysis. RESULTS: The results showed that the macrophage density in keratocystic odontogenic tumor (35.72±7.74) and ameloblastoma (46.12±9.84) was not significantly different from that in dentigerous cyst (43.87±8.13). Interestingly, the macrophage density in keratocystic odontogenic tumor was lower than that in dentigerous cyst. No significant difference was observed in macrophage density between the ameloblastoma and much less aggressive lesions like dentigerous cyst (p= 0.59). Macrophage density in radicular cyst (81.53±11.04) was significantly higher than other odontogenic lesions (p< 0.001). CONCLUSION: The lack of significant differences in macrophage density between the known aggressive odontogenic tumors and much less aggressive lesions implied that macrophages might not contribute to the biological behavior of the odontogenic lesions. Therefore, it could support the notion that targeted therapy would not have prominent clinical potential to decrease the extent of mutilating surgeries in odontogenic lesions.