QM-FISH analysis of the genes involved in the G1/S checkpoint signaling pathway in triple-negative breast cancer

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• 作者：Sheng Zhang (1) (2) (3)
  Yingbo Shao (1) (2) (3)
  Guofang Hou (1) (2) (3)
  Jingchao Bai (1) (2) (3)
  Weiping Yuan (4) (5)
  Linping Hu (4) (5)
  Tao Cheng (4) (5)
  Anders Zetterberg (6)
  Jin Zhang (1) (2) (3) (7)
  
• 关键词：Triple ; negative breast cancer ; Copy number alterations ; Quantitative multi ; gene fluorescence in situ hybridization
• 刊名：Tumor Biology
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：35
• 期：3
• 页码：1847-1854
• 全文大小：955 KB
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• 作者单位：Sheng Zhang (1) (2) (3)
  Yingbo Shao (1) (2) (3)
  Guofang Hou (1) (2) (3)
  Jingchao Bai (1) (2) (3)
  Weiping Yuan (4) (5)
  Linping Hu (4) (5)
  Tao Cheng (4) (5)
  Anders Zetterberg (6)
  Jin Zhang (1) (2) (3) (7)
  
  1. 3rd Department of Breast Cancer, China Tianjin Breast Cancer Prevention, Treatment and Research center, Tianjin Medical University Cancer Institute and Hospital, Tianjin, People’s Republic of China
  2. Key Laboratory of Breast Cancer Prevention and Therapy of Ministry of Education, Tianjin, People’s Republic of China
  3. Key Laboratory of Cancer Prevention and Therapy, Tianjin, People’s Republic of China
  4. Beijing Union Medical College Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin, People’s Republic of China
  5. The State Key Laboratory of Experimental Hematology, Tianjin, People’s Republic of China
  6. Clinical Pathology Department of the Karolinska Hospital, Karolinska Institute, Solna, Sweden
  7. 3rd Department of Breast Cancer, Tianjin Medical University Cancer Hospital, West Beihuanhu Rd, Tianjin, 300060, People’s Republic of China
  
• ISSN：1423-0380

文摘

This study was conducted to analyze copy number alterations (CNAs) of the genes involved in the G1/S checkpoint signaling pathway of triple-negative breast cancer (TNBC) and to evaluate their clinical value in the prognosis of TNBC. Quantitative multi-gene fluorescence in situ hybridization was used to study CNAs of the genes involved in the G1/S checkpoint signaling pathway, including cyclin d1 (CCND1), c-Myc, p21, cell-cycle-checkpoint kinase 2 gene, p16, retinoblastoma (Rb1), murine double minute 2 (Mdm2) and p53, in 60 TNBC samples and 60 non-TNBC samples. In comparison with the non-TNBC samples, CNAs of the genes involved in the G1/S checkpoint signaling pathway were more frequently observed in the TNBC samples (p--.000). Out of a total of eight genes, six (CCND1, c-Myc, p16, Rb1, Mdm2, and p53) exhibited significantly different CNAs between the TNBC group and the non-TNBC group. Univariate survival analysis revealed that the gene amplification of c-Myc (p--.008), Mdm2 (p--.020) and the gene deletion of p21 (p--.004), p16 (p--.015), and Rb1 (p--.028) were the independent predictive factor of 5-year OS for patients with TNBC. Cox multivariate analysis revealed that the gene amplification of c-Myc (p--.026) and the gene deletion of p21 (p--.019) and p16 (p--.034) were independent prognostic factors affecting the 5-year OS for TNBC. CNAs of the genes involved in the G1/S checkpoint signaling pathway presented a higher rate of incidence in TNBC than in non-TNBC, which could indicate one of the molecular mechanisms for the specific biological characteristics of TNBC. The genes c-Myc, p21, and p16 were correlated with the prognosis of TNBC and therefore may have potential clinical application values in the prognostic prediction of TNBC.