Clinical signifcance and prospective mechanism of increased CDKN2A expression in small cell lung cancer

• Dong Ming Li ^[1] ; Wan Ying Huang ^[1] ; Zhi Guang Huang ^[1] ; Jian Di Li ^[1] ; Yi Wu Dang ^[1] ; Yu Lu Tang ^[1] ; Wen Jia Tang ^[1] ; Gang Chen ^[1] ; Hui Ping Lu ^[1] ; Guo Sheng Li ^[2] ; Feng Chen ^[3] ; Hong Huang ^[4] ; Zhong Qing Tang ^[5]
  1. [1] Department of Pathology, The First Afliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, People’s Republic of China
  2. [2] Cardiothoracic Surgery, The First Afliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, People’s Republic of China
  3. [3] Medical Oncology, The First Afliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, People’s Republic of China
  4. [4] Department of Respiratory and Critical Care Medicine, The First Afliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, People’s Republic of China
  5. [5] Department of Pathology, Wuzhou Gongren Hospital, The Seventh Afliated Hospital of Guangxi Medical University, No.1, Nansanxiang Gaodi Road, Guangxi Zhuang Autonomous Region, Wuzhou 543000, People’s Republic of China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 26, Nº. 6, 2024, págs. 1519-1531
• Idioma: inglés
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• Resumen

  • Background Although it has been shown that cyclin dependent kinase inhibitor 2A (CDKN2A) plays a signifcant role in a number of malignancies, its clinicopathological value and function in small cell lung cancer (SCLC) is unclear and warrants additional research.

    Methods The clinical signifcance of CDKN2A expression in SCLC was examined by multiple methods, including comprehensive integration of mRNA level by high throughput data, Kaplan–Meier survival analysis for prognostic value, and validation of its protein expression using in-house immunohistochemistry.

    Results The expression of CDKN2A mRNA in 357 cases of SCLC was evidently higher than that in the control group (n=525) combing the data from 20 research centers worldwide. The standardized mean diference (SMD) was 3.07, and the area under the curve (AUC) of summary receiver operating characteristic curve (sROC) was 0.97 for the overexpression of CDKN2A. ACC, COAD, KICH, KIRC, PCPG, PRAD, UCEC, UVM patients with higher CDKN2A expression had considerably worse overall survival rates than those with lower CDKN2A expression with the hazard ratio (HR)>1.

    Conclusion CDKN2A upregulation extensively enhances the carcinogenesis and progression of SCLC.