Biological agents involved in malignant mesothelioma: relevance as biomarkers or therapeutic targets

Our plain-English summary of Biological agents involved in malignant mesothelioma: relevance as biomarkers or therapeutic targets, by S. Crispi, I. Cardillo, E.P. Spugnini, et al (Current Cancer Drug Targets, 2010).

The study

• Authors: S. Crispi, I. Cardillo, E.P. Spugnini, G. Citro, S. Menegozzo, A. Baldi
• Journal: Current Cancer Drug Targets
• Published: 2010;10(1):19-26
• Type of article: Review
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Malignant mesothelioma (MM) is a rare, highly aggressive tumor that arises from the surface serosal cells (pleural, peritoneal and pericardial cavities). Epidemiological and clinical data show that there is an association between asbestos exposure and MM development, even if the exact mechanism whereby asbestos induces MM is unknown. The continuing identification and elucidation of the molecular defects involved in mesothelioma pathogenesis and progression should lead to better disease control and greater therapeutic options in the near future. Goal of this article is to summarize the most recent advances in molecular pathogenesis of mesothelioma with particular emphasis on genes that could be considered as biomarkers or therapeutic targets and discuss possible clinical implications of these findings.

In plain English

This article was a narrative review, not a new study. The authors summarized published research on the molecular changes in malignant mesothelioma. They focused on genes and proteins that might serve as biomarkers or treatment targets. As background, they wrote that epidemiological and clinical data show an association between asbestos exposure and mesothelioma, but that the exact mechanism is unknown. The review covered studies of chromosome deletions, gene silencing by methylation, gene-expression profiling, and blood and tissue markers such as mesothelin and osteopontin. One cited study found a significant association between MT1A and MT2A methylation and asbestos exposure. Another reported a median survival of 7 months for patients with high mesothelin levels, compared with 19 months for those with low levels. The authors also described their own earlier profiling of about 40,000 genes, which found increased expression of several genes involved in cell division. They wrote that none of the markers studied to help early diagnosis had yet been proven reliable in clinical practice, and that the number of genome-wide studies in mesothelioma was still low.

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: Narrative review of published genomic, transcriptomic and biomarker studies of malignant mesothelioma
• Who was studied: No study population of its own. The article summarized previously published studies of malignant mesothelioma tumors, patients, cell lines and animal models.
• Exposure: Asbestos was discussed as background. The authors described asbestos fibers as serpentine (mainly chrysotile) and amphibole (including crocidolite, tremolite and amosite). The review itself focused on molecular changes in mesothelioma rather than on exposure levels.
• Main results:
  • A cited study of genomic gains and losses in mesothelioma reported deletions that occurred preferentially at chromosome regions 9p21.3, 22q12.2 and 17p13.1.
  • A cited study that analyzed 28 methylation markers in mesothelioma found a significant association between MT1A and MT2A methylation and asbestos exposure.
  • A cited study reported that mesothelioma patients with high mesothelin levels (above 3.5 nmol/L) had a median survival of 7 months, compared with 19 months for the low mesothelin group.
  • The same cited study reported that patients with high serum osteopontin (above 350 ng/mL) had significantly shorter survival (median 5 months) than patients with low serum osteopontin (median 15 months).
  • In a cited phase II trial of gefitinib, median failure-free survival was 2.7 months both in patients with low EGFR levels and in those with high EGFR levels.
  • The authors described their own earlier study, which profiled mesothelioma tumor samples for about 40,000 genes. It identified as up-regulated (increased expression) several genes related to DNA replication and cell division, including condensin, kinesin and cyclin genes.
• The authors' conclusion: The authors concluded that, although several markers had been studied to help early diagnosis, none had yet been proven reliable in clinical practice. They wrote that identifying tumor biomarkers could greatly facilitate surveillance of people exposed to asbestos, and that genome-wide analyses are being performed to find candidate therapeutic targets.
• Limitations the authors state:
  • The authors noted that the total number of genome-wide analyses in mesothelioma was still low compared with other tumors. They attributed this to the low incidence of the disease and the difficulty of obtaining large numbers of tumor samples.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Mesothelioma, Peritoneal mesothelioma.

Medical terms in this study, explained in our Lexicon: Malignant Mesothelioma, Biomarker, Pericardial, Asbestos Exposure, Mesothelioma.

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