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The Expression of VEGF-C and It’s Receptor VEGFR-3 Correlates with Lymph Node Metastasis in Gastric Cancer  [PDF]
Chun Yang, Zhaoda Zhang
Open Journal of Gastroenterology (OJGas) , 2014, DOI: 10.4236/ojgas.2014.412050
Abstract: Background: Regional lymph node invasion and metastasis may happen early during the progres-sion of gastric cancer. The lymphadenectomy is still the key method to treat lymph nodemetastasis. In the recent years, scientists have found some growth factors and receptors that can promote angiogenesis which also play an important role in adjusting the formation of the new lymph vessel, and lymphangiogenesis may play a key role in the process of lymph node metastasis. Objectives: This study aims to explore the correlation between the expression of vascular endothelial growth factor-C (VEGF-C), vascular endothelial growth factor receptor 3 (VEGFR-3) and lymph node me-tastasis (LNM), and its impact on prognosis of patients with gastric cancer. Methods: The samples were collected from gastric cancer database of Sichuan Provincial People’s Hospital from 2005 to 2007, which were registered and followed up. The samples were divided into two groups according to situation whether there is lymph node metastasis, which is lymph node metastasis N(+) and without lymph node metastasis N(﹣). The expression of VEGF-C, VEGFR-3 and CD34 were measured by immuno histochemistry staining with monoclonal antibody (anti-VEGF-C, anti-VEGFR-3, and anti-CD34). Kaplan-meier, logistic and Cox regression was performed to explore their impact on the prognosis of patients with gastric cancer. Results: In total 186 cases were collected, 96 cases in N(+) group and 90 cases in N(﹣) group. The percentage of VEGF-C expression is 54.83% (102/186) in all groups, 73.9% (71/96) in N(+) group, and 34.44% (31/90) in N(﹣) group (p = 0.001). The percentage of VEGFR-3 expression is 33.33% (62/186) in all groups, 44.78% (43/96) in N(+) group, and 21.11% (19/90) in N(﹣) group (p = 0.001). There are no statistical differences in microvessel density (MVD) between N(﹣) and N(+) group. The average lymphatic vessel density (LVD) was significant different between N(+) and N(﹣) group (26.23 ± 8.2 and 18.46 ± 7.4, t = ﹣2.427, p = 0.016). The five-year overall survival rate of N(+) group is 31% and the N(﹣) group is 66%; there are statistical differences between the two groups (Log rank = 27.15, p = 0.001). The five-year overall survival rates of VEGF-C positive group and VEGF-C negative group are 36% and 59%, with the statistical differences (Log rank = 27.15, p = 0.001). And the five-year overall survival rates of VEGFR-3 positive group and VEGFR-3 negative group are 31% and 43%, also with the statistical differences (Log rank = 5.241, p = 0.041). Conclusions: The
Nuclear Odontogenic Ameloblast-Associated Protein (ODAM) Correlates with Melanoma Sentinel Lymph Node Metastasis  [PDF]
Sagar S. Gandhi, Daniel P. Kestler, Charles T. Bruker, James M. McLaughlin, Robert E. Heidel, Sabina Siddiqui, James S. Foster, Keith D. Gray, John Bell, Alan Solomon, James Lewis
Journal of Cancer Therapy (JCT) , 2013, DOI: 10.4236/jct.2013.48151
Abstract:

We have examined primary tumor sections from melanoma patients by immunohistochmistry (IHC) for the presence of the odontogenic ameloblast-associated protein (ODAM). Within these patient tissues we have observed a correlation of nuclear ODAM staining in the primary tumors with sentinel lymph node (SLN) metastasis. Surgically, SLN invasion in melanoma is considered an important indicator of more aggressive, invasive melanoma and to date there are limited biomarkers which strongly correlate with metastatic disease. The observation that ODAM staining in melanoma associates with SLN invasion may have important prognostic implications which could assist in the management of melanoma. Notably, ODAM expression may correlate with pathway-signaling we have previously reported to be affected by ectopic ODAM expression in cultured melanoma and breast cancer cell lines.

MUC4 and MUC1 Expression in Adenocarcinoma of the Stomach Correlates with Vessel Invasion and Lymph Node Metastasis: An Immunohistochemical Study of Early Gastric Cancer  [PDF]
Yukihiro Tamura, Michiyo Higashi, Sho Kitamoto, Seiya Yokoyama, Masahiko Osako, Michiko Horinouchi, Takeshi Shimizu, Mineo Tabata, Surinder K. Batra, Masamichi Goto, Suguru Yonezawa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0049251
Abstract: We have previously reported that MUC4 expression is a poor prognostic factor in various carcinomas. Our previous study also showed that MUC1 expression in gastric cancers, including the early and advanced stages is a poor prognostic factor. In the present study, the expression profiles of MUC4 and MUC1 were examined by immunohistochemistry (IHC) using two anti-MUC4 monoclonal antibodies (MAbs), 8G7 and 1G8, and anti-MUC1 MAb DF3 in 104 gastrectomy specimens of early gastric adenocarcinoma with submucosal invasion (pT1b2), including 197 histological subtype lesions. Before the IHC study of the human specimens, we evaluated the specificity of the two MAbs by Western blotting and IHC of two MUC4 mRNA expressing gastric cancer cell lines. MAb 8G7 reacted clearly, whereas MAb 1G8 did not show any reactivity, in either Western blotting or IHC. In the IHC of the gastric cancers, the expression rates of MUC4/8G7 detected by MAb 8G7, MUC4/1G8 detected by MAb 1G8 and MUC1/DF3 detected by MAb DF3 in well differentiated types (70%, 38/54; 67%, 36/54; 52%, 28/54) were significantly higher than those in poorly differentiated types (18%, 10/55; 36%, 20/55; 13%, 7/55) (P<0.0001; P = 0.0021; P<0.0001), respectively. The MUC4/8G7 expression was related with lymphatic invasion (r = 0.304, P = 0.033). On the other hand, the MUC4/1G8 expression was related with lymphatic invasion (r = 0.395, P = 0.001) and lymph node metastasis (r = 0.296, P = 0.045). The MUC1/DF3 expression was related with lymphatic invasion (r = 0.357, P = 0.032) and venous invasion (r = 0.377, P = 0.024). In conclusion, the expression of MUC4 as well as MUC1 in early gastric cancers is a useful marker to predict poor prognostic factors related with vessel invasion.
Vascular endothelial growth factor C (VEGF-C) in esophageal cancer correlates with lymph node metastasis and poor patient prognosis
Tatsuya Tanaka, Hideyuki Ishiguro, Yoshiyuki Kuwabara, Masahiro Kimura, Akira Mitsui, Takeyasu Katada, Midori Shiozaki, Yasuhiro Naganawa, Yoshitaka Fujii, Hiromitsu Takeyama
Journal of Experimental & Clinical Cancer Research , 2010, DOI: 10.1186/1756-9966-29-83
Abstract: KYSE series of esophageal cancer cell lines and 106 patients with primary esophageal squamous cell carcinomas who had undergone radical esophagectomy were analyzed. VEGF-C mRNA expression was determined by quantitative RT-PCR.High expression of VEGF-C was detected in most of the KYSE cell lines, especially KYSE410, yet, in an esophageal normal epithelium cell line, Het-1A, VEGF-C was not detected. In the clinical specimen, the expression of VEGF-C in the cancerous tissue was higher than in the corresponding noncancerous esophageal mucosa (p = 0.026). The expression of VEGF-C was found to be higher in Stage2B-4A tumors than in Stage0-2A tumors (p = 0.049). When the patients were divided into two groups according to their expression levels of VEGF-C (a group of 53 cases with high expression and a group of 53 cases with low expression), the patients with high VEGF-C expression had significantly shorter survival after surgery than the patients with low expression (p = 0.0065). Although univariate analysis showed that high expression of VEGF-C was a statistically significant prognostic factor, this was not shown in multivariate analysis. In the subgroup of patients with Tis and T1 tumors, the expression of VEGF-C was higher in N1 tumors than in N0 tumors (p = 0.029). The survival rate of patients from the high expression group (n = 10) was lower than that in the low expression group (n = 11), and all the patients in the low VEGF-C expression group survived.The expression of VEGF-C correlates with lymph node metastasis and poor prognosis. In patients with Tis and T1 esophageal tumors, the expression of VEGF-C may be a good diagnostic factor for determining metastasis of the lymph node.Esophageal cancer is a disease with poor prognosis. Of many prognostic factors, the metastatic lymph nodes are one of the most significant. To avoid highly invasive surgery, endoscopic mucosal resection (EMR), endoscopic submucosal dissection (ESD), chemoradiotherapy, and their combinations
Overexpression of the secretory small GTPase Rab27B in human breast cancer correlates closely with lymph node metastasis and predicts poor prognosis  [cached]
Zhang Jia-Xing,Huang Xiao-Xia,Cai Man-Bo,Tong Zhu-Ting
Journal of Translational Medicine , 2012, DOI: 10.1186/1479-5876-10-242
Abstract: Background The secretory small GTPase Rab27b was recently identified as an oncogene in breast cancer (BC) in vivo and in vitro studies. This research was designed to further explore the clinical and prognostic significance of Rab27B in BC patients. Methods The mRNA/protein expression level of Rab27B was examined by performing Real-time PCR, western blot, and immunohistochemistry (IHC) assays in 12 paired BC tissues and matched adjacent noncancerous tissues (NAT). Then we carried out IHC assay in a large cohort of 221 invasive BC tissues, 22 normal breast tissues, 40 fibroadenoma (FA), 30 ductual carcinoma in situ (DCIS) and 40 metastatic lymph nodes (LNs). The receiver operating characteristic curve method was applied to obtain the optimal cutoff value for high Rab27B expression. Epithelial-mesenchymal transition (EMT) marker expression levels were detected in relation to Rab27B expression. Results We observed that the increased expression of Rab27B was dependent upon the magnitude of cancer progression (P < 0.001). The elevated expression of Rab27B was closely correlated with lymph node metastasis, advanced clinical stage, ascending pathology classification, and positive ER status. Furthermore, patients with high expression of Rab27B had inferior survival outcomes. Multivariate Cox regression analysis proved that Rab27B was a significantly independent risk factor for patients’ survival (P < 0.001). Furthermore, a significant positive relationship was observed between Rab27B expression and elevated mesenchymal EMT markers. Conclusion Our findings suggest that overexpression of Rab27B in BC coincides with lymph node metastasis and acquisition of a poor prognostic phenotype.
Upregulated Expression of Indoleamine 2, 3-Dioxygenase in Primary Breast Cancer Correlates with Increase of Infiltrated Regulatory T Cells In Situ and Lymph Node Metastasis  [PDF]
Jinpu Yu,Jingyan Sun,Shizhen Emily Wang,Hui Li,Shui Cao,Yizi Cong,Juntian Liu,Xiubao Ren
Journal of Immunology Research , 2011, DOI: 10.1155/2011/469135
Abstract: IDO has been reported to induce immunotolerance and promote metastasis in solid malignancy, but the mechanisms involved were not fully understood. In this study, the expression of IDO in primary breast cancer was examined and the correlation between the expression levels of IDO and the densities of Foxp3+ Tregs in situ was studied. The IDO stably-expressing CHO cells(IDO/CHO) were generated to evaluate the induction of Foxp3+ Tregs after coculturing with CD3+ T cells in vitro. The IDO expression in cancer was higher than that in benign diseases both at RNA and protein levels. The IDO expression was significantly upregulated in tumors of more advanced stages and with more extensive lymph node metastasis, and displayed positive linear correlation with the density of Foxp3+ Tregs. We further demonstrated that CD4+CD25+CD127？ Tregs could be amplified by coculturing CD3+ T cells with IDO/CHO cells in vitro which displayed increasing Foxp3 expression both at mRNA and protein levels. Our results implied that up-regulation of IDO in primary breast cancer may inhibit local immune surveillance and promote metastasis by favoring development and infiltration of Foxp3+ Tregs in the tumor microenvironment. 1. Introduction Breast cancer is the most common solid malignancy in women worldwide. A substantial fraction of breast cancer patients develop distant metastases shortly after diagnosis. Metastatic breast cancer is associated with poor prognosis with shorter survival time and refractoriness to therapies. Previous studies have proposed the mechanisms of early metastasis, including overexpression of growth factor receptors and resistant to apoptosis [1, 2], downregulation of adherent molecules during epithelial-mesenchymal transition (EMT) [3–5], degradation of extracellular matrix after activation of matrix metalloproteinases (MMPs) [6, 7], enhanced tumor angiogenesis [8, 9], and inhibition of effective antitumor immunity [10, 11]. Breast cancer cells can evade the immune attack through a variety of complex mechanisms, among which tumor-derived immunosuppression resulting from upregulation of metabolistic enzymes, such as indoleamine 2,3-dioxygenase (IDO), has shown a crucial role in the recent studies [12–15]. IDO is a rate-limiting enzyme in the catabolic process of extrahepatic tryptophan which is an essential amino acid for T-cell proliferation and activation. Deprivation of tryptophan in the microenvironment directly affects the cytotoxicity and cytokine secretion of T cells. In addition, the toxic metabolites generated from tryptophan via the Kynurenine
Upregulated Expression of Indoleamine 2, 3-Dioxygenase in Primary Breast Cancer Correlates with Increase of Infiltrated Regulatory T Cells In Situ and Lymph Node Metastasis  [PDF]
Jinpu Yu,Jingyan Sun,Shizhen Emily Wang,Hui Li,Shui Cao,Yizi Cong,Juntian Liu,Xiubao Ren
Clinical and Developmental Immunology , 2011, DOI: 10.1155/2011/469135
Abstract: IDO has been reported to induce immunotolerance and promote metastasis in solid malignancy, but the mechanisms involved were not fully understood. In this study, the expression of IDO in primary breast cancer was examined and the correlation between the expression levels of IDO and the densities of Foxp3
PRC2/EED-EZH2 Complex Is Up-Regulated in Breast Cancer Lymph Node Metastasis Compared to Primary Tumor and Correlates with Tumor Proliferation In Situ  [PDF]
Hongxiang Yu, Diana L. Simons, Ilana Segall, Valeria Carcamo-Cavazos, Erich J. Schwartz, Ning Yan, Neta S. Zuckerman, Frederick M. Dirbas, Denise L. Johnson, Susan P. Holmes, Peter P. Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051239
Abstract: Background Lymph node metastasis is a key event in the progression of breast cancer. Therefore it is important to understand the underlying mechanisms which facilitate regional lymph node metastatic progression. Methodology/Principal Findings We performed gene expression profiling of purified tumor cells from human breast tumor and lymph node metastasis. By microarray network analysis, we found an increased expression of polycomb repression complex 2 (PRC2) core subunits EED and EZH2 in lymph node metastatic tumor cells over primary tumor cells which were validated through real-time PCR. Additionally, immunohistochemical (IHC) staining and quantitative image analysis of whole tissue sections showed a significant increase of EZH2 expressing tumor cells in lymph nodes over paired primary breast tumors, which strongly correlated with tumor cell proliferation in situ. We further explored the mechanisms of PRC2 gene up-regulation in metastatic tumor cells and found up-regulation of E2F genes, MYC targets and down-regulation of tumor suppressor gene E-cadherin targets in lymph node metastasis through GSEA analyses. Using IHC, the expression of potential EZH2 target, E-cadherin was examined in paired primary/lymph node samples and was found to be significantly decreased in lymph node metastases over paired primary tumors. Conclusions/Significance This study identified an over expression of the epigenetic silencing complex PRC2/EED-EZH2 in breast cancer lymph node metastasis as compared to primary tumor and its positive association with tumor cell proliferation in situ. Concurrently, PRC2 target protein E-cadherin was significant decreased in lymph node metastases, suggesting PRC2 promotes epithelial mesenchymal transition (EMT) in lymph node metastatic process through repression of E-cadherin. These results indicate that epigenetic regulation mediated by PRC2 proteins may provide additional advantage for the outgrowth of metastatic tumor cells in lymph nodes. This opens up epigenetic drug development possibilities for the treatment and prevention of lymph node metastasis in breast cancer.
Lymph Node Metastasis of Gastric Cancer  [PDF]
Tomonori Akagi,Norio Shiraishi,Seigo Kitano
Cancers , 2011, DOI: 10.3390/cancers3022141
Abstract: Despite a decrease in incidence in recent decades, gastric cancer is still one of the most common causes of cancer death worldwide [1]. In areas without screening for gastric cancer, it is diagnosed late and has a high frequency of nodal involvement [1]. Even in early gastric cancer (EGC), the incidence of lymph node (LN) metastasis exceeds 10%; it was reported to be 14.1% overall and was 4.8 to 23.6% depending on cancer depth [2]. It is important to evaluate LN status preoperatively for proper treatment strategy; however, sufficient results are not being obtained using various modalities. Surgery is the only effective intervention for cure or long-term survival. It is possible to cure local disease without distant metastasis by gastrectomy and LN dissection. However, there is no survival benefit from surgery for systemic disease with distant metastasis such as para-aortic lymph node metastasis [3]. Therefore, whether the disease is local or systemic is an important prognostic indicator for gastric cancer, and the debate continues over the importance of extended lymphadenectomy for gastric cancer. The concept of micro-metastasis has been described as a prognostic factor [4-9], and the biological mechanisms of LN metastasis are currently under study [10-12]. In this article, we review the status of LN metastasis including its molecular mechanisms and evaluate LN dissection for the treatment of gastric cancer.
Gastrointestinal stromal tumor of the stomach with lymph node metastasis
Aras Canda, Yucel Ozsoy, Olcay Nalbant, Ozgul Sagol
World Journal of Surgical Oncology , 2008, DOI: 10.1186/1477-7819-6-97
Abstract: A 32-year-old female presented with anemia. Diagnostic investigations including thoracoabdominopelvic computed tomography (CT) scan and gastroscopy revealed a 8 cm gastric antral submucosal tumor without any metastasis. Enlarged periantral LNs were detected during laparotomy and patient underwent distal gastrectomy with en bloc perigastric LN dissection. Pathologic investigation revealed antral stromal tumor with high mitotic and Ki-67 index. Lymph node metastasis was observed in 7 of 12 resected perigastirc nodes. Immunohistochemically, tumor cells were positive for CD117. She was diagnosed as high grade gastric GIST due to the presence of LN metastasis, large tumor size and unfavorable histopathologic features thus underwent adjuvant imatinib treatment (400 mg, daily). No recurrence or metastasis has been detected during a 12-month of postoperative follow-up.Surgery remains the mainstay of treatment in patients with localized, resectable GISTs. Although lymphatic metastasis rarely occurs in patients with GIST, LN dissection should be considered for patients with any suspicion of nodal metastasis. Adjuvant imatinib treatment is recommended according to the well defined prognostic factors.Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. They most commonly arise from the stomach; which account for ~1% of gastric malignancies [1]. Their origin has been proposed to be the intestinal cells of Cajal [2]. The mainstay of primary treatment for GIST is R0 resection. Unlike gastric adenocarcinomas, routine lymphadenectomy is not recommended unless there is no suspicion of intraoperative lymph node (LN) metastasis. Approximately 95% of GISTs express mutation in the C-KIT proto-oncogen [3]. A tyrosine kinase inhibitor, Imatinib mesylate (Glivec？; Novartis Pharma, Istanbul, Türkiye) which blocks KIT proteins is the main agent for targeted adjuvant and neoadjuvant treatment as well as used for palliation. Risk assessment a
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