Absence of amplification of the FGFR1-gene in human malignant mesothelioma of the pleura: a pilot study

Our plain-English summary of Absence of amplification of the FGFR1-gene in human malignant mesothelioma of the pleura: a pilot study, by T. Plönes, F. Beckers, W. Engel-Riedel, et al (BMC Research Notes, 2014).

The study

• Authors: T. Plönes, F. Beckers, W. Engel-Riedel, E. Stoelben, M. Brockmann, V. Schildgen, O. Schildgen
• Journal: BMC Research Notes
• Published: 2014;7:549
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Background: Mesothelioma (MPM) is a rare malignant disease with a worse outcome. Fibroblast growth factor 1 (FGFR1) may be an interesting target for selective tyrosine kinases inhibitors (TKI) in MPM. The aim of this study was to evaluate the amplification of the FGFR1 gene in patients suffering from MPM.

Findings: We identified nineteen male patients treated in our department between August 2008 and July 2010 matching the inclusion criteria. Mean age was 68 years. Histopathological examination confirmed thirteen patients with epitheloid subtype, five with biphasic and one patient with sarcomatoid. Fluorescence in situ hybridization analysis revealed no polysomy nor an amplification of the FGFR gene copy number in any case.

Conclusion: Regarding that also EGFR amplifications in MPM are absolute rarities, our findings may be a hint that TKI's will not satisfy the hope for a new era in the treatment of MPM.

In plain English

This short report from a thoracic surgery department in Cologne, Germany, was a retrospective pilot study of whether the FGFR1 gene is amplified (present in extra copies) in malignant pleural mesothelioma. FGFR1 had been suggested as a possible target for drugs called tyrosine kinase inhibitors. The authors examined tumour tissue from nineteen men, mean age 68 years, treated between August 2008 and July 2010. None had received chemotherapy before tissue sampling or had any other cancer. The text reports thirteen epitheloid, five biphasic and one sarcomatoid tumour, but the table lists 20, 4 and 1. The text reports that ten patients disclosed asbestos exposure, while the table lists eleven. Exposure was not confirmed by tissue examination in any case. Using fluorescence in situ hybridization, a laboratory method that counts gene copies in cells, the authors found no amplification and no polysomy (extra chromosome copies) of the FGFR gene in any sample. The authors concluded that, since EGFR amplifications in this cancer are also very rare, their findings may hint that these drugs will not bring a new era in mesothelioma treatment.

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: Retrospective pilot study; laboratory (FISH) analysis of tumour tissue, descriptive only
• Who was studied: Nineteen male patients with malignant pleural mesothelioma treated in the authors' department (Lung Clinic Merheim, Cologne, Germany) between August 2008 and July 2010. All had no chemotherapy before tissue sampling, no other malignancy, and sufficient tumour tissue. Mean age was 68 years. The text gives 13 epitheloid, 5 biphasic and 1 sarcomatoid tumours; Table 1 gives 20, 4 and 1.
• Exposure: Not an asbestos exposure study. Asbestos exposure was taken from patient history (anamnestic): 10 patients according to the text, 11 according to Table 1. It was not confirmed histologically in any case. The measured factor was FGFR1 gene copy number by FISH. A ratio above 2.2 counted as amplification and a ratio below 1.8 as not amplified.
• Main results:
  • None of the 19 tumour samples showed amplification or polysomy of the FGFR gene.
  • Neither high nor low polysomy was found in any of the tissue samples.
• The authors' conclusion: The authors concluded that, because EGFR amplifications in malignant pleural mesothelioma are also very rare, their findings may be a hint that tyrosine kinase inhibitors will not bring a new era in its treatment. They called for further investigation.
• Limitations the authors state:
  • The authors described the study as descriptive and used no statistical methods beyond description.

Topics

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

Medical terms in this study, explained in our Lexicon: Mesothelioma, Pleura, Fibroblast, Biphasic Mesothelioma, Sarcomatoid, Fluorescence In Situ Hybridization (FISH), EGFR.

Related studies

• Nonamplified FGFR1 is a growth driver in malignant pleural mesothelioma — L.A. Marek, T.K. Hinz, et al. (2014)
• Inhibition of FGF/FGFR autocrine signaling in mesothelioma with the FGF ligand trap, FP-1039/GSK3052230 — C. Blackwell, C. Sherk, et al. (2016)
• The inhibition of FGF receptor 1 activity mediates sorafenib antiproliferative effects in human malignant pleural mesothelioma tumor-initiating cells — A. Pattarozzi, E. Carra, et al. (2017)
• Correlation of MET-Receptor Overexpression with MET Gene Amplification and Patient Outcome in Malignant Mesothelioma — E. Santoni-Rugiu, M.J.S. Lü, et al. (2021)
• Expression of FGFR1-4 in Malignant Pleural Mesothelioma Tissue and Corresponding Cell Lines and its Relationship to Patient Survival and FGFR Inhibitor Sensitivity — G. Vlacic, M.A. Hoda, et al. (2019)
• Genomic gains and losses in malignant mesothelioma demonstrated by FISH analysis of paraffin-embedded tissues — M. Takeda, T. Kasai, et al. (2012)

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