Objective: Laryngeal squamous cell carcinoma (LSCC) belongs to head and neck squamous cell carcinoma (HNSCC), with dismal prognosis. Here, this study aims to disclose the role of LINC-PINT in cancer development, which may contribute to improving the clinical outcomes of LSCC treatment. Methods: LINC-PINT expression in LSCC tissues and in TU-177 and Hep-2 cells was quantified, and subsequently, the association between LINC-PINT and LSCC malignancies was analyzed. pcDNA3.1-LINC-PINT or pcDNA3.1-EZH2 was introduced into Hep-2 and TU-177 cells. qRT-PCR and Western blot analyses examined the levels of proteins related to the AKT/mTOR pathway and their phosphorylated proteins in Hep-2 and TU-177 cells. The viability as well as migration and invasion abilities of Hep-2 and TU-177 cells were determined. Also, the distribution of LINC-PINT in Hep-2 cells was investigated as well as the interplay between LINC-PINT and EZH2. The downstream genes that might interact with EZH2 were screened. Results: LINC-PINT expression was inhibited in LSCC tissues and in Hep-2 and TU-177 cells, whose downregulation was associated with unsatisfactory prognosis. LINC-PINT overexpression suppressed the proliferative, migratory and invasive capacities of Hep-2 and TU-177 cells. LINC-PINT, mainly expressing in nuclei, could enrich EZH2 to silence ZEB1. In Hep-2 and TU-177 cells, the inhibition of LINC-PINT or overexpression of ZEB1 could enhance cell proliferation, migration and invasion. The phosphorylated levels of proteins related to the AKT/mTOR pathway were declined in cells with LINC-PINT overexpression, and the levels of these phosphorylated proteins were increased in cells with LINC-PINT inhibition. Conclusion: LINC-PINT enriches EZH2 to silence ZEB1 and thus inhibits the proliferative, migratory, and invasive capacities of Hep-2 and TU-177 cells. In addition, LINC-PINT might exert its biological function through the AKT/mTOR pathway.

Objectives The purpose of this study was to determine the safety and efficacy of superselective neck dissection(SSND) (levels IIA and III) for patients with supraglottic squamous cell carcinoma (SCC) of the larynx and clinically negative (N0) neck. Study design This was a prospective analysis of consecutive patients. Methods A prospective analysis of 60 patients with SCC of the supraglottic larynx and N0 neck who underwent surgical treatment of the primary lesion with simultaneous SSND (levels IIA and III). The incidence of occult metastasis in the lymph nodes, regional recurrence, survival rate, and spinal accessory nerve function were evaluated. Results Ninety-eight superselective neck dissection (levels IIA and III) procedures were performed for 60 patients. The occult metastasis rate was 20% (12 of 60). Four patients (6.7%) developed regional recurrence, none of them was in level IIB. The 5-year overall, cancer-specific and disease-free survival rate was 82.8%, 87.6%, and 80.7%, respectively. Spinal accessory nerve function was maintained in all patients. Conclusion Superselective neck dissection removing lymph nodes in levels IIA and III was safe and effective for supraglottic SCC of the larynx with clinically negative neck. The spinal accessory nerve function was maintained without compromising clinical outcome.

Thyroid cancer is the most common malignancy of the endocrine system,and its incidence is increasing worldwide.In China,its incidence has increased from 1.78/104 in 1988 to 10.58/104 in 2013.

AFAP1-AS1 is a long non-coding RNA that is associated with tumorigenesis and poor prognosis in a variety of cancers. We have been suggested that AFAP1-AS1 increases tumorigenesis in laryngeal carcinoma specifically by enhancing stemness and chemoresistance. We assessed AFAP1-AS1 expression in human laryngeal specimens, paired adjacent normal tissues and human HEp-2 cells. Indeed, we found not only that AFAP1-AS1 was up-regulated in laryngeal carcinoma specimens and cells, but also that stemness-associated genes were overexpressed. Silencing of AFAP1-AS1 promoted HEp-2 cell chemoresistance under cisplatin treatment. Expression of AFAP1-AS1 was increased in drug-resistant Hep-2 cells. We then probed the mechanism of AFAP1-AS1 activity and determined that miR-320a was a potential molecular target of AFAP1-AS1. Luciferase reporter and qRT-PCR assays of AFAP1-AS1 and miR-320a levels in human specimens and cell cultures indicated that AFAP1-AS1 negatively regulates miR-320a. To discover the molecular mechanism of miR-320a, we again used the DIANA Tools algorithm to predict its genetic target, RBPJ. After cloning the 3'-untranslated regions (3'-UTR) of RBPJ into a luciferase reporter, we determined that miR-320a did in fact reduce RBPJ mRNA and protein levels. Ultimately, we determined that AFAP1-AS1 increases RBPJ expression by negatively regulating miR-320a and RBPJ overexpression rescues stemness and chemoresistance inhibited by AFAP1-AS1 silencing. Taken together, these results suggest that AFAP1-AS1 can serve as a prognostic biomarker in laryngeal carcinoma and that miR-320a has the potential to improve standard therapeutic approaches to the disease, especially for cases in which cancer cell stemness and drug resistance present significant barriers to effective treatment.

AFAP1‐AS1 is a long non‐coding RNA that is associated with tumorigenesis and poor prognosis in a variety of cancers. We have been suggested that AFAP1‐AS1 increases tumorigenesis in laryngeal carcinoma specifically by enhancing stemness and chemoresistance. We assessed AFAP1‐AS1 expression in human laryngeal specimens, paired adjacent normal tissues and human HEp‐2 cells. Indeed, we found not only that AFAP1‐AS1 was up‐regulated in laryngeal carcinoma specimens and cells, but also that stemness‐associated genes were overexpressed. Silencing of AFAP1‐AS1 promoted HEp‐2 cell chemoresistance under cisplatin treatment. Expression of AFAP1‐AS1 was increased in drug‐resistant Hep‐2 cells. We then probed the mechanism of AFAP1‐AS1 activity and determined that miR‐320a was a potential molecular target of AFAP1‐AS1. Luciferase reporter and qRT‐PCR assays of AFAP1‐AS1 and miR‐320a levels in human specimens and cell cultures indicated that AFAP1‐AS1 negatively regulates miR‐320a. To discover the molecular mechanism of miR‐320a, we again used the DIANA Tools algorithm to predict its genetic target, RBPJ. After cloning the 3′‐untranslated regions (3′‐UTR) of RBPJ into a luciferase reporter, we determined that miR‐320a did in fact reduce RBPJ mRNA and protein levels. Ultimately, we determined that AFAP1‐AS1 increases RBPJ expression by negatively regulating miR‐320a and RBPJ overexpression rescues stemness and chemoresistance inhibited by AFAP1‐AS1 silencing. Taken together, these results suggest that AFAP1‐AS1 can serve as a prognostic biomarker in laryngeal carcinoma and that miR‐320a has the potential to improve standard therapeutic approaches to the disease, especially for cases in which cancer cell stemness and drug resistance present significant barriers to effective treatment.

This study aimed to further understand the functional synergy between microRNAs in the pathogenesis of nasopharyngeal carcinoma (NPC). The microarray dataset GSE46172 was downloaded from Gene Expression Omnibus. After missing values imputation using the Impute package (default K value of 10) and across-array normalization by the quantile normalization method using the PreprocessCore package, the differential expression analysis was performed using the LIMMA (Linear Models for Microarray Data) package of R. MiRNAs with |log(2)FC (Fold change)| > 1 and adjusted P-value < 0.05 were considered as differentially expressed miRNAs (DEMs). Totally, 47 DEMs were screened, including 30 up-regulated and 17 down-regulated ones. And 33 miRNAs formed 515 miRNA-miRNA pairs, sharing with at least one common target gene, and miR-203 and miR-526b shared the most common target genes (1169). 365 miRNA pairs have functional synergism, and miR-139-5p and miR-141 shared the most common GO terms (703). In conclusions, MiR-141 and miRNA-138 may have critical roles in NPC pathogenesis, mainly working via functional synergy with many other miRNAs to regulate genes that are involved in cell cycle regulation and apoptosis in NPC pathogenesis.

Targeting cancer cells is crucial for improving the efficiency of laryngeal cancer treatment. However, the signaling pathway and therapeutic strategy, related to the tumor, still need further research. Dietary flavonoid fisetin (3,3′,4′,7-tetrahydroxyflavone) found in many fruits and vegetables has been shown in preclinical studies to inhibit cancer growth through regulating cell cycle, apoptosis, angiogenesis, invasion and metastasis without causing any toxicity to normal cells. PI3K/AKT and ERK1/2 have been known as essential signaling pathways to modulate cell proliferation, apoptosis as well as autophagy via mTOR, Caspase-3 and NF-κB signals. In our study, flow cytometry and western blot assays suggested that apoptosis was induced by fisetin administration, promoting Caspase-3 expressions by regulating PI3K/AKT/NF-κB. Additionally, fisetin suppressed TU212 cells proliferation, which was linked with ERK1/2 inactivation. Further, the activation of PI3K/AKT-regulated mTOR was inhibited by fisetin, leading to transcription suppression and proliferation inhibition of TU212 cells. In vivo studies also showed that the tumor volume and weight of nude mice were reduced for fisetin use with KI-67 decrease and LC3II increase in tumor tissue samples. Together, our data indicated that fisetin had a potential role in controlling human laryngeal cancer through inhibiting tumor cell proliferation, inducing apoptosis and autophagy regulated by ERK1/2 and AKT/NF-κB/mTOR signaling pathways, which might provide a therapeutic strategy for laryngeal cancer inhibition in future.

Aims: This study aimed to investigate the expression of EphA7 in human laryngeal squamous cell carcinoma (LSCC) tissues and disclose the potential roles and molecular mechanisms of EphA7 in LSCC. Methods: In the present study, we examined EphA7 expression and its function and mechanism in LSCC. EphA7 expression levels were investigated by quantitative real-time PCR (qRT-PCR), western blotting, and immunohistochemistry in a panel of 35 LSCC patient cases. To investigate the potential mechanism of EphA7 in human laryngeal cancer, we employed EphA7 siRNA to knockdown EphA7 expression in LSCC cell line Hep-2 and AMC-HN-8. Subsequently, MTT, TUNEL, qRT-PCR, and western blotting were performed to disclose the roles of EphA7 on proliferation, invasion and migration, and apoptosis in LSCC cell line Hep-2 and AMC-HN-8. Results: Depletion of EphA7 remarkably inhibited the proliferation and invasion of Hep-2 and AMC-HN-8 cells in comparison to control and EphA7 siRNA negative control (NC)-transfected cells. TUNEL staining assay demonstrated that, compared with the control group, the rate of apoptosis in the EphA7 siRNA group was significantly increased. In addition, knockdown of EphA7 in Hep-2 or AMC-HN-8 cells markedly decreased the expression of EphA7 and PTEN, which could contribute to apoptosis. However, the bpV(phen), a PTEN inhibitor, could attenuate anti-proliferation and pro-apoptotic effects of EphA7 siRNA in Hep-2 and AMC-HN-8 cells. Conclusion: Up-regulation of EphA7 was observed in human LSCC samples and down-regulation of EphA7 effectively suppressed laryngeal carcinoma cell growth and promoted its apoptosis. Thus, EphA7 has a critical role in modulating cell growth and apoptosis, which serves as a potential therapeutic target in human LSCC.

Objective To investigate the expression of CXCL12 and CXCR4 in gallbladder cancer,and to explore its clinical significance. Methods From January 2010 to December 2014,132 cases of surgically confirmed gallbladder cancer were selected,74 males and 58 females,and 24 cases of normal gallbladder were taken as controls. Expression of CXCL12 and CXCR4 was determined by immunohistochemistry in gallbladder cancer and normal gallbladder. Results The positive CXCL12 and CXCR4 cells were expressed in gallbladder cancer cytoplasm. The positive rates of CXCL12 and CXCR4 expression were 69. 7%( 92 /132) and 62. 1%( 82 /132) in gallbladder cancer,and 16. 7%( 4 /24) and 8. 3%( 2 /24) in normal gallbladder,respectively,and the expression in gallbladder cancer was significantly higher than that in normal gallbladder( P 0. 01). The expression of CXCL12 and CXCR4 was closely related with Nevin stage and lymph node metastasis( P 0. 05). Conclusion The results suggest that the CXCL12 and CXCR4 expression may have some clinical significance for the diagnosis of primary gallbladder cancer.

Tongue squamous cells carcinoma (TSCC) is the most common type in oral cancers. Recently, accumulating evidence suggests that microRNAs (miRNAs) play critical roles in tumorigenesis. Here, we demonstrated that miR-219 was significantly downregulated in TSCC tissues and cell lines. miR-219 overexpression remarkably suppressed cell proliferation, colony formation, migration and invasion of TSCC cells. In addition, protein kinase CI (PRKCI) was identified as a target of miR-219, and overexpression of PRKCI could significantly attenuated the tumor suppressive effects of miR-219. Furthermore, PRKCI inversely correlates with miR-219 in TSCC tissues. Taken together, miR-219 inhibited growth and metastasis by targeting PRKCI and might be used as a potential target for the treatment of TSCC.

In the present study, we aimed to detect microRNA-9 (miR-9) expression level and its clinical significance in laryngeal squamous cell carcinomas (LSCC). 103 patients who were diagnosed with LSCC and treated between March 2010 and June 2013 were enrolled in this study. Expression levels of miR-9 were detected by real-time quantitative RT-PCR assay. Survival curves were estimated using the Kaplan-Meier method, and differences between them were evaluated by the log-rank test. Cox proportional hazard regression test was used to estimate univariate and multivariate hazard ratios for prognosis. We found that miR-9 levels were significantly higher in LSCC tissues compared with matched non-cancerous tissues [4.55 (164-6.75) vs. 2.07 (0.89-2.65), P < 0.05]. The level of miR-9 in LSCC was strongly correlated with tumor differentiation (P = 0.031), thyroid cartilage invasion (P = 0.024), lymph node metastasis (P = 0.009) and clinical TNM stage (P = 0.011). The log-rank test showed that the survival time was significantly different between groups with high and low expression of miR-9 (Log Rank test, P = 0.014). Furthermore, Cox regression multivariate analysis demonstrated that miR-9 expression was an independent prognostic factor of outcomes in patients with LSCC after tumour resection (HR = 3.18, 95% CI = 2.19-11.91, P = 0.012). In conclusion, miR-9 expression was up-regulated in LSCC and was significantly associated with the progression and poorer prognosis of LSCC. Therefore, it might be utilized as a useful prognostic biomarker for LSCC.

Objective:To obs erve the clinical effect of Kang'ai Injection adjuvant chemotherapy for advanced es ophageal cancer with liver metas tas is. Methods: Seventy- three cas es of advanced es ophageal cancer with liver metas tas is were divided into obs ervation group(37 cas es) and control group(36 cas es). The control group was treated with routine chemotherapy,and the obs ervation group was treated with Kang'ai Injection combined with chemotherapy. The s hort- term clinical effect was evaluated after treatment, and the changes of blood routine, liver and renal function were obs erved. Results:The total effective rate was 48.65% in the obs ervation group,and was 30.56% in the control group,the difference being s ignificant(P0.05). The differences of white blood cells and aminotrans feras e,as well as s erum creatinine(SCr),blood urea nitrogen(BUG),and endogenous creatinine clearance rate(CCr) in both groups were ins ignificant(P0.05) before and after treatment,and the differences of BUN,SCr,and CCr in the two groups after treatment were als o ins ignificant(P0.05). The level of hemoglobin in the obs ervation group was increas ed after treatment(P0.05 compared with before treatment),and the increas e was s uperior to that in the control group after treatment(P 0.05). Conclusion: Kang'ai Injection can improve the s hort- term efficacy of chemotherapy for advanced es ophageal cancer with liver metas tas is by increas ing hemoglobin, and protecting the liver function and renal function of patients,and is worth of clinical promotion.

Krüppel-like factor 5 (KLF5), a zinc finger-containing transcription factor, is involved in important biological processes including cell transformation, proliferation, and carcinogenesis. However, its clinical significance has remained largely unknown in laryngeal cancer. Here, specimens from 144 patients with laryngeal tumors were investigated by immunohistochemical staining for KLF5, integrin-linked kinase (ILK), and E-cadherin expressions. A clinicopathological study revealed that the KLF5 expression level in tumor cells was significantly correlated with lymph node metastasis (P < 0.05) and local recurrence (P < 0.05). In addition, KLF5, ILK, and E-cadherin (epithelial–mesenchymal transition (EMT) biomarker) expressions were correlated with each other. These findings suggest that KLF5 may be an epithelial–mesenchymal transition-associated biomarker in human laryngeal carcinomas and play important roles in the progression of laryngeal carcinomas. KLF5 immunoreactivity is therefore considered a potential lymph node metastasis and recurrence factor in human laryngeal cancers. In addition, the KLF5-mediated pathway is a potential target for elimination of laryngeal cancer in the future.

In our previous study, a potential antitumor polysaccharide (LSPc1) was screened from the fruiting bodies of Lepista sordida. However, its molecular mechanism of cell death induction on Hep-2 human laryngocarcinoma cells has still not been determined. The present study evaluated the anticancer efficacy and associated mechanisms of LSPc1 on Hep-2 cells in vitro. We found that LSPc1-induced inhibition of cell proliferation was associated with an increase in G2/M-phase arrest at 48 h. Typical morphological and biochemical features of apoptosis were also observed in LSPc1-treated cells. Furthermore, LSPc1 led a loss of mitochondrial membrane potential (ΔΨm), increased the ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2, induced cytochrome c release, and increased the activity of caspase-3 and -9, which altogether account for apoptotic cell death. Taken together, our study suggests that intrinsic mitochondrial caspase dependent pathway plays a very important role in LSPc1-induced cancer apoptosis and these results provided strong experimental evidence for the use of LSPc1 as a potential therapeutic agent in cancer for laryngocarcinoma.

Four water-soluble polysaccharides (LSPa1, LSPb1, LSPb2 and LSPc1) extracted from the fruiting bodies of Lepista sordida were prepared by DEAE cellulose-52 anion-exchange and Sepharose 6 Fast Flow gel-permeation chromatography. LSPa1 was composed of Glc, Man and Gal with a molar ratio of 3.2: 1.3: 0.6. LSPb1, LSPb2 and LSPc1 were composed of Glc, Man, Gal, Rha and Ara in the proportions of 2.6: 2.1: 0.9: 0.6: 0.3, 1.2: 1.0: 2.3: 0.6: 0.5, 0.2: 0.3: 2.3: 0.3: 2.0, respectively. The high-performance gel-permeation chromatography (HPGPC) analysis showed that the average molecular weight (Mw) of four polysaccharides were approximately 156, 134, 96 and 57 kDa, respectively. MTT and lactate dehydrogenase (LDH) assays indicated that three acidic polysaccharides, namely LSPb1, LSPb2 and LSPc1, possessed more potent antiproliferative effect on human laryngocarcinoma Hep-2 cells than neutral polysaccharide LSPa1 in a dose- and time-dependent manner and the effect increased in the order of LSPa1<LSPb2<LSPb1<LSPc1, which is the same as their uronic acid content. Furthermore the tumor volume and tumor weight were also obviously suppressed after two weeks' treatment of LSPc1 to mice engrafted with Hep-2 cancer cells. Results of these studies demonstrated that the polysaccharide LSPc1 had a potential application as natural antitumor drugs.

Aims: We aimed to investigate the incidence rates and risk factors for different subgroups of central neck lymph node (LN) metastasis (prelaryngeal, ipsilateral paratracheal, pretracheal, and contralateral paratracheal) in unilateral papillary thyroid carcinoma (PTC) patients with clinically negative neck nodes (cN₀). Methods: We evaluated 184 patients from 2007 to 2009. The relationships between different subgroups of LN metastasis and clinical pathological factors were analyzed. Results: The incidence rates of different central LN metastases were diverse. Multivariate analysis indicated that lymphovascular invasion, perithyroidal invasion, and tumor size were risk factors for ipsilateral paratracheal central LN metastasis; tumor size was an independent risk factor for pretracheal central LN metastasis, and pretracheal or/and ipsilateral paratracheal central LN metastasis were risk factors for contralateral paratracheal central LN metastasis. Conclusion: The extent of elective central LN dissection (CLND) should be decided based on different clinical pathological factors in cN₀ PTC patients. Moreover, elective prelaryngeal CLND may be unnecessary.

OBJECTIVE:To investigate the metastatic rule and management methods of occult lymphatic metastasis in patients with supraglottic cancer.METHOD:The results of 139 cN0 patients with supraglottic cancer treated by neck dissection (ND) were reviewed retrospectively. Each lymph node was studied pathologically in order to define the level of the lymph node metastasis.RESULT:Of the 139 patients with supraglottic cancer and cN0 neck, 113 cases received ipsilateral ND and 26 cases with bilateral ND. Thirty-six (25.9%) of 139 patients were found to have occult lymphatic metastasis on pathological examination, 6 patients without metastasis in dissected side at pathologic examination showed metastasis in the contralateral undissected neck later. Therefore the total occult metastasis rate was 30.2% (42 of 139). The unilateral and bilateral neck occult metastases were determined in 37 cases (26.6%) and 5 cases (3.6%) respectively. A total of 3594 lymph nodes were harvested in 165 specimens, with 83 positive nodes. The distributions of the 83 positive nodes were as follows: level I 1.2% (1 node), level II 78.3% (65 nodes), level III 19.3% (16 nodes), level IV 1.2% (1 node), level V (0 node). The 3-year regional recurrence rate was 5.0% (7/139). The 5-year survival rate was 76.3% (106/139). Patients with positive neck metastasis had higher regional recurrence rates (P < 0.05).CONCLUSION:Occult metastasis rate of supraglottic cancer is as high as 30.2%, the selective lateral neck dissection of level II, III is recommended.

Objective To study the expressions of inducible nitric oxide synthase(iNOS) and CD105 in laryngeal squamous cell carcinoma(LSCC) and their clinical significance.Methods The immunohistochemical SP method was used to examine the expressions of iNOS and CD105 in 40 cases of LSCC and 10 cases of normal mucosae,and the microvessel density(MVD) highlighted by CD105 were counted.Results iNOS expression in tumour tissue was significantly higher than normal mucosa(P<0.01),which was related with the metastasis of cervical glands,TNM stage and pathology grading of laryngeal cancer(P<0.05),but no relation with gender,age and tumor site(P>0.05).MVD highlighted by CD105 in tumour tissue [(23.45±8.27)/HPF] was significantly higher than normal mucosa(P<0.01).The degree of iNOS expression and MVD in tumor showed positive correlation(P<0.05).Conclusion Higher expression of iNOS is related to the invasion and metastasis of LSCC,The high MVD in LSCC may be related with the expression of iNOS.iNOS may facilitate the pathogenesis and development of LSCC via accelerating the angiogenesis of the tumor.

The aim of this study was to observe the effects of rapamycin on proliferation, apoptosis and invasion of SW579 in vitro. The proliferation and apoptosis of SW579 cells were detected by methyl thiazolyl tetrazolium and flow cytometry. Transwell assay was used to observe the changes of invasive ability of SW579 cells after being treated with rapamycin. The effects of rapamycin on the expression of mammalian target of rapamycin (mTOR) signalling and vascular endothelial growth factor C (VEGF-C) were observed by Western blot. The inhibition and apoptosis rates increased obviously when the concentration of rapamycin was 20 nm. When the rapamycin concentration was 10 nm, the invasive ability of SW579 cells changed significantly than when it was 5 nm. Our data showed that when the concentrations of rapamycin were over 20 nm, the expression of mTOR and p70S6K decreased significantly, and the expression of PTEN increased notably. There were no remarkable variations observed when we detected the expression of Akt. We found the expression of VEGF-C was high in SW579 cells and decreased slightly when the cells were treated with 5 nm rapamycin. When the concentration of rapamycin was over 5 nm, significant changes were observed. Rapamycin could inhibit the proliferation and induce the apoptosis of human thyroid cancer cells in vitro by mTOR inhibition. No obvious changes observed in the expression of AKT indicated that there might be a feedback loop effect by the mTOR inhibition induced by rapamycin. Rapamycin could inhibit the invasive ability of SW579 cells by down-regulating the expression of VEGF-C.

目的 研究CD105在声门上型喉癌组织中的表达,评价其标记的微血管密度(IMVD)的临床病理意义.方法 应用免疫组化技术检测CD105在40例声门上型喉癌标本及20例正常喉黏膜标本中的表达情况,并计数其标记的微血管密度(IMVD).结果 40例声门上型喉癌组织中IMVD值(23.45±8.27个/HPF)明显高于正常喉黏膜组织(P＜0.01),有淋巴结转移组IMVD值(29.72±2.97个/HPF)明显高于无淋巴结转移组(15.10±3.49个/HPF)(P＜0.01),IMVD值随临床分期增加而明显增加(P＜0.05),而IMVD值与肿瘤的分化程度以及病人的年龄、性别等因素无明显相关(P＞0.05).结论 CD105是肿瘤新生血管的标志,其标记的微血管密度与声门上型喉癌的侵袭转移密切相关,可能作为一种新的肿瘤标志物来监控喉鳞状细胞癌的发生、浸润和转移.