Arpc1b gene is a candidate prediction marker for choroidal malignant melanomas sensitive to radiotherapy.

نویسندگان

  • Ken Kumagai
  • Yoshinori Nimura
  • Atsushi Mizota
  • Nobuyuki Miyahara
  • Mizuho Aoki
  • Yoshiya Furusawa
  • Masaki Takiguchi
  • Shuichi Yamamoto
  • Naohiko Seki
چکیده

PURPOSE Choroidal malignant melanomas (CMMs) are the most common primary intraocular tumors in adult humans. Although radiotherapy is commonly used to treat the melanomas, the therapeutic effects are unpredictable. The purpose of this study was to search for a gene(s) that can predict the success of radiotherapy for CMMs. METHODS The cell lines 92-1, OCM-1, and OMM-1 were established from patients with CMM, and radiation sensitivity was determined using the colony-formation assay. RNA was extracted from nonirradiated cells, and gene expression analysis was performed using a microarray containing 10,800 genes. The up- or downregulated genes were verified by real-time PCR using other cancerous cell lines in which radiation sensitivity had been documented. RESULTS Analysis of radiation survival curves showed that cell line 92-1 was radiation sensitive and OCM-1 and OMM-1 lines were radiation resistant. The results of microarray analyses showed that 34 genes were differentially expressed in the OCM-1 and OMM-1 cell lines compared with the 92-1 cell line. The validity of the expression level of 13 of the 34 genes that were identified by microarray was confirmed by PCR. From the analysis of the different radio-sensitivity cancer cell lines, the Arpc1b gene was selected as a prediction marker gene for sensitivity of CMM to radiotherapy. CONCLUSIONS Gene expression analysis of CMM cell lines can be used to search for radiation sensitivity prediction markers. Comprehensive gene expression profiles of radiation-sensitive and/or resistant cell lines may provide new insights into the mechanisms of resistance or sensitivity to radiation therapy.

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عنوان ژورنال:
  • Investigative ophthalmology & visual science

دوره 47 6  شماره 

صفحات  -

تاریخ انتشار 2006