K-ras and rho A mutations in malignant pleural effusion

Our plain-English summary of K-ras and rho A mutations in malignant pleural effusion, by M. Nakamoto, H. Teramoto, S. Matsumoto, et al (International Journal of Oncology, 2001).

The study

• Authors: M. Nakamoto, H. Teramoto, S. Matsumoto, T. Igishi, E. Shimizu
• Journal: International Journal of Oncology
• Published: 2001;19(5):971-6
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Mutations of the Kristen ras (K-ras) gene have been implicated in the pathogenesis of human lung cancer, especially adenocarcinoma, and have been proposed to be a prognostic factor. The K-ras mutation in codon 12 is detectable even in cell-free fluids by using the enriched polymerase chain reaction (PCR) technique. On the other hand, based on experimental results, the rho A mutation in codon 14 is also proposed to be oncogenic as observed in the K-ras mutation. Malignant pleural effusion is a common complication of lung cancer. We studied the point mutation of K-ras codon 12 and rho A codon 14 using enriched PCR in specimens of pleural effusion. Forty patients with pleural effusion were enrolled in this study. The causes of pleural effusion were non-small cell lung cancer (18 cases), small cell lung cancer (6 cases), malignant mesothelioma (2 cases), metastatic lung tumor (5 cases), thymoma (1 case), malignant lymphoma (1 case), and pleuritis tuberculosa (7 cases). The K-ras mutation was detected in 4 of 14 cases with adenocarcinoma, 1 of 3 cases with squamous cell carcinoma, 1 of 1 case with large cell carcinoma, and 1 of 5 cases with metastatic lung tumor, respectively. The rho A mutation was not detected in any pleural effusion examined in this study. Our study demonstrates the usefullness of pleural effusion as a clinical specimen for a search of point mutation of oncogenes. The K-ras codon 12 mutation is readily detected in pleural effusion, and the demonstration of this mutation has potentially important implications for the diagnosis of malignant pleural effusion.

In plain English

This laboratory study, from Tottori University in Japan, tested fluid from around the lungs (pleural effusion) for two gene changes: a mutation in codon 12 of the K-ras gene and a mutation in codon 14 of the rho A gene. The fluid came from 40 patients. Most had lung cancer, two had malignant mesothelioma, and seven had tuberculosis. The authors used a sensitive DNA-copying method, enriched PCR, on DNA taken from the cell-free part of the fluid. In lab tests, the method found mutant DNA diluted to 1 in 1,000. The K-ras mutation was found in 7 of the 40 fluids: 4 of 14 adenocarcinomas, 1 of 3 squamous cell carcinomas, 1 of 1 large cell carcinoma, and 1 of 5 metastatic lung tumors. It was not found in the 2 mesothelioma cases, the small cell cancer cases, or the tuberculosis cases. The rho A mutation was found in none of the 40. The authors concluded that pleural fluid is a useful specimen for finding such mutations. This article does not study asbestos exposure.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory study of pleural fluid samples from a series of patients, using enriched PCR to look for gene mutations
• Who was studied: 40 patients with pleural effusion at Tottori University, Japan (study dates not given). Causes: non-small cell lung cancer 18 (adenocarcinoma 14, squamous cell carcinoma 3, large cell carcinoma 1), small cell lung cancer 6, malignant mesothelioma 2, metastatic lung tumor 5, thymoma 1, malignant lymphoma 1, and pleuritis tuberculosa 7
• Main results:
  • In lab sensitivity tests, both methods detected mutant DNA diluted with normal DNA down to 1 in 1,000
  • The K-ras codon 12 mutation was found in 7 of 40 pleural fluids: 4 of 14 adenocarcinomas, 1 of 3 squamous cell carcinomas, 1 of 1 large cell carcinoma, and 1 of 5 metastatic lung tumors. Overall this was 6 of 18 non-small cell cancers (33%) and none of 6 small cell cancers
  • No K-ras mutation was found in the fluids from patients with small cell carcinoma, thymoma, lymphoma or tuberculosis. The table also shows 0 of 2 in malignant mesothelioma
  • The rho A codon 14 mutation was not found in any of the 40 pleural fluids, including the 2 from patients with malignant mesothelioma
• The authors' conclusion: The authors concluded that pleural fluid is a useful clinical specimen for searching for point mutations. They added that the K-ras codon 12 mutation is readily detected in pleural fluid and that finding it has potential clinical implications
• Limitations the authors state:
  • The authors noted that failing to find the rho A mutation does not necessarily mean rho A is not involved in naturally occurring tumors, and that further study is needed

Topics

Medical terms in this study, explained in our Lexicon: Pleural Effusion, Lung Cancer, Adenocarcinoma, Non-Small Cell Lung Cancer, Small Cell Lung Cancer, Malignant Mesothelioma, Squamous Cell Carcinoma, Carcinoma.

Related studies

• K-ras mutations in human adenocarcinoma of the lung: association with smoking and occupational exposure to asbestos — K. Husgafvel-Pursiainen, P. Hackman, et al. (1993)
• Gender comparisons in human lung cancer: analysis of p53 mutations, anti-p53 serum antibodies and C-erbB-2 expression — D.G. Guinee, W.D. Travis, et al. (1995)
• Analysis of K-ras and p53 mutations in mesotheliomas from humans and rats exposed to asbestos — Z. Ni, Y. Liu, et al. (2000)
• Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer — J. Alguacil, M. Porta, et al. (2003)
• Fluorescence in situ hybridization in the definitive diagnosis of malignant mesothelioma in effusion cytology — S. Savic, N. Franco, et al. (2010)
• p53 and ras gene mutations in lung cancer: implications for smoking and occupational exposures — K. Husgafvel-Pursiainen, M. Ridanpää, et al. (1995)

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