The effect of neoadjuvant chemotherapy on the correlation of tumor-associated macrophages with CD31 and LYVE-1

Angiogenesis and lymphangiogenesis play a crucial role in tumor growth, invasion and metastasis. Tumor-associated macrophages (TAM) induce both angiogenesis and lymphangiogenesis in mouse breast cancer models and positively correlate with these processes in human breast cancer patients. Neoadjuvant chemotherapy (NAC) is a widely used therapeutic option for cancer treatment. However, the effect of NAC on the distribution of TAM within intratumoral compartments and their correlation with angiogenesis and lymphangiogenesis remained unknown. In the present study we analyzed the effect of NAC on the distribution of CD68+ and stabilin-1+ TAM in five functionally distinct areas of human breast cancer and their correlations with microvessel density (MVD) and lymphatic microvessel density (LMVD), identified by CD31 and LYVE1, respectively. We found that NAC enhances blood vessel density in soft fibrous stroma and in coarse fibrous stroma. Without NAC the amount of CD68+ TAM in gaps of ductal tumor structures positively correlate with CD31+ microvessel density in soft fibrous stroma. NAC had enhancing effect on the amount of CD68+ TAM but not stabilin-1+ TAM in soft fibrous stroma. However, no correlation between TAM and CD31+ microvessel density was identified after NAC. NAC did not enhance the lymphatic microvessel density. But after NAC stabilin-1 expressing subpopulation of TAM positively correlated with expression of LYVE-1. We hypothesized that CD68+ TAM can support tumor angiogenesis primarily before NAC, while stabilin-1+ TAM can contribute to the maintenance of lymphatic microvessel density after NAC.     

血管内皮生长因子C及其受体3在非小细胞肺癌组织中的表达及意义

目的　探讨血管内皮生长因子C(VEGF C)和受体 (VEGFR) 3在人非小细胞肺癌(NSCLC)组织中的表达及其与微血管、微淋巴管形成、淋巴转移、预后之间的关系。方法　对 76例人NSCLC及相应癌旁组织行VEGF C、VEGFR 3及CD34免疫组织化学染色链霉素抗生物素蛋白 过氧化物酶 (SP)法检测 ,进行淋巴管密度计数、微血管密度 (MVD)计数 ,并结合临床和病理资料进行分析。结果　NSCLC中 ,VEGF C的表达与肺癌分化程度负相关 (P =0 0 0 9)。VEGF C和VEGFR 3的表达水平与淋巴结转移呈正相关 (分别P =0 0 0 8,P =0 0 13) ,与淋巴浸润呈正相关 (分别P =0 0 2 7,P =0 0 2 0 )。VEGF C的表达与VEGFR 3在肺癌细胞中的表达呈正相关 (P =0 0 0 9)。VEGF C与淋巴管密度 (P =0 0 0 6 )、MVD(P =0 0 4 6 )呈正相关。淋巴管密度与淋巴结转移 (P =0 0 10 )、淋巴浸润 (P =0 0 19)、TNM分期 (P =0 0 15 )呈正相关 ,MVD与血行转移 (P <0 0 0 1)、TNM分期 (P <0 0 0 1)呈正相关。VEGF C阳性表达与生存时间、5年生存率呈负相关 (P <0 0 0 1)。结论　NSCLC中 ,VEGF C通过自分泌方式作用于受体VEGFR 3,促进肺癌组织生长 ,抑制分化。VEGF C促使肺癌内淋巴管形成 ,促进肺癌淋巴结转移。VEGF C和VEGFR 3表达增高、淋巴管密度增加     

Importance of lymph vessels in gastric cancer: a prognostic indicator in general and a predictor for lymph node metastasis in early stage cancer

BACKGROUND: Metastasis to regional lymph nodes (LNs) through lymphatic vessels is common in cancer progression and is an important prognostic factor in many cancers. Recent evidence suggests that tumour lymphangiogenesis promotes lymphatic metastasis. AIMS: To study the role of lymph vessel density (LVD) in gastric cancer and investigate whether LVD is associated with LN metastasis/prognosis. METHODS: Lymphatics of 117 primary human gastric cancer cases were investigated by quantitative immunohistochemical staining for podoplanin. The relation between LVD and LN metastasis and other established clinicopathological parameters was analysed. The relation between LVD and prognosis was also studied. RESULTS: Mean LVD of "hot spots" was 11.6/case. LVD significantly correlated with LN and podoplanin positive lymphatic invasion. High LVD was associated with worse overall survival. In multivariate analysis, positive LVD was a significant independent predictor of overall survival, depth of invasion, and TNM stage. LVD significantly correlated with LN metastasis at surgery and podoplanin positive lymphatic invasion. In multivariate analysis, positive LVD was an independent significant predictor of LN metastasis. CONCLUSIONS: Increased podoplanin expression is significantly associated with LN metastasis, and may play an important role in detecting LN metastasis in gastric cancer. Furthermore, LVD may be a significant prognostic factor in gastric cancer at any stage. In addition, LVD and lymph vessel invasion detected by podoplanin immunohistochemistry are associated with LN metastasis in T1 early gastric cancer. LVD assessment by podoplanin immunohistochemistry may become a useful predictor of LN metastasis in T1 early gastric cancer and may influence the decision making process for additional surgery.     

Nuclear and cytoplasmic Id-1 expression patterns play different roles in angiogenesis and lymphangiogenesis in gastric carcinoma

The purpose of the study was to investigate the expression and impact of Id-1 (inhibitor of differentiation) on tumor progression, angiogenesis, and lymphangiogenesis in gastric adenocarcinoma. The study included 97 cases of gastric adenocarcinoma, which were surgically excised at the Second Hospital of Shandong University. Immunohistochemistry was used to detect the Id-1 expression, and dual-labeling immunohistochemistry was used to evaluate the microvessel density (MVD) and lymphatic vessel density (LVD). The Id-1 protein was mainly expressed with nuclear staining in well-differentiated carcinoma, but with cytoplasmic staining in moderately and poorly differentiated carcinoma, which showed a significant difference (P < .0001). Moreover, the expression patterns had different and crucial effects on angiogenesis and lymphangiogenesis. Nuclear staining of Id-1 inhibited angiogenesis, but cytoplasmic staining promoted angiogenesis (MVD, 110.57 ± 32.32 vs 141.45 ± 55.60) (P < .05). Consistent with their roles in angiogenesis, the nuclear and cytoplasmic expressions of Id-1 had similar effects on lymphangiogenesis: nuclear expression inhibited and cytoplasmic expression promoted lymphangiogenesis (LVD, 2.62 ± 1.03 vs 4.05 ± 2.04) (P < .05). Microvessel density and LVD showed no significant difference in low-and high-Id-1 expression groups (P > .05). Aberrant expression of Id-1 from nuclear to cytoplasm is accompanied with tumor malignant progression, which promotes angiogenesis and lymphangiogenesis; and Id-1 should be developed as a target for gastric carcinoma therapy.     

Correlation of vascular endothelial growth factor-D expression and VEGFR-3-positive vessel density with lymph node metastasis in gastric carcinoma

Lymph node metastasis is an important prognostic factor in gastric cancer. Vascular endothelial growth factor-D (VEGF-D) is a lymphangiogenic growth factor that activates VEGF receptor (VEGFR)-3, a receptor expressed in the lymphatic endothelium. We investigated the clinical value of VEGF-D expression and VEGFR-3 positive vessel density in gastric carcinoma with regard to lymphangiogenesis. Immunohistochemical staining was used to determine the expression of VEGF-D and VEGFR- 3 in specimens from 104 cases of resected gastric cancer. VEGF-D expression was observed in 62.5% of the gastric cancers and in 9.6% of the non-neoplastic gastric tissue. The VEGFR-3-positive vessel density was significantly greater in the VEGFD positive group than the negative group. VEGF-D expression was significantly associated with lymph node metastasis, increased serum CEA levels, and the nonsignet ring cell type. The VEGFR-3-positive vessel density was correlated with tumor size, lymphatic invasion, and lymph node metastasis. The VEGF-D expression and high VEGFR-3-positive vessel density were significant poor prognostic factors for relapse-free survival. These results suggest that VEGF-D and VEGFR-3-positive vessel density are potential molecular markers that predict lymphatic involvement in gastric carcinoma.     

Angiogenic and lymphangiogenic microvessel density in breast carcinoma: correlation with clinicopathologic parameters and VEGF-family gene expression.

Angiogenesis and lymphangiogenesis are essential for breast cancer progression and are regulated by vascular endothelial growth factors (VEGF). To determine clinical and molecular correlates of these processes, we measured blood and lymphatic vascular microvessel density in 29 invasive carcinomas (22 ductal, six lobular, one papillary), using the vascular marker CD31 and the novel lymphatic marker D2-40. Microvessel density was assessed microscopically and by image cytometry, and was compared with tumor histology, grade, stage, lymph node metastasis, hormone receptors, HER2/neu status, and expression of VEGF, VEGF-C and VEGF-D by immunohistochemistry or quantitative RT-PCR. Strong correlation was observed between visual and image cytometric microvessel density using D2-40 but not CD31 (P=0.016 and 0.1521, respectively). Image cytometric CD31 microvessel density correlated with tumor size, grade, stage and lymph node metastasis (P=0.0001, 0.0107, 0.0035 and 0.0395, respectively). D2-40 microvessel density correlated with tumor stage (P=0.0123 by image cytometry) and lymph node metastasis (P=0.0558 by microscopy). Immunohistochemical VEGF signal in peritumoral blood vessels correlated with image cytometric CD31 and D2-40 microvessel density (P=0.022 and 0.0012, respectively), consistent with the role of VEGF in blood and lymphatic vascular growth. Intratumoral VEGF-C and VEGF-D expression by quantitative RT-PCR correlated with D2-40 (P=0.0291 by image cytometry) but not with CD31 microvessel density, which could suggest a selective role of VEGF-C and VEGF-D in lymphangiogenesis. CD31 and D2-40 microvessel density correlated significantly with several prognostic factors, including lymph node metastasis. Thus, measurements of angiogenesis and lymphangiogenesis may have utility for breast cancer pathology, particularly for estimation of metastatic risk.     

Lack of lymphangiogenesis in human primary cutaneous melanoma. Consequences for the mechanism of lymphatic dissemination.

Cutaneous melanoma has an initial preference for lymphatic spread. Remarkably, melanoma progression toward this metastasizing phenotype is accompanied by intense blood vessel angiogenesis (hemangiogenesis), but lymphangiogenesis, the formation of new lymph vessels in the tumor, has never been reported. To investigate how primary melanoma cells interact with the existing lymphatic microvasculature, and whether lymphangiogenesis occurs, an immunostaining was developed that differentially decorates blood and lymph vessels in frozen tissue sections. The density and distribution of both these vessel types in and around thin (< or = 1.5 mm) and thick (> or = 1.5 mm) primary melanoma lesions and in normal and uninvolved skin were determined. Although especially in thick melanoma lesions a significant increase in blood vessel density was observed, lymphatic density remained unaltered, showing that lymphangiogenesis did not occur. Morphological analysis indicated, however, that melanoma progression is accompanied by a sequence of events that involves hemangiogenesis supporting tumor expansion, especially in the vertical growth phase. Often, stromal sepia are formed around the blood capillaries in the tumor neovasculature protecting them from invasion. Lymph vessels inside the tumor were infrequently observed. However, subepidermal lymph vessels often seemed to be entrapped and penetrated by the expanding tumor mass. In this way, hemangiogenesis, as the driving force behind tumor expansion, might indirectly increase the chance of lymphatic invasion in the absence of lymphangiogenesis. This model explains the paradox that, although melanoma metastasis seems to require angiogenesis, a consistent relation of prognosis with blood capillary density in primary cutaneous melanoma is lacking.     

Inducible nitric oxide synthase activity correlates with lymphangiogenesis and vascular endothelial growth factor-C expression in head and neck squamous cell carcinoma

Nitric oxide (NO) is a diatomic free radical molecule that has been implicated in tumour angiogenesis and progression of head and neck squamous cell carcinoma (HNSCC). However, the mechanism underlying the effect of NO on tumour spread remains largely unknown. Tumour lymphangiogenesis has recently received considerable attention and there is increasing evidence that it is relevant for metastasis to lymph nodes in HNSCC. Here, we study the correlation between inducible NOS synthase (iNOS) activity and lymphangiogenesis in a series of 60 HNSCCs and the possible involvement of the lymphangiogenic factor vascular endothelial growth factor (VEGF)-C. HNSCC presenting with lymph node metastasis had a significantly higher lymphatic vessel density in both the tumour mass and the peritumour area (p = 0.006 and p = 0.001, respectively). Similarly, tumours with lymph node metastasis showed greater lymphatic vessel area than tumours with no lymph node involvement (p = 0.001 for intratumour lymphatics and p < 0.001 for peritumour lymphatics). iNOS activity measured in specimens from the tumour periphery correlated strongly with both lymphatic vessel density and lymphatic vessel area (p = 0.01, rs = 0.45 and p < 0.001, rs = 0.725, respectively). Conversely, these correlations were not observed in specimens from the tumour core. In addition, VEGF-C mRNA expression was significantly elevated in tumours with high iNOS activity (p = 0.008, rs = 0.563), and VEGF-C expression correlated positively with the presence of lymph node metastases (p = 0.03). In vitro, in the A431 human squamous carcinoma cell line, exogenous and endogenous stimulation of the iNOS pathway led to up-regulation of VEGF-C, which was blocked by the NOS inhibitor L-NNA. Taken together, our results indicate that iNOS activity may promote lymphangiogenesis and spread to lymph nodes in HNSCC, with the possible involvement of VEGF-C.     

血浆纤维蛋白原水平在胃癌淋巴结转移诊断中的临床意义

目的观察胃癌患者血浆纤维蛋白原水平与肿瘤临床分期、浸润程度和淋巴结转移的关系。方法结合临床资料,回顾分析我科收治的1064例胃癌患者的血浆中纤维蛋白原含量。结果血浆纤维蛋白原和胃癌分化程度、TNM分期、浸润深度、淋巴结转移及是否有远处转移有密切关系。PN0～PN3血浆纤维蛋白原水平分别为(2.43±0.74)g/L,(3.57±1.16)g/L,(3.98±0.81)g/L,(4.52±0.74)g/L。多因素Logistic回归分析表明高纤维蛋白原血症是胃癌淋巴结转移的一个危险因素。结论术前血浆纤维蛋白原水平可以作为预测胃癌淋巴结转移的一个指标。     

The extent of retraction clefts correlates with lymphatic vessel density and VEGF-C expression and predicts nodal metastasis and poor prognosis in early-stage breast carcinoma

Although the earliest feature of disseminated disease in breast cancer is regional lymph node involvement, little is known about the mechanisms whereby cancer cells interact with lymphatic endothelial cells and enter the lymphatic system. We have previously reported that the extensive presence of retraction clefts in breast carcinomas highly significantly correlates with lymphatic tumor spread and predicts poor outcome, suggesting that retraction clefts are not just fixation artifacts, but real potential spaces that are exaggerated by tissue processing and may reflect an early stage of lymphatic invasion. In this study, we examined the correlation between the extent of retraction clefts and lymphangiogenesis, as assessed by lymphatic vessel density and vascular endothelial growth factor-C (VEGF-C) expression in a series of 256 early-stage breast carcinomas. The presence and extent of retraction clefts around tumor cell nests was determined by review of all hematoxylin- and eosin-stained tumor sections. Lymphatic vessels were detected by podoplanin immunohistochemistry and lymphatic vessel density was measured using the hot-spot method. The expression of VEGF-C in the tumor cells was determined by immunohistochemistry and analyzed semiquantitatively on a four-tiered scale. High levels of retraction clefts, peritumor lymphatic vessel density and VEGF-C expression at the invasive edge in breast carcinomas significantly correlated with tumor size, histological grade, lymphatic invasion and nodal metastasis. Breast carcinomas showing extensive retraction clefts (>20% of tumor volume) were found to have significantly higher lymphatic vessel density and VEGF-C expression levels compared to tumors without this feature. High retraction clefts, peritumor lymphatic vessel density and VEGF-C expression predicted poor outcome in breast carcinomas. Our results support the hypothesis that retraction clefts are real potential spaces that may represent 'pre-lymphatic spaces' facilitating initial lymphatic invasion and that growth factors secreted by the tumor cells may stimulate tumor-associated lymphangiogenesis by promoting the endothelialization of these 'pre-lymphatic channels'.     

Lateral peritumoral lymphatic vessel invasion can predict lymph node metastasis in esophageal squamous cell carcinoma.

Lymph node metastasis is an important prognostic factor in many types of cancer. We investigated the clinical significance of lymphangiogenesis and lymphatic vessel invasion in esophageal squamous cell carcinoma. We evaluated lymphatic vessel density and lymphatic vessel invasion in the intratumoral, peritumoral and normal compartments using D2-40 immunostaining. In addition, the peritumoral compartment was divided into the lateral peritumoral compartment and the non-lateral peritumoral compartment. The lymphatic vessel density was higher in the peritumoral and intratumoral compartments than in the normal compartment. However, the lymphatic vessel density did not correlate with any pathological parameters including lymph node metastasis. Intratumoral and peritumoral lymph vessels were small and collapsed while normal lymphatic vessels and lymphatic vessels with lymphatic vessel invasion were dilated and large. The presence of lymphatic vessel invasion, in the lateral peritumoral compartment but nowhere else, significantly correlated with lymph node metastasis. These results suggest that lymphangiogenesis might occur with esophageal cancer, but it does not play a direct role in lymphatic vessel invasion and lymph node metastasis. Peritumoral lymphatic vessel invasion, especially in the lateral peritumoral compartment, should imply a high probability of regional lymph node metastasis.     

Overexpression of TrkB promotes the progression of colon cancer

Yu Y, Zhang S, Wang X, Yang Z, Ou G. Overexpression of TrkB promotes the progression of colon cancer. APMIS 2010; 118: 188–95. Studies have confirmed that TrkB plays important roles in facilitating metastasis in various types of malignant tumors. In the present study, 30 cases of colon cancer and matched non‐tumors were examined for the expression of TrkB by Western blot. The expression of TrkB was also examined in 90 colon tumor sections by immunohistochemical methods, and D2‐40 staining was used to evaluate the correlation between TrkB expression and lymphatic vessel density. To investigate the effects of TrkB on the progression of colon cancer, siRNA specific for TrkB was transfected into LoVo cells, and proliferation, apoptosis and invasion of trasfected cells were examined using MTT [3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide], flow cytometry and Transwell assays, respectively. Our results showed that TrkB was up‐regulated in colon tumors compared with the non‐tumorous counterparts, and the overexpression of TrkB was closely correlated with lymphatic vessel density (LVD) and metastasis. Inhibition of TrkB by siRNA increased the apoptotic rates of transfected cells, while the numbers of proliferative and invasive cells were decreased. In summary, our data suggest that overexpression of TrkB in colon cancer possibly plays roles in inhibiting apoptosis, promoting proliferation and invasion, facilitating tumor progression by lymphangiogenesis‐associated metastasis.     

血管内皮生长因子D的表达与乳腺癌淋巴管生成及淋巴结转移的相关性

目的 探讨乳腺癌患者不同区域淋巴管生成、淋巴管浸润特点以及与血管内皮生长因子D(VEGF-D)的表达关系,并结合腋淋巴结转移状态进行分析. 方法 选取乳腺癌根治术石蜡标本79例,分4个区域(肿瘤区、癌周区、近癌区、远癌区)取材.切片行免疫组织化学染色,采用D2-40对淋巴管进行标记,检测各区域淋巴管密度(LVD)、淋巴管浸润(LVI)及VEGF-D表达情况. 结果 癌周区LVD最高(20.25±2.03),肿瘤区VEGF-D和LVI阳性率最高,分别为87.34%和63.29%.肿瘤区VEGF-D表达与LVD之间、LVD与LVI之间、VEGF-D表达与LVI之间差异无统计学意义(P>0.05),但在其他各区域它们之间差异有统计学意义(P<0.05),且呈正相关.癌周区LVD与腋淋巴结转移状态有关(P<0.05);癌周区和近癌区的VEGF-D表达及LVI与腋淋巴结转移之间差异有统计学意义(P<0.05),但在其他区域差异无统计学意义(P>0.05). 结论 VEGF-D可能促进乳腺癌淋巴管生成,增加淋巴管浸润机会.LVD的增高易致淋巴管浸润,促进腋淋巴结转移.癌周区和近癌区在乳腺癌淋巴道转移以及评估腋淋巴结转移状态的研究中可能更具有意义.     

Expression of angiopoietin 1, 2 and their common receptor Tie2 in human gastric carcinoma: implication for angiogenesis

Angiogenesis, formation of new microvessels providing oxygen and nutrient supply, is essential for tumor growth. It is dependent on the production of angiogenic growth factors by tumor cells. Angiopoietin 1 (Ang-1) and 2 (Ang-2) and their common receptor, Tie2, are thought to be critical regulators of tumor angiogenesis. We examined expression of Ang-1, Ang-2, and their common receptor Tie2 mRNAs and proteins in gastric cancers using in situ hybridization and immunohistochemistry. We also investigated the relationship between their expression and differentiation of cancer cells, lymph node metastasis, tumor size, depth of cancer cell invasion, TNM staging and microvessel density (MVD). The expression of Ang-1, Ang-2, and Tie2 mRNA in cancer cells significantly correlated with the MVD (p<0.001, <0.001 and =0.019, respectively). Ang-1 and Tie2 positivity correlated with advanced gastric cancers (p<0.05) and larger cancers had higher positive rates of Ang-1, Ang-2, and Tie2 mRNA expression (p<0.001, =0.010 and =0.039, respectively). Significant positive correlations were also found between mRNA expression of Tie2 and those of Ang-1 and Ang-2 (p<0.01 and <0.001, respectively). These findings indicate that the expression of Ang-1 and Ang-2 is important for tumor angiogenesis, and suggest a possible role of autocrine/paracrine function of angiopoietin/Tie2 system in gastric cancer progression.     

乙酰肝素酶、碱性成纤维细胞生长因子在胃癌中表达及对血管新生和肿瘤进展的影响

目的：探讨乙酰肝素酶(Hpa)、碱性成纤维细胞生长因子(bFGF)在胃癌组织中表达及其对血管新生和肿瘤生物学行为的影响。方法：应用免疫组化SABC法检测60例胃癌组织中Hpa、bFGF表达及计数肿瘤微血管密度(MVD)。结果：Hpa、bFGF表达和MVD、浸润深度、TNM分期和淋巴结转移有关，且Hpa、bFGF共表达病例有更高MVD与单独一种阳性表达相比。Hpa表达和bFGF表达呈正相关。结论：Hpa、bFGF可加速肿瘤浸润和转移，促进肿瘤间质微血管生成。且Hpa、bFGF在促进肿瘤间质微血管生成方面有协同作用。     

Vascular endothelial growth factor-C expression in human gallbladder cancer and its relationship to lymph node metastasis

Lymph node metastasis is a major prognostic factor in human cancer. Vascular endothelial growth factor C (VEGF-C) is a lymphangiogenic polypeptide that has been implicated in several human solid tumors. However, the clinical significance of VEGF-C has remained unknown in gallbladder carcinoma. Paraffin-embedded tumor specimens of 52 surgically resected gallbladder cancers were immunohistochemically stained for VEGF-C, VEGF, and CD34. The correlations among VEGF-C expression, VEGF expression, microvessel density (MVD), clinicopathologic features, and clinical outcomes were statistically analyzed. Thirty-three (63%) of the 52 gallbladder cancers were highly positive for VEGF-C protein by immunohistochemistry. VEGF-C expression was significantly correlated with lymphatic vessel involvement, lymph node metastasis, and worse outcomes after operation (p<0.001, p<0.001, p<0.001, respectively), but not with MVD. By the Cox regression model, lymphatic vessel involvement emerged as an independent prognostic parameter. These results suggest that VEGF-C may play a role in tumor progression via lymphangiogenesis and lymph node metastasis in human gallbladder cancer.     

胃癌组织中微淋巴管密度与侵袭转移的关系

目的:探讨胃癌微淋巴管密度(LMVD)与侵袭转移的相关性。方法:应用免疫组化SP法检测胃癌组织和正常胃组织淋巴管内皮细胞透明质酸受体-1(LYVE-1)的表达,并计数LMVD,分析LMVD与侵袭转移的关系。结果:胃癌组织癌周区处于开放状态的功能性微淋巴管明显增多。胃癌组织LMVD较正常胃组织LMVD增多,差异有统计学意义(P0.05)。有淋巴结转移胃癌中LMVD明显多于无淋巴结转移者,直径≥5cm胃癌LMVD明显多于直径5cm者,侵及浆膜胃癌组织LMVD明显多于未侵及浆膜者,差异均有统计学意义(P0.05)。结论:胃癌组织LMVD与肿瘤大小、浸润深度和淋巴转移有密切关系,可以作为肿瘤诱导生成淋巴管研究的量化指标,有助于胃癌的预后判断及治疗方案的评价。     

Galectin-3与CDC25B在胃癌中的表达及意义

目的 探讨半乳糖凝集素3 mRNA(Galectin-3)和细胞分裂周期蛋白25B mRNA(cell division cycle 25B,CDC25B)在胃癌中的表达及其与临床病理参数及预后的关系.方法 应用组织微阵列技术和原位杂交法检测220例胃癌组织和31份正常胃黏膜组织中Galectin-3 mRNA和CDC25B mRNA 的表达情况.结果 220例胃癌中Galectin-3 mRNA和CDC25B mRNA的阳性表达率分别为58.6%、54.1%;Galectin-3 mRNA表达与肿瘤大小、TNM(tumor,lymph node,metastasis)分期、浸润深度、脉管侵犯、淋巴结转移及远处转移呈正相关;CDC25B mRNA表达也与肿瘤大小、TNM分期、脉管侵犯、淋巴结转移及远处转移呈正相关;Galectin-3 mRNA表达与CDC25B mRNA表达呈正相关;Galectim3 mRNA和CDC25B mRNA阳性表达病例的平均生存时间和5年生存率均明显低于阴性表达的病例.结论 Galectin-3 和CDC25B基因的表达促进了胃癌的发生和发展,是指导临床治疗及评估预后的有效指标.     

Galectin-3与CDC25B在胃癌中的表达及意义

目的 探讨半乳糖凝集素3 mRNA(Galectin-3)和细胞分裂周期蛋白25B mRNA(cell division cycle 25B,CDC25B)在胃癌中的表达及其与临床病理参数及预后的关系.方法 应用组织微阵列技术和原位杂交法检测220例胃癌组织和31份正常胃黏膜组织中Galectin-3 mRNA和CDC25B mRNA 的表达情况.结果 220例胃癌中Galectin-3 mRNA和CDC25B mRNA的阳性表达率分别为58.6%、54.1%;Galectin-3 mRNA表达与肿瘤大小、TNM(tumor,lymph node,metastasis)分期、浸润深度、脉管侵犯、淋巴结转移及远处转移呈正相关;CDC25B mRNA表达也与肿瘤大小、TNM分期、脉管侵犯、淋巴结转移及远处转移呈正相关;Galectin-3 mRNA表达与CDC25B mRNA表达呈正相关;Galectim3 mRNA和CDC25B mRNA阳性表达病例的平均生存时间和5年生存率均明显低于阴性表达的病例.结论 Galectin-3 和CDC25B基因的表达促进了胃癌的发生和发展,是指导临床治疗及评估预后的有效指标.     

Galectin-3与CDC25B在胃癌中的表达及意义

目的 探讨半乳糖凝集素3 mRNA(Galectin-3)和细胞分裂周期蛋白25B mRNA(cell division cycle 25B,CDC25B)在胃癌中的表达及其与临床病理参数及预后的关系.方法 应用组织微阵列技术和原位杂交法检测220例胃癌组织和31份正常胃黏膜组织中Galectin-3 mRNA和CDC25B mRNA 的表达情况.结果 220例胃癌中Galectin-3 mRNA和CDC25B mRNA的阳性表达率分别为58.6%、54.1%;Galectin-3 mRNA表达与肿瘤大小、TNM(tumor,lymph node,metastasis)分期、浸润深度、脉管侵犯、淋巴结转移及远处转移呈正相关;CDC25B mRNA表达也与肿瘤大小、TNM分期、脉管侵犯、淋巴结转移及远处转移呈正相关;Galectin-3 mRNA表达与CDC25B mRNA表达呈正相关;Galectim3 mRNA和CDC25B mRNA阳性表达病例的平均生存时间和5年生存率均明显低于阴性表达的病例.结论 Galectin-3 和CDC25B基因的表达促进了胃癌的发生和发展,是指导临床治疗及评估预后的有效指标.