Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma

Shunsuke Kondo, Hidenori Ojima, Hitoshi Tsuda, Jun Hashimoto, Chigusa Morizane, Masafumi Ikeda, Hideki Ueno, Kenji Tamura, Kazuaki Shimada, Yae Kanai, Takuji Okusaka

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Background: c-Met is an oncogene encoding a receptor for hepatocyte growth factor and, as such, plays a key role in hepatocellular carcinomas (HCC). We evaluated c-Met protein expression and its gene amplification in order to assess whether they were related to tumor recurrence and survival rates among patients who had undergone tumor resection. Methods: We used the polymer-based method to perform an immunohistochemistry analysis of c-Met expression on 59 formalin-fixed, paraffin-embedded sections of surgical specimens. c-Met gene amplification was investigated with fluorescence in-situ hybridization. Kaplan-Meier methods and Cox proportional hazards models were used to investigate relationships between c-Met expression, patient characteristics, tumor recurrence, and survival. Results: c-Met expression was associated with portal vein invasion (p = 0.006). Recurrence-free survival rates were significantly lower in patients with high levels of c-Met expression (p < 0.001). However, c-Met expression levels did not significantly affect overall survival rates (p = 0.12). Only 1 patient was found to have c-Met gene amplification; 22 patients were found to have aneuploidy of chromosome 7, on which the c-Met gene is located. Tumors with chromosome 7 polysomy tended to have higher levels of c-Met expression than those with chromosome 7 monosomy or disomy, but this difference was not statistically significant. Conclusion: Although c-Met expression was not significantly associated with c-Met gene amplification, it may be a useful predictive marker of recurrence in resected HCC patients.

Original languageEnglish
Pages (from-to)207-213
Number of pages7
JournalInternational Journal of Clinical Oncology
Volume18
Issue number2
DOIs
Publication statusPublished - 2013 Apr
Externally publishedYes

Fingerprint

Gene Amplification
Hepatocellular Carcinoma
Proto-Oncogene Proteins c-met
Recurrence
Chromosomes, Human, Pair 7
Survival Rate
Neoplasms
Aneuploidy
Portal Vein
Fluorescence In Situ Hybridization
Oncogenes
Proportional Hazards Models
Paraffin
Formaldehyde
Polymers
Immunohistochemistry
Survival
Genes

Keywords

  • Amplification
  • c-Met
  • Hepatocellular carcinoma
  • Recurrence

ASJC Scopus subject areas

  • Oncology
  • Surgery
  • Hematology

Cite this

Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma. / Kondo, Shunsuke; Ojima, Hidenori; Tsuda, Hitoshi; Hashimoto, Jun; Morizane, Chigusa; Ikeda, Masafumi; Ueno, Hideki; Tamura, Kenji; Shimada, Kazuaki; Kanai, Yae; Okusaka, Takuji.

In: International Journal of Clinical Oncology, Vol. 18, No. 2, 04.2013, p. 207-213.

Research output: Contribution to journalArticle

Kondo, S, Ojima, H, Tsuda, H, Hashimoto, J, Morizane, C, Ikeda, M, Ueno, H, Tamura, K, Shimada, K, Kanai, Y & Okusaka, T 2013, 'Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma', International Journal of Clinical Oncology, vol. 18, no. 2, pp. 207-213. https://doi.org/10.1007/s10147-011-0361-9
Kondo, Shunsuke ; Ojima, Hidenori ; Tsuda, Hitoshi ; Hashimoto, Jun ; Morizane, Chigusa ; Ikeda, Masafumi ; Ueno, Hideki ; Tamura, Kenji ; Shimada, Kazuaki ; Kanai, Yae ; Okusaka, Takuji. / Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma. In: International Journal of Clinical Oncology. 2013 ; Vol. 18, No. 2. pp. 207-213.
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AU - Kondo, Shunsuke

AU - Ojima, Hidenori

AU - Tsuda, Hitoshi

AU - Hashimoto, Jun

AU - Morizane, Chigusa

AU - Ikeda, Masafumi

AU - Ueno, Hideki

AU - Tamura, Kenji

AU - Shimada, Kazuaki

AU - Kanai, Yae

AU - Okusaka, Takuji

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AB - Background: c-Met is an oncogene encoding a receptor for hepatocyte growth factor and, as such, plays a key role in hepatocellular carcinomas (HCC). We evaluated c-Met protein expression and its gene amplification in order to assess whether they were related to tumor recurrence and survival rates among patients who had undergone tumor resection. Methods: We used the polymer-based method to perform an immunohistochemistry analysis of c-Met expression on 59 formalin-fixed, paraffin-embedded sections of surgical specimens. c-Met gene amplification was investigated with fluorescence in-situ hybridization. Kaplan-Meier methods and Cox proportional hazards models were used to investigate relationships between c-Met expression, patient characteristics, tumor recurrence, and survival. Results: c-Met expression was associated with portal vein invasion (p = 0.006). Recurrence-free survival rates were significantly lower in patients with high levels of c-Met expression (p < 0.001). However, c-Met expression levels did not significantly affect overall survival rates (p = 0.12). Only 1 patient was found to have c-Met gene amplification; 22 patients were found to have aneuploidy of chromosome 7, on which the c-Met gene is located. Tumors with chromosome 7 polysomy tended to have higher levels of c-Met expression than those with chromosome 7 monosomy or disomy, but this difference was not statistically significant. Conclusion: Although c-Met expression was not significantly associated with c-Met gene amplification, it may be a useful predictive marker of recurrence in resected HCC patients.

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