E-cadherin and urokinase-type plasminogen activator tissue status in gastric carcinoma

Yonemura, Yutaka; Nojima, N; Kaji, Masahide; Fujimura, Takashi; Itoh, Hiroshi; Ninomiya, Itasu; Miyazaki, Itsuo; Endo, Yuichi; Sasaki, Takuma

doi:10.1002/1097-0142(19950915)76:6<941::aid-cncr2820760606>3.0.co;2-i

Cited by 66 publications

(40 citation statements)

References 23 publications

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“…detected gastric cancer exist, prognosis of advanced gastric cancer still remains poor (40). Prognosis of gastric carcinoma patients depends on several pathological and genetic variables, such as TNM grading and p53, MUC1, and E-cadherin (41)(42)(43)(44). However, patient outcome is difficult to predict using classic histological and molecular classifications.…”

Section: Discussionmentioning

confidence: 99%

Absence of RKIP expression is an independent prognostic biomarker for gastric cancer patients

et al. 2012

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Abstract. Gastric cancer is a leading cause of cancer-related mortality, and the presence of lymph node metastasis an important prognostic factor. Downregulation of RKIP has been associated with tumor progression and metastasis in several types of neoplasms, being currently categorized as a metastasis suppressor gene. Our aim was to determine the expression levels of RKIP in gastric tissues and to evaluate its impact in the clinical outcome of gastric carcinoma patients. RKIP expression levels were studied by immunohistochemistry in a series of gastric tissues. Overall, we analysed 222 non-neoplastic gastric tissues, 152 primary tumors and 42 lymph node metastasis samples. We observed that RKIP was highly expressed in ~83% of non-neoplastic tissues (including normal tissue and metaplasia), was lost in ~56% of primary tumors and in ~90% of lymph node metastasis samples. Loss of RKIP expression was significantly associated with several markers of poor clinical outcome, including the presence of lymph node metastasis. Furthermore, the absence of RKIP protein constitutes an independent prognostic marker for these patients. In conclusion, RKIP expression is significantly lost during gastric carcinoma progression being almost absent in lymph node metastasis samples. Of note, we showed that the absence of RKIP expression is associated with poor outcome features of gastric cancer patients, this being also an independent prognostic marker.

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Section: Discussionmentioning

confidence: 99%

Absence of RKIP expression is an independent prognostic biomarker for gastric cancer patients

et al. 2012

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“…These activated forms digest the extracellular matrix of SGC tissues. 44,45 In addition, HGF stimulates the production of plasminogen activator and promatrix metalloproteinase. 46,47 The effects of NK4 on these candidates for gefitinib-resistance may be elucidated by further studies.…”

Section: Figurementioning

confidence: 99%

Preclinical study of a “tailor-made” combination of NK4-expressing gene therapy and gefitinib (ZD1839, Iressa™) for disseminated peritoneal scirrhous gastric cancer

Namiki¹,

Namiki²,

Yoshida³

et al. 2005

Int. J. Cancer

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We evaluated the effect of a ''tailor-made'' chemo-gene therapy in scirrhous gastric cancer (SGC)-bearing nude mice. For this tailormade approach, we first selected gefitinib (epidermal growth factor receptor-tyrosine kinase inhibitor)-sensitive SGC cell lines, and 5/8 cell lines demonstrated various degrees of gefitinib-sensitivity. In the highly gefitinib-sensitive NUGC-4, the biological response to NK4 (HGF antagonist/angiogenesis inhibitor) was examined. Subsequently, the composition of an NK4-expressing ternary complex (cationic lipid/nucleic acid/HMG-1, 2 protein) was optimized for maximum transfection activity in NUGC-4. Finally, mice were peritoneally coinoculated with NUGC-4 and scirrhous-associated gastric fibroblasts, NF22, on day 0. Animal models were orally administrated gefitinib (50 mg/kg/day, on days 7-28), and peritoneally NK4-expressing ternary complex (on days 14, 21 and 28). NK4-expression suppressed the gefitinib-resistance induced by the interaction between fibroblasts and SGC, and eventually, this tailor-made combination synergistically decelerated the disease progression by inhibiting proliferative, angiogenic and antiapoptotic effects in tumor tissues. On day 28, both the hemoglobin concentration (g/dl) (control (n 5 8), 11.9; treated (n 5 8), 17.3; p 5 0.0014) and the numbers of mice in good condition (control, 2; treated, 8; p 5 0.0012) were significantly greater, and the abdominal girth (mm) (control, 81.1; treated, 70.3; p 5 0.0036) was significantly reduced. The median points of bloody ascite-free survival time (days) (control, 22; treated, 44; p < 0.0001) and time to euthanasia (days) (control, 36.5; treated, 56; p < 0.0001) were also significantly prolonged. This combination is a potentially useful approach to the treatment of peritoneal gefitinib-sensitive SGC dissemination. ' 2005 Wiley-Liss, Inc.

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“…Several studies have reported that decreased function of E-cadherin is associated with tumour progression in many cancers, and in particular E-cadherin acts as a suppressor of invasive ability (Behrens et al, 1989;Vleminckx et al, 1991;Hirohashi, 2000). Many immunohistochemical studies evaluating E-cadherin expression in tumour tissues have demonstrated that reduced expression of E-cadherin is frequently observed in cancer progression (Katagiri et al, 1995;Lipponen and Eskelinen, 1995;Yonemura et al, 1995;Tamura et al, 1996;Nakanishi et al, 1997;Umbas et al, 1997;Bankfalvi et al, 1999;Ghadimi et al, 1999;Gofuku et al, 1999;Zheng et al, 1999;Kase et al, 2000).…”

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confidence: 99%

Prognostic significance of dysadherin expression in advanced colorectal carcinoma

Aoki

Shimamura²,

Shibata³

et al. 2003

Br J Cancer

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A novel glycoprotein, dysadherin, has an anti-cell -cell adhesion function through downregulating E-cadherin. In this study, we investigated the expressions of dysadherin and E-cadherin in 82 patients with stage II and III colorectal carcinomas to determine the correlation between the two molecules and the clinicopathologic features of each tumour. Dysadherin was not expressed in normal colorectal epithelium. Fifty-one per cent of tumours showed dysadherin immunopositivity in over 50% of cancer cells. Thirty-eight per cent of tumours showed reduced E-cadherin immunopositivity. The increased expression of dysadherin was significantly associated with lung metastasis (P ¼ 0.003). The increased expression of dysadherin had a significant impact on patient survival (P ¼ 0.0099 and 0.0036, log-rank test for overall and recurrence-free survival rate, respectively). Furthermore, tumour with increased expression of dysadherin and reduced expression of E-cadherin showed the worst prognosis (P ¼ 0.0043 and 0.0028, log-rank test for overall and recurrence-free survival rate, respectively). These results suggest that increased dysadherin expression is a significant indicator of poor prognosis for patients with advanced colorectal carcinoma.

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E-cadherin and urokinase-type plasminogen activator tissue status in gastric carcinoma

Cited by 66 publications

References 23 publications

Absence of RKIP expression is an independent prognostic biomarker for gastric cancer patients

Absence of RKIP expression is an independent prognostic biomarker for gastric cancer patients

Preclinical study of a “tailor-made” combination of NK4-expressing gene therapy and gefitinib (ZD1839, Iressa™) for disseminated peritoneal scirrhous gastric cancer

Prognostic significance of dysadherin expression in advanced colorectal carcinoma

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