ERG rearrangement is present in a subset of transition zone prostatic tumors

Sara M. Falzarano, Maria Navas, Kelly Simmerman, Eric A. Klein, Mark A. Rubin, Ming Zhou, Cristina Magi-Galluzzi

Research output: Contribution to journalArticle

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Abstract

A majority of prostate cancers exhibit a recurrent gene rearrangement involving chromosome 21. In approximately 90% of cases, the rearrangement is characterized by fusion of the androgen-regulated gene TMPRSS2 with the oncogene ERG. A recent study suggested that TMPRSS2-ERG gene fusion is lacking in cancers arising from the transition zone of the prostate. A dominant transition zone cancer was detected in 62/397 (16%) patients who underwent radical prostatectomy at our institution and were reviewed and mapped by a single pathologist. In 46/62 specimens, a secondary tumor was identified in the peripheral zone of the prostate. A tissue microarray containing both transition and peripheral zone tumors was constructed and evaluated for gene fusion analysis. TMPRSS2-ERG fusion status was determined using a multicolor interphase fluorescence in situ hybridization assay for ERG break-apart. The median age of the patients was 59 years. Prostatectomy Gleason score was 6 in 21, 7 in 34, and 8 in 7 cases. Median tumor volume was 200 mm 2. TMPRSS2-ERG gene fusion was present in 7/59 (12%) transition zone, and in 12/35 (34%) peripheral zone tumors. Transition zone fusion-positive cases were larger than their negative counterparts. No significant correlation was found between fusion status and Gleason score or pathologic stage. Gene fusion through deletion occurred in 4/7 transition zone and 7/12 peripheral zone tumors. Transition zone prostate cancers are considered biologically and genetically different from peripheral zone tumors. Although ERG rearrangement is more common in peripheral zone tumors, we have detected TMPRSS2-ERG fusion in a subset of transition zone cancers (12%). The lower frequency of gene fusion in transition zone prostate cancer may suggest distinct molecular alterations from peripheral zone tumors and the association with a high tumor volume may indicate a growth advantage for transition zone tumors harboring the gene fusion. Further studies are necessary to confirm this hypothesis.

Original languageEnglish (US)
Pages (from-to)1499-1506
Number of pages8
JournalModern Pathology
Volume23
Issue number11
DOIs
StatePublished - Nov 1 2010

Fingerprint

Gene Fusion
Neoplasms
Prostatic Neoplasms
Neoplasm Grading
Prostatectomy
Tumor Burden
Prostate
Chromosomes, Human, Pair 21
Gene Rearrangement
Interphase
Fluorescence In Situ Hybridization
Oncogenes
Androgens
Growth
Genes

Keywords

  • ERG rearrangement
  • peripheral zone
  • prostate cancer
  • transition zone

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Falzarano, S. M., Navas, M., Simmerman, K., Klein, E. A., Rubin, M. A., Zhou, M., & Magi-Galluzzi, C. (2010). ERG rearrangement is present in a subset of transition zone prostatic tumors. Modern Pathology, 23(11), 1499-1506. https://doi.org/10.1038/modpathol.2010.150

ERG rearrangement is present in a subset of transition zone prostatic tumors. / Falzarano, Sara M.; Navas, Maria; Simmerman, Kelly; Klein, Eric A.; Rubin, Mark A.; Zhou, Ming; Magi-Galluzzi, Cristina.

In: Modern Pathology, Vol. 23, No. 11, 01.11.2010, p. 1499-1506.

Research output: Contribution to journalArticle

Falzarano, SM, Navas, M, Simmerman, K, Klein, EA, Rubin, MA, Zhou, M & Magi-Galluzzi, C 2010, 'ERG rearrangement is present in a subset of transition zone prostatic tumors', Modern Pathology, vol. 23, no. 11, pp. 1499-1506. https://doi.org/10.1038/modpathol.2010.150
Falzarano SM, Navas M, Simmerman K, Klein EA, Rubin MA, Zhou M et al. ERG rearrangement is present in a subset of transition zone prostatic tumors. Modern Pathology. 2010 Nov 1;23(11):1499-1506. https://doi.org/10.1038/modpathol.2010.150
Falzarano, Sara M. ; Navas, Maria ; Simmerman, Kelly ; Klein, Eric A. ; Rubin, Mark A. ; Zhou, Ming ; Magi-Galluzzi, Cristina. / ERG rearrangement is present in a subset of transition zone prostatic tumors. In: Modern Pathology. 2010 ; Vol. 23, No. 11. pp. 1499-1506.
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abstract = "A majority of prostate cancers exhibit a recurrent gene rearrangement involving chromosome 21. In approximately 90{\%} of cases, the rearrangement is characterized by fusion of the androgen-regulated gene TMPRSS2 with the oncogene ERG. A recent study suggested that TMPRSS2-ERG gene fusion is lacking in cancers arising from the transition zone of the prostate. A dominant transition zone cancer was detected in 62/397 (16{\%}) patients who underwent radical prostatectomy at our institution and were reviewed and mapped by a single pathologist. In 46/62 specimens, a secondary tumor was identified in the peripheral zone of the prostate. A tissue microarray containing both transition and peripheral zone tumors was constructed and evaluated for gene fusion analysis. TMPRSS2-ERG fusion status was determined using a multicolor interphase fluorescence in situ hybridization assay for ERG break-apart. The median age of the patients was 59 years. Prostatectomy Gleason score was 6 in 21, 7 in 34, and 8 in 7 cases. Median tumor volume was 200 mm 2. TMPRSS2-ERG gene fusion was present in 7/59 (12{\%}) transition zone, and in 12/35 (34{\%}) peripheral zone tumors. Transition zone fusion-positive cases were larger than their negative counterparts. No significant correlation was found between fusion status and Gleason score or pathologic stage. Gene fusion through deletion occurred in 4/7 transition zone and 7/12 peripheral zone tumors. Transition zone prostate cancers are considered biologically and genetically different from peripheral zone tumors. Although ERG rearrangement is more common in peripheral zone tumors, we have detected TMPRSS2-ERG fusion in a subset of transition zone cancers (12{\%}). The lower frequency of gene fusion in transition zone prostate cancer may suggest distinct molecular alterations from peripheral zone tumors and the association with a high tumor volume may indicate a growth advantage for transition zone tumors harboring the gene fusion. Further studies are necessary to confirm this hypothesis.",
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