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The class II tumour suppressor gene RARRES3 maps to 11q12, not 11q23

Leukemia volume 16, page 1396 (2002)Cite this article

We read with interest the paper by Casanova et al1 who have analysed expression of the class II tumour suppressor gene RARRES3 (TIG-3/RIG-1) in patients with B-CLL. They state ‘alterations of the retinoic acid receptor alpha (RARα) gene at 17q12 are a frequent abnormality in B-CLL’. However, this observation is based on changes suggestive of a constitutional polymorphism of RARα gene in three out of 47 patients with B-CLL;2 somatic alterations of 17q12 have not been identified in B-CLL in a large (325 patients) study.3 Analysis of the RARRES3 gene, which is retinoid inducible, was performed, in part because this gene ‘maps to chromosome band 11q23, a region frequently deleted in lymphoproliferative disorders’. They showed a significant correlation between down-regulation of RARRES3 and disease progression in B-CLL. However, no mutations were found in either patients with or without deletions of 11q23. The authors suggest that this gene may play a role in B-CLL progression. Their assignment to this region is incorrect and the assumptions made upon this must also be incorrect.

We have formed a YAC/BAC/PAC contig between 11q22 and the telomere, which includes the minimal region of deletion for B-CLL4,5 (C Jones, F Bertoni, R Auer, unpublished data), but have failed to locate RARRES3 within our contig. Moreover, analysis of the NCBI database (www.ncbi.nlm.nih.gov) reveals that RARRES3 maps to 11q12, genomic contig NT—009296.5. BLAST (Basic Local Alignment Search Tool) analysis of the genome database with cDNA sequence of RARRES3 identified alignment with chromosome 11 BAC clone CTC-343D6 (GenBank accession No. AC090271) also within 11q12 contig NT_009296.5. DiSepio et al6 described the original mapping of RARRES3 to 11q23 after database analysis revealed that the cDNA sequence showed homology with a cosmid clone 187D6 (GenBank accession No. U73641). We have performed BLAST analysis on 187D6 which again aligns with 11q12 BAC CTC-343D6. Work published by Duvic et al7 also incorrectly quotes the location of RARRES3 as 11q23. RARRES3 therefore lies outside the 11q minimal region of deletion for B-CLL. We are not surprised that the authors failed to identify any mutations in B-CLL patients, particularly those with 11q deletions. Although, as the authors suggest, RARRES3 may affect cell proliferation and hence disease progression, in light of the mapping data, RARRES3 seems an unlikely candidate for the 11q abnormality; other novel tumour suppressor genes are likely to exist.

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References

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  1. Department of Haematology, Barts and The London School of Medicine, London, UK

    RL Auer, F Bertoni, C Jones & FE Cotter

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Auer, R., Bertoni, F., Jones, C. et al. The class II tumour suppressor gene RARRES3 maps to 11q12, not 11q23. Leukemia 16, 1396 (2002). https://doi.org/10.1038/sj.leu.2402505

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