Early and late recurrence after gastrectomy for gastric carcinoma

Shiraishi, Norio; Ito, Masafumi; Osawa, Naofumi; Yasuda, Kazuhiro; Adachi, Yosuke; Kitano, Seigo

doi:10.1002/1097-0142(20000715)89:2<255::aid-cncr8>3.0.co;2-n

Cited by 156 publications

(127 citation statements)

References 14 publications

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“…Either as described in the previous studies or in our multivariate survival analysis, the depth of invasion, lymph node or distant metastasis, and TNM staging are independent prognostic indicators in gastric cancers (25,26). The heparanase mRNA expression had a statistical correlation with those indicators.…”

Section: Discussionsupporting

confidence: 67%

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Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma

et al. 2002

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Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro. Recently, it was found that the human heparanase gene was cloned and highly expressed in malignant cell lines and human solid malignant tumors. In the present study, we investigated the heparanase mRNA expression by using in situ hybridization in 116 paraffin-embedded tissues of primary gastric carcinomas. To explore its clinicopathologic significance, it was detected in the various steps of tumor progression and then compared with prognostic indicators. As a result, the heparanase expression was more prevalent in late-stage rather than early-stage carcinomas (P < .0001) and was more frequent in tumors of large size (P ‫؍‬ .0212). Expression also correlated with lymphatic (P ‫؍‬ .0086) and venous (P ‫؍‬ .0171) invasion and with negative prognostic factors such as lymph nodal (P < .0001) and distant (P ‫؍‬ .0221) metastases. However, in a multivariate analysis, messenger RNA expression of heparanase was not an independent prognostic factor. It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.

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Section: Discussionsupporting

confidence: 67%

“…Increased lymphatic and venous invasion is possible evidence of tumor angiogenesis. Many reports have shown that the presence of lymphatic and/or venous invasion is a strong risk factor for nodal metastasis, distant metastasis, and tumor recurrence in gastric cancer (25,26).…”

Section: Discussionmentioning

confidence: 99%

Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma

et al. 2002

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“…In previous studies, it was demonstrated that both the macroscopic appearance and depth of invasion are independent prognostic indicators in gastric carcinoma. 13 Thus, the expression of heparanase in gastric carcinoma may correlate with a more aggressive course.…”

Section: Discussionmentioning

confidence: 99%

“…A Volume of 7 ml of total RNA isolated from approximately 10 000 cells were mixed with 1 ml of oligo-(dT) [12][13][14][15][16][17][18] primer, 1 ml of random hexamers primer (N 6 ), and 1 ml of 10 mM dNTPs in a total volume of 10 ml. They were heat denaturated at 651C for 5 min, and then chilled in ice.…”

Section: Rt-pcr Of Microdissected Cellsmentioning

confidence: 99%

Positive association of heparanase expression with tumor invasion and lymphatic metastasis in gastric carcinoma

Wang

Jiang

et al. 2005

Modern Pathology

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Tumor invasion and metastasis are the most common causes of death in gastric carcinoma. Human heparanase influences tumor invasiveness and angiogenesis. Analysis of its expression in gastric carcinoma has been hindered by our inability to procure pure cancer cells from heterogeneous tissue. In the present study, we analyzed heparanase expression in human primary and metastatic gastric carcinoma cells as well as in paired normal gastric epithelial cells by laser capture microdissection coupled with reverse transcriptionpolymerase chain reaction (RT-PCR). Tumor tissues, metastatic lymph nodes, and apparently uninvolved normal gastric tissues were collected from 30 patients who had undergone gastrectomy with radical lymph node dissection for gastric carcinoma without preoperative treatment. Bulk tissues and laser capture microdissected cell groups were separately subjected to RT-PCR analysis with heparanase-specific primers. For bulk tissues, heparanase-specific transcripts were detectable in all primary tumor tissues, metastatic lymph nodes, and almost all matching normal tissues. RT-PCR analysis after laser capture microdissection showed no detectable heparanase expression in matching normal epithelial cell groups. Of the laser capture microdissected primary gastric carcinoma cells, 47% (14/30) were heparanase positive. Expression was closely associated with greater tumor invasiveness, including Borrmann gross type and depth of wall infiltration. For metastatic cell groups dissected from lymph nodes, 95% showed clear heparanase expression. Furthermore, the extent of lymphatic spread was directly correlated to heparanase expression at the primary site. In conclusion, laser capture microdissection coupled with RT-PCR is a reliable approach for molecular analysis of heparanase expression in gastric carcinoma. Heparanase may facilitate invasion and metastasis of gastric carcinoma cells. Keywords: gastric carcinoma; laser capture microdissection; lymphatic metastasis; heparanase expression It is generally accepted that the invasion of the basement membrane and extracellular matrix is one of the critical steps for cancer cell metastasis. 1 Heparan sulfate proteoglycans, composed of a protein core covalently linked to heparan sulfate side-chains, represent a principal component of the extracellular matrix and, in particular, basement membranes. Cell surface heparan sulfate can also serve as coreceptors, along with the other cell surface molecules, to form functional receptor complexes that facilitate signal transduction. 2 Furthermore, heparan sulfate chains bind a large number of bioactive molecules and regulate their availability and function. These include growth factors, chemokines, cytokines, and enzymes that are essential for angiogenesis, cell adhesion, and locomotion. 3 Accordingly, enzymatic degradation of heparan sulfate may play a critical role in cancer cell invasion and metastasis. Heparanase is an endoglycosidase that cleaves heparan sulfate side chains of heparan sulfate proteoglycans at a limited number ...

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“…Statistically significant differences in risk factors for metastases at different time intervals after definitive treatment have been demonstrated in other cancers, such as gastric and hepatocellular carcinomas. 8,9 Shiraishi et al 8 have demonstrated that, compared with patients who had a late recurrence, patients who had an early recurrence of gastric carcinoma had a significantly increased likelihood of having a larger tumor size at presentation, lymphatic invasion, extensive lymph node metastasis, and more advanced initial stage of disease. In examining hepatocellular carcinoma, multivariate analysis by Poon et al 9 observed that preoperative ''tumor rupture'' and vascular invasion were significant risk factors for early intrahepatic recurrence, whereas cirrhosis was a significant risk factor for late intrahepatic recurrence.…”

mentioning

confidence: 99%

Characteristics associated with early and late melanoma metastases

Brauer

Wriston

Troxel

et al. 2009

Cancer

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BACKGROUND: Differences in risk factors for metastases at different time intervals after treatment have been described in several malignancies; however, to the authors' knowledge, no extensive study examining this issue in melanoma has been conducted to date. METHODS: The authors performed a nested case-control study of patients with melanoma who presented with only local disease. Patients in the case group included 549 patients who developed metastases 6 months after surgery. Of these, 320 patients developed metastasis within 3 years after undergoing definitive surgery (early metastases [EM]), and 70 patients developed metastasis 8 years after undergoing definitive surgery (late metastases [LM]). For each case, a control patient was chosen who had melanoma but who did not develop metastases in the same interval. Univariate and conditional multivariate logistic regression were used in the analysis of 34 clinical and tumor characteristics. RESULTS: Multivariate analysis confirmed previously established risk factors for metastases, such as increasing tumor thickness. In addition, the authors discovered that a personal history of nonmelanoma skin cancer (P ¼ .006) and a history of cancer other than skin cancer (P ¼ .020) also were associated with metastasis. In comparing the 320 EM patients with the 70 LM patients, EM patients were more likely to have thicker lesions (P < .001), ulcerated lesions (P ¼ .016), and a history of nonmelanoma skin cancer (P ¼ .024). CONCLUSIONS: In this study, 2 potentially novel risk factors for melanoma metastases were identified, and different profiles of risk factors were constructed for EM versus LM. These differences may be important in future risk identification and stratification for clinical trials and for the management and treatment of patients with melanoma.

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Early and late recurrence after gastrectomy for gastric carcinoma

Cited by 156 publications

References 14 publications

Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma

Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma

Positive association of heparanase expression with tumor invasion and lymphatic metastasis in gastric carcinoma

Characteristics associated with early and late melanoma metastases

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