Oral Carcinoma Cells (oral + carcinoma_cell)

Distribution by Scientific Domains


Selected Abstracts


Antiangiogenic and Chemopreventive Activities of Celecoxib in Oral Carcinoma Cell,,

THE LARYNGOSCOPE, Issue 5 2002
Zhi Wang MD
Abstract Objectives Chemoprevention is a promising strategy to inhibit carcinoma before invasive tumors develop, but a new molecular target is desirable. Celecoxib is a newly developed cyclo-oxygenase (COX)-2 inhibitor with significantly less toxicity. The study was conducted to determine whether celecoxib is effective and safe in prevention of oral cancer. The antiangiogenic activity of celecoxib was studied to explore the potential mechanism involved. Study Design Randomized animal study. Methods The study consisted of two phases. In the phase 1, 10 mice were used to determine the efficacy and safety of celecoxib with intradermal inoculation with oral carcinoma cells. The 10 mice were equally divided into two groups 5 mice (30 inoculated sites) in each group to receive 1,500 parts per million (ppm) celecoxib mixed in with the diet or to eat a normal diet, respectively, for 21 days. In phase 2, 10 more mice were inoculated to determine the effect of celecoxib on angiogenesis. Five mice received 3,000 ppm celecoxib in the diet, with the other five mice as control animals. The antiangiogenic activity was evaluated by comparing the density of newly growing microvessels after the inoculation. Results The results indicated that celecoxib significantly delayed cell growth and reduced tumor volume. There was statistical significance in the quantity of new vasculature in the tumor sites between the two groups. No toxic effect was found by means of measurement of body weight loss and microscopic dissection of organs. Conclusions The study provided the first evidence to show the chemopreventive efficacy of celecoxib on oral cancer in a nude mouse model. Clinical trials are warranted to determine the efficacy in humans. [source]


Radiation-induced changes in oral carcinoma cells , a multiparametric evaluation

CYTOPATHOLOGY, Issue 5 2003
L. Bindu
The aim of this study was to see whether serial cytological evaluation of various cellular abnormalities in tumours from patients receiving fractionated radiotherapy can predict radio-response in oral carcinoma. Cytological assessment was carried out in scrape smears collected prior to and during the course of radiotherapy in 68 patients with squamous cell carcinoma of the oral cavity planned for radical radiotherapy with accelerated fraction schedule. Smears were evaluated for a set of 15 radiation-induced cellular abnormalities. The relationship between the cellular alterations and the cumulative radiation dose was analysed by Kruskal,Wallis one-way anova. The results showed that among the various quantifiable changes that occur in irradiated cancer cells, karyolysis, karyorrhexis, pyknosis, cytolysis, multinucleation, micronucleation and nuclear budding show significant increase depending on the dose of radiation. The radio-resistant group of patients exhibited a lesser degree of change compared with the radio-sensitive group. This suggests that radio-resistance may be due to the defective induction of cell damage and that these cytological features may have potential use as predictive markers of radio-sensitivity in oral carcinoma. [source]


Nuclear STK15 expression is associated with aggressive behaviour of oral carcinoma cells in vivo and in vitro,

THE JOURNAL OF PATHOLOGY, Issue 1 2010
Shou-Yen Kao
Abstract Oral squamous cell carcinoma (OSCC) is one of the most commonly diagnosed cancers worldwide. Chromosome 20q is a hotspot for gene amplification in OSCC and the serine/threonine kinase STK15 (also named Aurora-A) maps to 20q13. The amplification and over-expression of STK15 is common in neoplasia but the functional and clinical impact of STK15 in OSCC remains poorly understood. STK15 copy number is amplified in 12% of OSCCs and nuclear STK15 protein expression increases with tumour progression. In vivo elevated nuclear STK15 protein expression is significantly associated with the worse prognosis of OSCC patients. The combination of high nuclear STK15 and Ki-67 expression has a 2.55-fold hazard for cancer-associated mortality. In vitro knockdown of STK15 reduced the oncogenic phenotypes of OECM-1 cells. Injection of lentivirus carrying shRNA vectors against STK15 significantly reduced the growth of SAS xenografts on nude mice. Knockdown of STK15 also induced autophagy and apoptosis of OSCC cells. Our data provide evidence that STK15 is oncogenic for OSCC and that its nuclear expression is a predictor of clinical behaviour. Knockdown of STK15 could be a potential therapeutic option in OSCC and other tumours. Copyright 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]


Antiangiogenic and Chemopreventive Activities of Celecoxib in Oral Carcinoma Cell,,

THE LARYNGOSCOPE, Issue 5 2002
Zhi Wang MD
Abstract Objectives Chemoprevention is a promising strategy to inhibit carcinoma before invasive tumors develop, but a new molecular target is desirable. Celecoxib is a newly developed cyclo-oxygenase (COX)-2 inhibitor with significantly less toxicity. The study was conducted to determine whether celecoxib is effective and safe in prevention of oral cancer. The antiangiogenic activity of celecoxib was studied to explore the potential mechanism involved. Study Design Randomized animal study. Methods The study consisted of two phases. In the phase 1, 10 mice were used to determine the efficacy and safety of celecoxib with intradermal inoculation with oral carcinoma cells. The 10 mice were equally divided into two groups 5 mice (30 inoculated sites) in each group to receive 1,500 parts per million (ppm) celecoxib mixed in with the diet or to eat a normal diet, respectively, for 21 days. In phase 2, 10 more mice were inoculated to determine the effect of celecoxib on angiogenesis. Five mice received 3,000 ppm celecoxib in the diet, with the other five mice as control animals. The antiangiogenic activity was evaluated by comparing the density of newly growing microvessels after the inoculation. Results The results indicated that celecoxib significantly delayed cell growth and reduced tumor volume. There was statistical significance in the quantity of new vasculature in the tumor sites between the two groups. No toxic effect was found by means of measurement of body weight loss and microscopic dissection of organs. Conclusions The study provided the first evidence to show the chemopreventive efficacy of celecoxib on oral cancer in a nude mouse model. Clinical trials are warranted to determine the efficacy in humans. [source]