Acute severe hypokalemia caused by treatment of tongue squamous cell carcinoma with docetaxel and cisplatin:A case report

BACKGROUND The tongue squamous cell carcinoma(TSCC)is an oral malignant tumor arising from the squamous epithelium of the tongue mucosa,characterized by a high malignant degree,invasive growth,early lymph node metastasis,and poor prognosis.Paclitaxel,represented by docetaxel,is now the standard first-line treatment for head and neck squamous cell carcinoma.Docetaxel,which belongs to the class of drugs known as paclitaxel,is an antitumor drug that inhibits cell mitosis and proliferation.Its adverse effects include myelosuppression,hair loss,gastrointestinal reactions,fluid retention,and allergic reactions.However,hypokalemia is rare,most cases are mild or moderate,and severe hypokalemia is seldom reported.symptoms of adverse effects early.It is necessary to be considerate regarding individual differences between patients when selecting chemotherapy regimens and adhere to the principle of individualized treatment.Following multiple cycles of chemotherapy,patients should be aware of the accumulation of toxic side effects and receive blood tests reviewed within 24 hours of completion.It is essential to monitor electrolyte levels in patients suffering from severe gastrointestinal reactions to avoid complications that may result in death.

Current Research Status of MicroRNAs in Squamous Cell Carcinoma of the Tongue

Tongue squamous cell carcinoma (TSCC) is the most invasive type of oral malignant tumor, posing a serious threat to human life and health. Its pathogenesis is complex and has a high degree of malignancy. Recurrence and metastasis often lead to poor prognosis. MicroRNAs are a type of single stranded small molecule RNA with only 18 - 25 nucleotides, which can regulate the expression of various genes and participate in the occurrence and development of tumors. Studies have found that microRNA expression profiling can serve as a reliable and stable biological indicator for early diagnosis and prognosis of tumors. This article provides a review of the research status of MicroRNAs in squamous cell carcinoma of the tongue.

Galectin 2 regulates JAK/STAT3 signaling activity to modulate oral squamous cell carcinoma proliferation and migration in vitro

Background:Galectin 2(LGALS2)is a protein previously reported to serve as a mediator of disease progression in a range of cancers.The function of LGALS2 in oral squamous cell carcinoma(OSCC),however,has yet to be explored,prompting the present study to address this literature gap.Methods:Overall,144 paired malignant tumor tissues and paracancerous OSCC patient samples were harvested and the LGALS2 expression levels were examined through qPCR and western immunoblotting.The LGALS2 coding sequence was introduced into the pcDNA3.0 vector,to enable the overexpression of this gene,while an LGALS2-specific shRNA and corresponding controls were also obtained.The functionality of LGALS2 as a regulator of the ability of OSCC cells to grow and undergo apoptotic death in vitro was assessed through EdU uptake and CCK-8 assays,and flow cytometer,whereas a Transwell system was used to assess migratory activity and invasivity.An agonist of the Janus Kinase 2(JAK2)/Signal Transducer and Activator of Transcription 3(STAT3)pathway was also used to assess the role of this pathway in the context of LGALS2 signaling.Results:Here,we found that lower LGALS2 protein and mRNA expression were evident in OSCC tumor tissue samples,and these expression levels were associated with clinicopathological characteristics and patient survival outcomes.Silencing LGALS2 enhanced proliferation in OSCC cells while rendering these cells better able to resist apoptosis.The opposite was instead observed after LGALS2 was overexpressed.Mechanistically,the ability of LGALS2 to suppress the progression of OSCC was related to its ability to activate the JAK/STAT3 signaling axis.Conclusion:Those results suggest a role for LGALS2 as a suppressor of OSCC progression through its ability to modulate JAK/STAT3 signaling,supporting the potential utility of LGALS2 as a target for efforts aimed at treating OSCC patients.

TCGA-based analysis of oncogenic signaling pathways underlying oral squamous cell carcinoma

Background:Oral squamous cell carcinoma(OSCC)represents a prevalent malignancy in the oral and maxillofacial area,having a considerable negative impact on both the quality of life and overall survival of affected individuals.Our research endeavors to leverage bioinformatic approaches to elucidate oncogenic signaling pathways,with the ultimate goal of gaining deeper insights into the molecular underpinnings of OSCC pathogenesis,and thus laying the groundwork for the development of more effective therapeutic and preventive strategies.Methods:Differential expression analysis was performed on mRNA data from tumor and normal tissue groups to identify genes associated with OSCC,using The Cancer Genome Atlas database.Predictions of oncogenic signaling pathways linked to differentially expressedmRNAs were made,and these results were presented visually using R software,using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichments.Results:GO and KEGG analyses of 2938 differentially expressed genes in OSCC highlighted their significant involvement in various biological processes.Notably,these processes were related to the extracellular matrix,structural organization,connective tissue development,and cell cycle regulation.Conclusions:The comprehensive exploration of gene expression patterns provides valuable insights into potential oncogenic mechanisms in OSCC.

Molecular signaling in cancer stem cells of tongue squamous cell carcinoma:Therapeutic implications and challenges

Head and neck squamous cell carcinoma is the seventh most common cancer worldwide with high mortality rates.Amongst oral cavity cancers,tongue carcinoma is a very common and aggressive oral cavity carcinoma.Despite the implementation of a multimodality treatment regime including surgical intervention,chemo-radiation as well as targeted therapy,tongue carcinoma shows a poor overall 5-year survival pattern,which is attributed to therapy resistance and recurrence of the disease.The presence of a rare population,i.e.,cancer stem cells(CSCs)within the tumor,are involved in therapy resistance,recurrence,and distant metastasis that results in poor survival patterns.Therapeutic agents targeting CSCs have been in clinical trials,although they are unable to reach into therapy stage which is due to their failure in trials.A more detailed understanding of the CSCs is essential for identifying efficient targets.Molecular signaling pathways,which are differentially regulated in the CSCs,are one of the promising targets to manipulate the CSCs that would provide an improved outcome.In this review,we summarize the current understanding of molecular signaling associated with the maintenance and regulation of CSCs in tongue squamous cell carcinoma in order to emphasize the need of the hour to get a deeper understanding to unravel novel targets.

Effects of hsa-circ-0001862 on Phenotype of Tongue Squamous Cell Carcinoma Cells

[Objectives]To investigate the molecular mechanism of hsa_circ_0001862 on the proliferation,migration,invasion and apoptosis of tongue squamous cell carcinoma Tca-8113 cells.[Methods]hsa_circ_0001862 plasmid was constructed,and the interaction relationship between hsa_circ_0001862 and miR-23a-3p was verified by dual luciferase reporter gene and qRT-PCR.CCK8 assay,colony formation assay,scratch assay and Transwell assay were used to detect the proliferation,migration and invasion ability of Tca-8113 cells.Western blot was used to detect the expression level of apoptosis-related protein molecules.The effects of hsa_circ_0001862 on the apoptosis of Tca-8113 cells was detected.[Results]hsa_circ_0001862 and miR-23a-3p could interact,and their expression was negatively correlated in tongue squamous cell carcinoma cells.In Tca-8113 cells,hsa_circ_0001862 inhibited cell proliferation,migration,and invasion(P<0.01),and promoted cell apoptosis(P<0.01).[Conclusions]The hsa_circ_0001862 interacts with miR-23a-3p,and hsa_circ_0001862 plays an inhibitory role in the development of tongue squamous cell carcinoma.The hsa_circ_0001862 may be a new biomarker and target for the treatment of tongue squamous cell carcinoma.

Sternocleidomastoid flap for reconstruction of tongue small cell carcinoma: A case report

BACKGROUND The management of tongue carcinoma is excision and radical neck dissection followed with reconstruction.This is a case report of a patient with tongue squamous cell carcinoma(SCC)who underwent the procedure with sternocleidomastoid(SCM)flap reconstruction.CASE SUMMARY A 52-year-old woman without smoking history complained tongue ulcer since 3 years ago.Based on the histopathological examination,the patient was diagnosed with T2N2M0 right tongue SCC and underwent wide excision of tumor;right mandibular;neck dissection and were reconstructed with SCM flap.CONCLUSION SCC of the tongue requires wide excision and dissection of the neck and mandible if infiltration into the surrounding lymph nodes has been found.The SCM flap reconstruction could be used post-surgery.

In vitro effect of iASPP on cell growth of oral tongue squamous cell carcinoma

iASPP is an inhibitory member of the apoptosis-stimulating proteins of P53 （ASPP） family. iASPP is over expressed in several malignant tumors and potentially affects cancer progression. However, the expression and potential role of iASPP in oral tongue squamous cell carcinoma （OTSCC） have not been addressed. In our study, we detected iASPP expression in OTSCC by immunohistochemistry, iASPP expression is up-regulated in OTSCC tissues. Moreover, in clinical pathology specimens, we found that increased iASPP expression correlates with poor differentiation and lymph node metastasis. Using multicellular tumor spheroids （MTS） and flow cytometry, we demonstrated that iASPP down-regulation arrests OTSCC cells at the G0/G1 phase, induces OTSCC cell apoptosis and inhibits OTSCC cell proliferation. These results indicate that iASPP plays a significant role in the progression of OTSCC and may serve as a biomarker or therapeutic target for OTSCC patients.

miR-221/222/PUMA Axis Promotes Oral Squamous Cell Carcinoma Apoptosis

Background: To investigate the therapeutic activity of the miR-221/222 inhibitor against OSCC in vitro and in vivo. Materials and Methods: HSC3 and HSC6 were treated with miR-221/222 inhibitor and the empty vector respectively. After the recombinants were transfected into HSC3 and HSC6 with LipofectamineTM MAX, the expression of miR-221/222 and PUMA was analyzed by RT-PCR. The proliferation and migration of HSC3 and HSC6 were detected by CCK-8 assay and Wound-healing assay. Cell cycle and apoptosis were detected by flow cytometry. The effect of the miR-221/222 inhibitor was also assessed in OSCC xenografts in BALB/c-nu mice. Results: Transfection of the miR-221/222 inhibitor increased cell apoptosis and upregulated PUMA expression in OSCC cell lines HSC3 and HSC6 with the significantly reduced expression of miR-221 and miR-222. Furthermore, the miR-221/222 inhibitor suppressed cell growth and invasion and blocked the cell cycle at the G1 phase. Obvious anti-tumor activity was achieved in BALB/c-nu mice by treatment with the miR-221/222 inhibitor, together with the upregulation of PUMA protein in tumors retrieved from the mice. Conclusions: There was a significant inhibitory effect of the miR-221/222 inhibitor on the growth of OSCC both in vitro and in vivo, and there might be a regulatory loop between miR-221/222 and PUMA. These findings demonstrated that downregulation of miR-221/222 could induce cell apoptosis, and it might be considered as a candidate target for gene therapy of OSCC.

POLE2 Regulates Apoptosis of Oral Squamous Cell Carcinoma Cells through the PI3K/AKT Signaling Pathway

Objective Oral squamous cell carcinoma(OSCC)is the most common malignant tumor of the head and neck,but its occurrence and progression mechanisms remain unclear.In addition-there is a lack of effective targeting drugs.The second major subunit of DNA polymerase(POLE2)catalyzes the prolongation of new strand replication and modifies exonuclease domain activity.Our previous study found that POLE2 was associated with OSCC progression,but the mechanism remains unclear.Methods The expression of POLE2 in OSCC tissues was detected using immunological assays.Mann-Whitney U analysis was used to investigate the relationship between POLE2 gene expression and tumor classification and prognosis of OSCC.POLE2 expression was inhibited in OSCC cells,and the effects of gene and protein expression were detected using RT-PCR and Western blotting.The POLE2 knockout model was constructed by transfecting a lentiviral vector.Cell proliferation,apoptosis,and migration were detected using various assays including colony formation,MTT,flow cytometry,wound healing assay,Transwell assay,and the Human Apoptosis Antibody Array.The animal model of OSCC was established by subcutaneous injection of transfected HN6 into 4-week-old female nude mice.After 30 days,tumors were removed under anesthesia and tumor weight and dimension were recorded.Tumor cell proliferation was analyzed using Ki67 staining.Results POLE2 gene levels were significantly higher in the OSCC tissues than in the normal tissues.In addition,POLE2 gene levels were statistically correlated with tumor classification and prognosis.Silencing POLE2 inhibited the proliferation of oral cancer cells and promoted apoptosis in vitro.Animal experiments also supported a positive correlation between POLE2 and OSCC tumor formation.We further demonstrated that POLE2 could upregulate the expression of apoptosis-related proteins such as caspase-3,CD40,CD40L,DR6,Fas,IGFBP-6,p21,and SMAC.In addition,POLE2 regulated OSCC development by inhibiting the PI3K/AKT signaling pathway.Conclusion POLE2 is closely related to the progression of OSCC.Thus,POLE2 may be a potential target for OSCC treatment.

KIF18A is a potential prognostic factor and promotes tumor progression in oral tongue squamous cell carcinoma

The kinesin family member 18A protein was dysregulated in several human cancers and involved in cancer progression.However,the significance in oral tongue squamous cell carcinoma(OTSCC)has not been studied.The present study was intended to explore the functions of KIF18A in oral tongue squamous cell carcinoma.The immunohistochemistry(IHC)assay was performed to assess the relationships between the KIF18A protein expression level and clinical-pathological features of the patients.The biological functions of KIF18A in OTSCC cells were investigated by the experiments in vitro and in vivo.Based on immunohistochemistry,we found that KIF18A was correlated with the clinical-pathological features of OTSCC patients.High expression of KIF18A was associated with the lymph node metastasis,and clinical stages.In vitro experiments revealed that silencing of KIF18A significantly inhibited the expression of the proliferation and migration related proteins such as Ki67,proliferating cell nuclear antigen,matrix metalloproteinase-7 and matrix metalloproteinase-9,and thereby inhibiting the proliferation,migration and invasion of tumor cells.In vivo,knocking-down of KIF18A could inhibit the tumor growth in nude mice.In conclusion,we found KIF18A promoted tumor progression in vivo and in vitro and might become an effective target for the treatment of OTSCC.

Effects of IL-6/JAK2/STAT3 on the Biological Behavior of Oral Squamous Cell Carcinoma

Objective:To investigate the effect of interleukin 6/Janus kinase 2/signal transducer and activator of transcription 3(IL-6/JAK2/STAT3)on the biological behavior of oral squamous cell carcinoma(OSCC).Methods:OSCC cells were transfected with the designed lentiviral vector plasmid pGMLV-SB3(experimental group)and the corresponding negative control plasmid pGMLV-SB3-shNC(control group);48 hours after transfection,a liposome transfection kit(Sigma,USA)was used for lentivirus packaging;after virus packaging,a medium containing pGMLV-SB3 lentiviral vector was added and cultured for 24 h;the cells were harvested,and RNA was extracted;Transwell chamber assay(Sigma,USA)was used to detect cell migration and invasion ability;dot-enzyme-linked immunosorbent assay(ELISA)kit was used to detect the level of interleukin 6(IL-6)in the culture supernatant,while serum IL-6 level was measured by ELISA.Results:The expressions of IL-6,JAK2,and STAT3 in the experimental group were significantly raised,as compared to the control group(P<0.05);the apoptosis rate of OSCC cells in the experimental group,which was detected by flow cytometry 48 h after transfection,was significantly higher than that of cells in the control group(P<0.05);and there was a significant improvement in the experimental group’s cell migration and invasion ability,as compared to that of the control group(P<0.05).Conclusion:The IL-6/JAK2/STAT3 signaling pathway plays an important role in the migration and invasion of OSCC cells.Inhibiting the expression of IL-6 can inhibit the growth and proliferation of OSCC cells as well as reduce their ability to invade and migrate.These results provide a new target for the treatment of OSCC.

The Effect of MMP-9 Inhibitors on the Biological Behavior of Human Oral Squamous Cell Carcinoma SCC15 Cell Line Through PI3K/Akt Signaling Pathway

Objective:To investigate the effect of MMP-9 inhibitor(Mki67)on the biology of human oral squamous cell carcinoma SCC15 cell line and to explore its mechanism of action through PI3K/Akt signaling pathway.Methods:SCC15 cells were extracted,and the supernatant was discarded.The cells were then rinsed twice with PBS,and 0,2.5,5,and 10μL of Mki67(50 mg/mL)were added to the culture respectively.The inhibition rate of cell proliferation was detected by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide(MTT)method,and the cell migration was measured by Transwell chamber test.The cell apoptosis rate was detected by cytometry,and the p-Akt protein content in the cells of each group was determined by a double-antibody sandwich enzyme-linked immunosorbent assay(ELISA)kit.Results:The cell proliferation rates of the 2.5μL,5μL,and 10μL dose groups were all lower than the 0μL group(P<0.05)before treatment,and the cell proliferation rates in the 2.5μL,5μL,and 10μL dose groups decreased overtime(P<0.05).After 24 h,with the increase of Mki67 concentration,the number of migration and invasion gradually decreased(P<0.05),and the number of apoptosis gradually increased(P<0.05);besides,the relative expression of MMP-9,PI3K,and Akt mRNA decreased gradually(P<0.05),and the expression level of Akt mRNA was not statistically significant(P>0.05).Conclusion:MMP-9 inhibitor(Mki67)can inhibit the proliferation and migration of SCC15 cell line and induce apoptosis,and its mechanism of action may be related to the inhibition of PI3K/Akt signaling pathway.

MiR-25-3p attenuates the proliferation of tongue squamous cell carcinoma cell line Tca8113

Objective:To investigate the effects of miR-25-3p on the occurrence,development and proliferation of tongue squamous cell carcinoma cells.Methods:To establish tongue squamous cell carcinoma cell line Tca8113 that stably and highly express miR-25-3p using recombinant reiroviral vector-mediated gene transfer method.The proliferation of transfected Tca8113 was detected by thiazolyl blue tetrazolium bromide(MTT)and cell colony formation assays.eyclnD1,p21^(cipt)and p27^(kipt)mRNA expressions in the transfected Tca-8113 were detected by quantitative PCR.cyclinD1,p21^(cipt),p27^(kipt),AKT,p-AKT,FOXOt and p-FOX01 expressions in the transfected Tca8113 were detected by western blot analysis.In addition,miR-25-3p expression in the tongue squamous cell carcinoma cell line and tissue specimen was also detected by quantitative PCR.Results:Quantitative PCR showed that mitt-25-3p expression in the tongue squamous cell carcinoma cell lines and tissue specimen was significantly lower than that in the adjacent tissue.MTT and cell colony formation assays showed that after miR-25-3p overexpression,the proliferation of transfected Tca8113 was obviously attenuated.Western blot analysis and quantitative PCR showed that after miR-25-3p overexpression.p21^(cipt)and p27^(kipt)expressions were upregulated,while cyclinD1,AKT,FOXO1 expressions were downregulated,and AKT and FOXO1 phosphorylation was inactivated in the transfected Tca8113 cells.Conclusions:MiR-25-3p inhibited the proliferation of tongue squamous cell carcinoma cells and regulated cell cycle-related protein expression,playing an important role in the occurrence and development of squamous cell carcinoma of the tongue.

OCCULT CERVICAL METASTASIS OF SQUAMOUS CELL CARCINOMA OF TONGUE AMONG CN0 PATIENTS AND ITS TREATMENT

Objective： To explore the treatment of clinically negative neck （CN0） patients with squamous cell carcinoma of the tongue. Methods： 165 CN0 patients with squamous cell carcinoma of the tongue from 1985 to 2002 were investigated retrospectively. Parts of the patients staged at T1, T2 and T3 underwent resection of primary lesion followed by neck observation, and other patients staged above T2 or at T1 but without follow-up were treated with elective neck dissection （END）. All patients were followed up for more than 3 y or until their death. Results： Lymphatic metastasis was identified histologically after operation in 33 of 120 patients treated with END, and 9 of 45 patients treated with resection of primary lesion alone. The overall rate of occult lymphatic metastasis was 25.45%, which increased with the elevating of clinical T stage. The overall rate of neck uncontrolled death was 20.00% for observation group and 5.00% for END group, and significant difference was found between them （P〈0.05）. For T~ patients in the two groups, the rate of neck uncontrolled death was 7.71% and 4.00% respectively, and no significance was found between them （P〉0.05）. When stage T2 and T3 were considered as middle stage together, significant difference （P〈0.05） could be obtained between observation （70.00%） and END group （0%）. Conclusion： The occult metastasis rate of squamous cell carcinoma of tongue increases with the elevating of clinical stage, and elective neck dissection could be considered for NO patients staged over T2 to improve neck control and survival rate; and regional resection alone of primary lesion could be considered for T1N0 patients to improve quality of life if closely followed up is conducted.

Neoneurogenesis in Squamous Cell Carcinoma of Tongue: A New Mechanism for Its Development

Objectives: To explore the role of the growth of new nerves (neo-neurogenesis) in the tumorogenesis of squamous cell carcinoma of tongue. Materials and Methods: 10 formalin-fixed specimens were gained from patients diagnosed with tongue squamous cell carcinoma. Animal models were made by subcutaneous injection in the dorsal midline with Tca-8113 cell line. Mice were sacrificed 2, 4, 6 weeks after cell injection, and tumor tissues were fixed in 4% paraformaldehyde, embedded in paraffin, sectioned. Detection of neo-neurogenesis was stained by Neurofila-ment-L antibody (NF-L) using immunohistochemistry method (IHC) in biopsy from both human body and animal model. Results: IHC staining of NF-L is positive in all 10 paraffins of tongue squamous cell carcinoma sections which suggest that newly formed nerves are observed in tumor microenvironment. NF-L staining is also positive in the paraffins from animal models indicating that the tongue cancer recruits newly formed nerves in its tumorogenesis. Conclusions: Tumor neo-neurogenesis may play an important role in the pathogenesis and development of tongue cancer. From a therapeutic perspective, further studies on the topic may provide new clinical opportunity.

EXPRESSION OF c-erbB-2, p53, p16 IN SQUAMOUS CELL CARCINOMA OF ANTERIOR TONGUE IN CHINA POPULATION

Objective: Aberrant expression of c-erbB-2, p53, p16 has been found in oral squamous cell carcinoma. We therefore examined expression of these proteins in squamous cell carcinoma of the anterior tongue and compared their relationship with clinical stages and prognosis. Methods: Seventy-six patients with squamous cell carcinoma of the anterior tongue never treated before were obtained from Cancer Hospital, CAMS. Archive tissues of carcinoma and paracarcinoma were examined for c-erbB-2, p53 and p16 expression by immunohistochemistry. Results: The rates of immunopositive staining of c-erbB-2, p53 and p16 were 64.5%, 61.8% and 23.7% respectively; the positive rates in paracarcinoma mucosa were 19.7%, 22.6% and 55.3% respectively. Overexpression of c-erbB-2 was significantly correlated with short overall survival, metastasis and staging. Overexpression of paracarcinoma p53 was significantly correlated with local recurrence. Conclusion. c-erbB-2 may be used as a prognosis marker for the patients with squamous cell carcinoma of the anterior tongue and p53 as a recurrence marker.

Expression and Significance of IL-6 and bFGF in Human Tongue Squamous Cell Carcinoma

Objective: To detect the expression and pathological significances of Interleukin-6 (IL-6) and basic fibroblast growth factor (bFGF) in tongue squamous cell carcinoma (TSCC). Methods: A tissue array was analyzed immunohistochemically. The expression levels of IL-6 and bFGF in tissues were recorded semi-quantitatively. Results: The positive expression of IL-6 in normal, benign tumor, and carcinoma groups was 12.50% ± 5.575%, 39.00% ± 1.41%, 77.26% ± 17.07% respectively, and the expression among the three groups showed significant differences (P P P Conclusion: It indicates that combining immunohistochemical examination of IL-6 and bFGF has an important reference value on the pathological diagnosis of tongue squamous cell carcinoma.

Inhibitory effect of celecoxib combined with cisplatin on growth of human tongue squamous carcinoma Tca8113 cell xenograft tumor

Objective:The aim of this study was to observe the inhibitory effect of application of COX-2 inhibitor,celecoxib,combined with cisplatin on the growth of human tongue squamous carcinoma Tca8113 cell xenograft by animal experiment.Methods:The nude mice were transplanted subcutaneously with Tca 8113 cells,and then were administrated with celecoxib,cisplatin or celecoxib combined with cisplatin respectively,and were sacrificed after 35 days.The weight of xenograft was measured to calculate the tumor inhibition rate.The histological change was studied under light and electron microscope.The COX-2 protein expression was observed by immunohistological staining.And the COX-2 mRNA expression was determined by RT-PCR.Results:Celecoxib,the COX-2 inhibitor,could not only inhibit the growth of Tca8113 cell xenograft tumor and COX-2 protein expression,but also enhance the inhibitory effect cisplatin on xenograft tumor growth significantly.The tumor inhibition rates of celecoxib group,cisplatin group and celecoxib plus cisplatin group were 15.63%,37.50% and 82.81% respectively that was statistically significant compared to control group(P < 0.01).The combined application of celecoxib and cisplatin could inhibit tumor growth more significantly than that of separated application(P < 0.01).The inhibitory effect of celecoxib on COX-2 mRNA expression of Tca 8113 cell was weaker and not significant(P = 0.073).Conclusion:Celecoxib can not only inhibit xenograft tumor growth in nude mice,but also enhance the inhibitory effect of CDDP on Tca 8113 transplanted tumor growth in nude mice.The mechanism maybe related to inhibition of COX-2 protein expression,which offers beneficial reference to further explore the mechanism between inhibition of COX-2 enzyme activity and prevention of head and neck tumor.

Development and validation of novel nomograms to predict survival of patients with tongue squamous cell carcinoma

BACKGROUND There is no unified standard to predict postoperative survival in patients with tongue squamous cell carcinoma(TSCC),hence the urgency to develop a model to accurately predict the prognosis of these patients.AIM To develop and validate nomograms for predicting overall survival(OS)and cancer-specific survival(CSS)of patients with TSCC.METHODS A cohort of 3454 patients with TSCC from the Surveillance,Epidemiology,and End Results(SEER)database was used to develop nomograms;another independent cohort of 203 patients with TSCC from the Department of Oral and Maxillofacial Surgery,First Affiliated Hospital of Zhejiang University School of Medicine,was used for external validation.Univariate and multivariate analyses were performed to identify useful variables for the development of nomograms.The calibration curve,area under the receiver operating characteristic curve(AUC)analysis,concordance index(C-index),net reclassification index(NRI),and decision curve analysis(DCA)were used to assess the calibration,discrimination ability,and clinical utility of the nomograms.RESULTS Eight variables were selected and used to develop nomograms for patients with TSCC.The Cindex(0.741 and 0.757 for OS and CSS in the training cohort and 0.800 and 0.830 in the validation cohort,respectively)and AUC indicated that the discrimination abilities of these nomograms were acceptable.The calibration curves of OS and CSS indicated that the predicted and actual values were consistent in both the training and validation cohorts.The NRI values(training cohort:0.493 and 0.482 for 3-and 5-year OS and 0.424 and 0.402 for 3-and 5-year CSS;validation cohort:0.635 and 0.750 for 3-and 5-year OS and 0.354 and 0.608 for 3-and 5-year CSS,respectively)and DCA results indicated that the nomograms were significantly better than the tumor-node-metastasis staging system in predicting the prognosis of patients with TSCC.CONCLUSION Our nomograms can accurately predict patient prognoses and assist clinicians in improving decision-making concerning patients with TSCC in clinical practice.