共信号分子B7-H4在人肺腺癌中的表达及临床意义

目的研究共信号分子B7-H4在人肺腺癌组织中的表达及临床意义。方法收集2013年10月-2014年10月手术切除的肺腺癌患者肺癌组织标本94份,正常肺组织标本20份,应用免疫组织化学法,分别检测组织标本中B7-H4的表达水平。结果 B7-H4在20份正常人肺组织中表达较低,在94份人肺腺癌组织中的阳性表达率为67.32%,在合并有淋巴结转移的肺腺癌组织中B7-H4的阳性表达率为73.24%。低分化组肺腺癌组织B7-H4阳性表达率(84.82%)明显高于中分化组(77.38%)和高分化组(62.51%)。结论共信号分子B7-H4在肺腺癌组织中表达上调,有可能成为评价肺腺癌分化程度和淋巴结转移的指标之一。     

卵巢上皮性肿瘤组织中泛素与Cyclin B1的表达及意义

采用免疫组化SP法检测20例正常卵巢组织、20例上皮性良性卵巢肿瘤组织及50例上皮性卵巢癌组织中的泛素和细胞周期蛋白B1（Cyclin B1）,分别与上皮性卵巢癌的组织学类型、病理分级、临床分期及淋巴结转移的关系。结果显示,泛素在上皮性卵巢癌、正常卵巢组织和良性卵巢肿瘤中的阳性表达率分别为34%（17/50）、5%（1/20）、10%（2/20）,Cyclin B1的阳性表达率分别为42%（21/50）、5%（1/20）、15%（3/20）,两者在卵巢癌中的阳性表达率均显著高于正常卵巢组织和良性卵巢肿瘤（P均〈0.05）;泛素和Cyclin B1在上皮性卵巢癌中的阳性表达率随细胞分化程度的降低、临床分期增加而增高（P均〈0.05）,伴区域淋巴结转移者,其表达增高（P〈0.05）;泛素和Cyclin B1在上皮性卵巢癌中的表达呈正相关（r=0.301,P〈0.05）。认为泛素、Cyclin B1与上皮性卵巢癌的发生发展密切相关,有可能成为评估上皮性卵巢癌恶性程度及判定预后的重要指标。     

ERα、EGFR 及 CyclinD1在上皮性卵巢癌中的表达及意义

目的：探讨雌激素受体α（ ERα）、表皮生长因子受体（ EGFR）及细胞周期蛋白D1（ CyclinD1）在上皮性卵巢癌中的表达及临床意义。方法采用免疫组化SP法观察ERα、EGFR及CyclinD1在上皮性卵巢癌组织58份（浆液性卵巢癌组织38份、非浆液性卵巢癌组织20份）、正常卵巢组织18份、卵巢良性肿瘤组织20份中的表达情况。结果 ERα、EGFR及CyclinD1在上皮性卵巢癌组织中的阳性表达率分别为74．13％、68．97％、51．72％,显著高于正常卵巢组织（33．33％、16．67％、0）及卵巢良性肿瘤组织（30．0％、25．0％、10．0％）（P均＜0．05）;但ERα、EGFR及CyclinD1在卵巢良性肿瘤、正常卵巢组织中的阳性表达率比较P均＞0．05。 ERα、EGFR及CyclinD1在上皮性卵巢癌中的表达与临床分期及细胞分化程度有关（P均＜0．05）。结论 ERα、EGFR及CyclinD1在上皮性卵巢癌中过表达,并在一定程度上反映其恶性程度及预后状况。     

食管鳞癌组织中B7-H4、CD3表达变化及意义

目的探讨B7-H4、CD3在食管鳞癌发生、发展中的作用。方法采用免疫组化SP法检测30例食管鳞癌组织（食管癌组）和20例癌旁正常食管黏膜组织（对照组）中B7-H4、CD3蛋白表达,采用等级相关方法分析B7-H4和CD3表达的相关性。结果食管癌组B7-H4阳性表达率高于对照组,CD3阳性表达率低于对照组（P均〈0.05）。不同临床分期及淋巴结转移情况者食管癌组织中B7-H4表达差异有统计学意义（P均〈0.05）。食管癌组织中B7-H4与CD3蛋白的表达呈负相关关系（r=-0.467,P〈0.05）。结论食管鳞癌组织中B7-H4呈高表达,CD3呈低表达,二者与食管鳞癌的发生发展及侵袭转移有关。     

上皮性卵巢癌DNA-PKcs和ERCC1表达与预后相关因素分析

目的探讨原发上皮性卵巢癌组织中DNA—PKcs和ERCC1表达与卵巢癌预后的关系。方法采用免疫组化SP法检测99例上皮性卵巢癌和16例正常卵巢组织中DNA-PKcs和ERCC1的表达。结果DNA-PKcs和ERCC1在卵巢癌组织中的阳性率分别为60．61％和53．54％,均显著高于正常卵巢组织（P〈0．01）;DNA-PKcs和ERCCI表达呈显著正相关（r=0．408,P=0．000）。单因素分析显示,DNA-PKcs与ER．CCl共表达,FIGO分期、淋巴结转移、CA125半衰期、残留灶直径均与卵巢癌患者的生存时间有关（P〈0．05）。多因素分析显示,ERCC1表达、FIGO分期、淋巴结转移与残留灶直径均是影响卵巢癌预后的独立危险因素。结论DNA-PKcs和ERCC1在上皮性卵巢癌组织中表达率明显高于正常卵巢组织;联合检测DNA-PKcs与ERCC1表达可作为早期诊断及预测卵巢癌预后的指标。     

Cx43和Fas在胃癌组织中的表达

目的研究间隙连接蛋白43（Cx43）和凋亡调节因子Fas在胃癌组织中的表达情况。方法应用免疫组化法检测70例胃癌患者手术切除的癌组织和癌旁正常组织中Cx43和Fas表达水平。结果Cx43在胃癌组织中的表达率为44．29％（31／70）,在癌旁正常组织中的表达率为92．86％（65／70）,P〈0．01;Fas在胃癌组织中的表达率为40．00％（28／70）,在癌旁正常组织中表达率为87．14％（61／70）,P〈0．01。Cx43表达水平与胃癌组织学分化程度、浸润深度、淋巴结转移有关（P〈0．05）,Fas表达水平与胃癌组织学分化程度、浸润深度、TMN分期、淋巴结转移有关（P〈0．05）。结论胃癌组织中Cx43和Fas表达水平的检测有助于判断胃癌的恶性程度。     

PTEN、survivin蛋白在食管癌中的表达及其相关性

应用免疫组织化学sP法检测60例食管癌组织及20例癌旁正常黏膜的survivin和PTEN的表达水平。结果：survivin在食管癌组织的阳性表达率为70．0％,癌旁正常黏膜为40．0％（P〈0．05）;低、高分化癌的阳性表达率差异显著（P〈0．05）;有、无淋巴结转移者的阳性表达率分别为88．9％、61．9％（P〈0、05）;其表达与肿瘤的浸润深度显著相关（P〈0．05）,与患者的性别、年龄无关（P〉0．05）。PTEN在癌旁正常黏膜阳性表达率为90．0％。食管癌组织为36．7％（P〈0．05）。低、高分化癌的阳性表达率差异显著（P〈0．05）;有、无淋巴结转移者的阳性表达率分别为16．7％、45．2％（P〈0．05）;与患者的性别、年龄及浸润深度无关（P〉0．05）。survivin和PTEN在食管癌中的表达呈负相关。认为PTEN低表达及survivin的过表达与食管癌的发生及其生物学行为密切相关,可作为食管癌早期诊断及评估预后的客观指标。     

生长抑素的表达与胃黏膜上皮癌变的关系

[目的]探讨生长抑素（ss）在胃黏膜上皮癌发生、发展中的作用及地位，从而为胃癌的诊断、治疗及预后判断提供一个新的途径。[方法]应用免疫组化SABC（Strept Avidin Biotin Complex）法检测78例胃癌组织和20例正常胃黏膜、53例胃黏膜上皮各级癌前病变标本中SS的表达。[结果]SS在正常胃黏膜中阳性表达率为85．0％，癌前病变组织中阳性表达率为43．4％，胃癌组织中阳性表达率为24．3％；高／中分化组和低分化组中的阳性表达率分别为34．2％、13．5％，随分化程度减低呈下降趋势；浸润黏膜层或黏膜下层和浸润肌层或浆膜层两组的阳性表达率分别为64．3％、15．6％，随浸润程度的加深其阳性表达率呈下降趋势；无淋巴结转移组和有淋巴结转移组的阳性表达率分别为38．7％、14．9％；TNMⅠ～Ⅱ期和Ⅲ～Ⅳ期的阳性表达率分别为45．5％、8．9％。以上两组间比较差异均有统计学意义（P〈0．05）。[结论]SS的低表达与胃癌的组织学分级、浸润深度、淋巴结转移及TNM分期密切相关。SS的失表达可能是胃黏膜上皮癌变过程中的重要机制之一。     

p16基因表达与胃癌生物学行为的关系

目的探讨P16蛋白表达与胃癌生物行为的关系．方法采取S－P免疫组织化学方法，检测51例胃癌组织中P16蛋白的表达，并与正常胃组织进行对比．结果正常胃组织和胃癌组织中P16蛋白的阳性表达率分别为100．0％（12／12）和39．2％（20／51），两组比较有非常显著性差异（P＜0．001）．P16蛋白的阳性表达与胃癌分化程度，浸润深度无明显关系（P＞0．05），但在有淋巴结转移的胃癌中，P16蛋白的阳性表达率仅25．8％（8／31），而无淋巴结转移组P16蛋白的阳性表达率为60．0％（12／20），两组间有显著性差异（P＜0．05）．结论P16蛋白表达缺失与胃癌的发生及淋巴结转移有密切关系．检测P16蛋白表达可作为诊断胃癌及判断患者预后的参考指标．     

Survivin在卵巢癌中的表达及其临床意义

目的探讨Survivin在卵巢癌中的表达及其临床意义。方法运用免疫组织化学SP法检测9例正常卵巢、17例卵巢交界性肿瘤以及26例卵巢癌组织中Survivin的表达情况。结果正常卵巢组织中无Survivin表达,卵巢交界性肿瘤、卵巢癌组织中Survivin表达阳性率分别为52．9％和80．8％,组间比较有统计学差异（P〈0．01）;卵巢癌组织中Survivin表达与临床分期、组织学分级及淋巴转移有关（P均〈0．01）。结论Survivin与卵巢癌的发生、发展有关。     

Expression of programmed death-1 ligand (PD-L) 1, PD-L2, B7-H3, and inducible costimulator ligand on human respiratory tract epithelial cells and regulation by respiratory syncytial virus and type 1 and 2 cytokines

BACKGROUND: Respiratory syncytial virus (RSV) is associated with wheezing illness, and infections can occur repeatedly throughout life. We hypothesized that RSV infection of respiratory tract epithelial cells up-regulates B7 molecules that regulate memory immune responses and that type 1 and 2 cytokines differentially modulate this induction. METHODS: We used flow-cytometric analysis to investigate programmed death-1 ligand (PD-L) 1, PD-L2, B7-H3, and inducible costimulatory ligand (ICOS-L) expression on tracheal (NCI-H292), bronchial (BEAS-2B), and alveolar (A549) epithelial cells; regulation of this expression by RSV, interferon (IFN)- gamma , and interleukin (IL)-4; and the effects of IFN-gamma and IL-4 on RSV-induced expression of these molecules. RESULTS: B7-H3 was strongly expressed, PD-L1 and ICOS-L were moderately expressed, and PD-L2 was weakly expressed on unstimulated tracheal, bronchial, and alveolar epithelial cells. RSV infection up-regulated PD-L1, PD-L2, and B7-H3 expression on all cells and ICOS-L expression on bronchial and alveolar epithelial cells. IL-4 treatment alone had no effect, whereas IFN-gamma treatment alone increased PD-L1 and PD-L2 expression on all cells and decreased B7-H3 expression on bronchial and alveolar epithelial cells. On RSV-infected alevolar epithelial cells, IFN-gamma treatment increased PD-L1 and PD-L2 expression and decreased B7-H3 and ICOS-L expression, and IL-4 treatment increased PD-L2 and B7-H3 expression and decreased ICOS-L expression. CONCLUSIONS: Respiratory tract epithelial cells express a wide range of B7 molecules. RSV infection increases their expression, and this expression is differentially regulated by IFN-gamma and IL-4. These processes may be involved in decreasing T cell antiviral immune responses to RSV and in RSV-associated wheezing.     

Expression and correlation of CD44v6, vascular endothelial growth factor, matrix metalloproteinase-2, and matrix metalloproteinase-9 in Krukenberg tumor

AIM: To explore the expression and correlation of CD44v6, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2 and matrix metalloproteinase (MMP)-9 in Krukenberg and primary epithelial ovarian carcinoma. METHODS: The expressions of CD44v6, VEGF, MMP-2 and MMP-9 were detected by immunohistochemical method in 20 cases of normal ovarian tissues, 38 cases of Krukenberg tumor and 45 cases of primary epithelial ovarian carcinoma. RESULTS: The expression of CD44v6 (primary epithelial ovarian carcinoma tissue vs normal ovarian tissue: x2 = 4.516, P= 0.034; Krukenberg tumor tissue vs normal ovarian tissue: x2 = 19.537, P= 0.001) and VEGF (primary epithelial ovarian carcinoma tissue vs normal ovarian tissue: P = 0.026; Krukenberg tumor tissue vs normal ovarian tissue: x2 = 22.895, P= 0.001) was significantly higher in primary epithelial ovarian carcinoma tissue and Krukenberg tumor tissue than in normal ovarian tissue. The positive expression rate of MMP-2 and MMP-9 was 0% in the normal ovarian tissue. The positive expression rate of CD44v6 (x2 = 10.398, P= 0.001), VEGF (x2 = 13.149, P= 0.001), MMP-2 (x2= 33.668, P= 0.001) and MMP-9 (x2 = 38.839, P = 0.001) was remarkably higher in Krukenberg tumor than in primary epithelial ovarian carcinoma. The correlation of CD44v6, VEGF, MMP-2, and MMP-9 was observed in primary epithelial ovarian carcinoma and Krukenberg tumor. CONCLUSION: CD44v6, VEGF, MMP-2, and MMP-9 are involved in ovarian carcinoma, gastric cancer and Krukenberg tumor. Detection of CD44v6, VEGF, MMP-2 and MMP-9 may contribute to the diagnosis of ovarian carcinoma, gastric cancer, and Krukenberg tumor.     

SDF-1／CXCR4在老年卵巢癌组织中的表达及意义

目的探讨趋化因子SDF-1及其受体CXCR4在老年人上皮性卵巢癌组织中的表达及意义。方法应用westernblotting方法定量检测43例老年患者上皮性卵巢癌组织中SDF-1和CXCR4的蛋白表达情况。结果老年人上皮性卵巢癌组织中SDF-1／CXCR4蛋白表达较卵巢良性肿瘤对照组明显增加,其相对表达量分别为（2．38±0．20）和（3．32±0．26）,差异具有统计学意义（P〈0．05）。结论SDF-1／CXCR4生物学轴可能在老年人卵巢癌的发生与转移过程中起着重要作用。     

B7-H4 expression in renal cell carcinoma and tumor vasculature: associations with cancer progression and survival

B7-H4 is a recently described B7 family coregulatory ligand that has been implicated as an inhibitor of T cell-mediated immunity. Although expression of B7-H4 is typically limited to lymphoid cells, aberrant B7-H4 expression has also been reported in several human malignancies. To date, associations of B7-H4 with clinical outcomes for cancer patients are lacking. Therefore, we examined B7-H4 expression in fresh-frozen tumor specimens from 259 renal cell carcinoma (RCC) patients treated with nephrectomy between 2000 and 2003 and performed correlative outcome analyses. We report that 153 (59.1%) RCC tumor specimens exhibited B7-H4 staining and that tumor cell B7-H4 expression was associated with adverse clinical and pathologic features, including constitutional symptoms, tumor necrosis, and advanced tumor size, stage, and grade. Patients with tumors expressing B7-H4 were also three times more likely to die from RCC compared with patients lacking B7-H4 (risk ratio = 3.05; 95% confidence interval = 1.51-6.14; P = 0.002). Additionally, 211 (81.5%) specimens exhibited tumor vasculature endothelial B7-H4 expression, whereas only 6.5% of normal adjacent renal tissue vessels exhibited endothelial B7-H4 staining. Based on these findings, we conclude that B7-H4 has the potential to be a useful prognostic marker for patients with RCC. In addition, B7-H4 represents a target for attacking tumor cells as well as tumor neovasculature to facilitate immunotherapeutic treatment of RCC tumors. Last, we demonstrate that patients with RCC tumors expressing both B7-H4 and B7-H1 are at an even greater risk of death from RCC.     

宫颈癌组织中B7-H3蛋白的表达变化及其与HPV感染的关系

目的观察宫颈癌组织中的B7家族同族3（B7-H3）蛋白的表达变化,探讨其与人乳头瘤病毒（HPV）感染的关系。方法采用免疫组化SP法检测50例宫颈癌组织肿瘤细胞和血管内皮细胞（宫颈癌组）中及15例子宫肌瘤组织（对照组）中的B7-H3蛋白。采用人乳头状瘤病毒核酸扩增分型检测试剂盒检测两组HPV感染情况。结果宫颈癌组肿瘤细胞B7-H3蛋白阳性41例,内皮细胞B7-H3蛋白阳性为24例;对照组宫颈组织细胞B7-H3蛋白阳性为3例,内皮细胞中无B7-H3表达,两组相比,P均〈0.05。宫颈癌组中HPV感染25例;对照组中无HPV感染者。宫颈癌组肿瘤细胞及血管内皮细胞中B7-H3蛋白表达与HPV感染呈正相关（r分别为0.364 4、0.400 3,P均〈0.05）。结论宫颈癌肿瘤细胞及血管内皮细胞中B7-H3呈高表达,且与HPV感染有关。     

卵巢肿瘤组织中EGFR、CK20表达及意义

目的探讨细胞角质蛋白20（CK20）和表皮生长因子受体（EGFR）mRNA在卵巢上皮性肿瘤发生中的作用。方法应用RT-PCR法检测12份正常卵巢（对照组）、18份卵巢良性肿瘤（良性组）、33份卵巢恶性肿瘤（恶性组）和14份胃肠道转移性卵巢肿瘤（转移组）组织中CK20、EGFR mRNA的表达。结果恶性组中CK20、EGFR mRNA阳性率显著高于对照组及良性组（P〈0.05）,与转移组比较无明显差异;恶性组CK20 mRNA表达与手术病理分期、淋巴结转移有关（P〈0.05）,EGFR mRNA表达与手术病理分期有关（P〈0.05）。结论CK20、EG-FR高表达可促进卵巢恶性肿瘤的发生、转移;其检测对判断预后有一定价值。     

The expression and distribution of immunomodulatory proteins B7-H1, B7-DC, B7-H3, and B7-H4 in rheumatoid synovium

CD28/B7 signals have been shown to have the capacity to regulate T cell activation and participate in regulating the development of rheumatoid arthritis (RA). However, the expression and anatomical distribution of some members of the B7 superfamily including B7-H1, B7-DC, B7-H3 and B7-H4 in RA synovium is still unclear. We analyzed the expression of these molecules in synovial tissues from RA patients. Immunohistochemistry showed that all of these molecules were observed in synovium. On the cellular level, all of them were found on cell membrane and in cytoplasma. The expression of B7-DC and B7-H3 was major on capillaries, synovicytes and infiltrated inflammatory cells in the lining layer, while B7-H1 and B7-H4 were detected in some inflammatory cells residing in the sublining and lining layer. Fluorescent dual staining indicated that all these molecules were principally associated with CD31⁺ endothelial cells and CD68⁺ macrophages. In addition, B7-H1 and B7-H3 were also observed on CD3⁺ T cells (including CD4⁺ and CD8⁺ T cells). Interestingly, B7-H1/B7-H4, B7-H3/B7-DC were co-expressed on the same cells. The characteristic expression and distribution of these molecules in synovium indicated that they probably have different effects during the progress of RA, and a clear understanding of their functional roles may further elucidate the pathogenesis of this disease.     

B7-H3 and B7x are highly expressed in human prostate cancer and associated with disease spread and poor outcome

B7-H3 and B7x are recently discovered members of the B7-CD28 family thought to dampen peripheral immune responses via negative costimulation. We evaluated their potential expression in human prostate cancer using a large cohort of patients with 7 years of follow-up. We identified 823 patients with tissue available treated with radical prostatectomy between 1985 and 2003. Immunohistochemistry was performed on tissue microarray sections using anti-B7-H3 and -B7x. The percentage and intensity of immunoreactivity by tumor cells were blindly evaluated by two urological pathologists, and outcome analyses were conducted. Both B7-H3 and B7x were highly expressed; 93% and 99% of tumors had aberrant expression, respectively. The median percentage of tumor cells staining positive was 80% for each molecule. Strong intensity for B7-H3 and B7x was noted in 212 (26%) and 120 (15%) patients, respectively. Patients with strong intensity for B7-H3 and B7x were significantly more likely to have disease spread at time of surgery (P < 0.001 and P = 0.005, respectively). Additionally, patients with strong intensity for B7-H3 and B7x were at significantly increased risk of clinical cancer recurrence (P < 0.001 and P = 0.005) and cancer-specific death (P = 0.004 and P = 0.04, respectively). To our knowledge, we present the largest investigation of B7 family molecules in a human malignancy and a previously undescribed evaluation of B7x in prostate cancer. B7-H3 and B7x are abundantly expressed in prostate cancer and associated with disease spread and poor outcome. Given the proposed immune-inhibitory mechanisms of B7-H3 and B7x, these molecules represent attractive targets for therapeutic manipulation in prostate cancer.     

肺癌CT征象与病理及血清可溶性B7－H4检测临床意义

目的探讨肺癌血清B7-H4与肺癌的CT征象及病理类型之间的相关性。方法回顾分析经病理确诊的74例肺癌患者的CT表现和血清137-H4检测结果。结果肺癌患者中鳞癌、腺癌血清B7＝H4水平为（46．61±4．48）uj/L、（44．76±3．78）ug／L,与肺良性疾病患者血清B7-H4水平（29．52±4．85）ug／L比较,差异有统计学意义（t值分别为15．5805、12．7966,均P〈0．01）;III～IV期肺癌患者血清B7-H4水平（46．16±4．27）uj/L,显著高于I～Ⅱ期患者（41．62±5．01）uj/L（t=4．1343,P〈0．01）。按鳞癌联系强度依次为毛刺征、分叶征、空泡征、细支气管充气征、胸膜凹陷征;按腺癌联系强度依次为毛刺征、分叶征、细支气管充气征、胸膜凹陷征、空泡征。结论CT联合应用血清B7一H4检测结果,可进一步提高肺癌诊断的准确率及检出率。     

Glycoprotein B7-H3 overexpression and aberrant glycosylation in oral cancer and immune response

The incidence and mortality rate of oral cancer continue to rise, partly due to the lack of effective early diagnosis and increasing environmental exposure to cancer-causing agents. To identify new markers for oral cancer, we used a sialylation probe to investigate the glycoproteins differentially expressed on oral cancer cells. Of the glycoproteins identified, B7 Homolog 3 (B7-H3) was significantly overexpressed in oral squamous cell carcinoma (OSCC), and its overexpression correlated with larger tumor size, advanced clinical stage, and low survival rate in OSCC patients. In addition, knockdown of B7-H3 suppressed tumor cell proliferation, and restoration of B7-H3 expression enhanced tumor growth. It was also found that the N-glycans of B7-H3 from Ca9-22 oral cancer cells contain the terminal α-galactose and are more diverse with higher fucosylation and better interaction with DC-SIGN [DC-specific intercellular adhesion molecule-3 (ICAM-3)–grabbing nonintegrin] and Langerin on immune cells than that from normal cells, suggesting that the glycans on B7-H3 may also play an important role in the disease.Oral cancer is the 11th most-common cancer worldwide. An estimated 300,373 new cases and 145,353 deaths from oral cavity cancer (including lip cancer) occurred worldwide in 2012 (1). According to the data in GLOBOCAN 2012 published by the World Health Organization, oral cancer incidence and mortality in men in South and Central Asia is increasing, and it has become the second most common cancer in the region. Epidemiological studies reveal the strong association between oral cancer and the use of betel quid, alcohol, and cigarettes. Cancers of buccal mucosa, tongue, and gingiva constitute the majority of oral cancer in the Asian population, and that is related to the exposure to the carcinogen in these anatomical areas (2). It is estimated that approximately 90–95% of oral cancers are squamous cell carcinoma (OSCC) (3), and oral cancer has been shown to progress from hyperplasia, to mild-to-moderate dysplasia, severe dysplasia, and carcinoma in situ (4). Surgery is the standard treatment for OSCC, but the differences in primary sites and the complex anatomy of the head and neck give rise to intricate patterns of local invasion and regional spread. This distinction makes primary tumors difficult to eradicate once they have grown large enough to spread into adjacent tissues. Radiotherapy is an integral part of primary or adjuvant treatment, and chemotherapy is used as a combination therapy in advanced OSCC (5). Despite numerous prospective trials using various combination therapies to improve locoregional control, survival rates for advanced carcinogen-associated OSCC remain dismal (6). In contrast to many other cancers in which metastasis is the primary cause of death, local recurrence is the common cause of treatment failure and death in patients with OSCC (5). Therefore, locoregional control is a key therapeutic objective (7).Glycosylation is an important biological process that occurs cotranslationally or posttranslationally on more than 50% of eukaryotic proteins and can affect protein folding, stability, solubility, and function. Aberrant glycosylation is often observed in pathological conditions such as inflammation and cancer metastasis. Altered terminal fucosylation and sialylation are believed to result from changes in expression and are associated with tumor malignancy (8). Atypical glycosylation of cell surface carbohydrates has been reported to be associated with malignant transformation of oral epithelium (9), and protein-bound sugar levels were higher in plasma and tissue samples of oral cancer patients (10). A series of studies about dysregulation of the N-glycosylation–regulating gene, DPAGT1, drives oral cancer cell discohesion by inhibiting adhesion of E-cadherin through Wnt signaling pathway were reported (11–13). It was also found that the expression of Lewis^y on EGFR promotes migration of oral cancer cells (14).To identify new markers as diagnostic and therapeutic targets for oral cancer, a sialylation probe was used to investigate the differential expression of glycoproteins in oral cancer and normal cells. Among the glycoproteins identified, receptor B7-H3 was selected for further study because it was more differentially expressed in cancer cells. B7-H3, also known as B7 homolog 3 or CD276 isoform 1, was discovered in 2001 (15) and is a 110-kDa, type I transmembrane glycoprotein with four Ig-like domains that contain a nearly exact tandem duplication of the IgV-IgC domain (4Ig-B7-H3). However, the potential binding partner of B7-H3 remains unclear (16), and the functional effect of B7-H3 on T cells is controversial (17). B7-H3 protein was also found on various cell types and organs. This broad expression pattern suggests more diverse immunological and probably nonimmunological functions of B7-H3, especially in peripheral tissues (18). Recently, B7-H3 has been found in a variety of different human cancers, including prostate (19, 20), nonsmall cell lung (NSCLC) (21), gastric (22, 23), pancreatic (24), ovarian (25), colorectal (26), urothelial cell (27), clear cell renal cell (ccRCC) (28), and hypopharyngeal (29) cancers.We are interested in understanding the expression pattern of B7-H3 in oral cancer and its possible underlying mechanisms. In this study, both the protein and the glycosylation profile of B7-H3 were investigated to explore their correlation with tumor progression with the expectation that the findings will provide more information to better understand oral cancer and improve therapies.