Additional chromosome 1q aberrations and der(16)t(1;16), correlation to the phenotypic expression and clinical behavior of the Ewing family of tumors

Batia Stark, Celia Mor, Marta Jeison, Rima Gobuzov, Ian J. Cohen, Yaacov Goshen, Jerry Stein, Salvi Fisher, Shifra Ash, Itzhak Yaniv, Rina Zaizov

Research output: Contribution to journalArticlepeer-review

Abstract

The cytogenetic hallmark of the Ewing family of tumors is t(11;22)(q24;q12) in its simple, complex or variant forms and/or its molecular equivalent EWS/FLI, EWS/ERG rearrangement. Additional secondary consistent chromosomal aberrations include the der(16)t(1;16) and, frequently, other chromosome 1q abnormalities leading to 1q overdosage. We studied whether these secondary cytogenetic changes are correlated to clinical features and phenotypic expression which may have a prognostic impact. Successful cytogenetic evaluation was performed in eight patients with a Ewing family tumor. In four of these, in addition to the primary aberration, chromosome 1q overdosage (including two with der(16)t(1;16)) was noted. Out of these four patients, two had metastatic disease at the time of evaluation, while in the other four, disease was localized. Morphologically, the tumors with the additional 1q aberration, revealed the pPNET sub type more frequently than the typical Ewing. They also expressed a higher degree of neural differentiation by neural marker immunocytochemistry, in comparison to tumors without the 1q aberration. Determination of the prognostic significance of this finding requires a longer follow-up with a larger group of patients.

Original languageEnglish
Pages (from-to)3-8
Number of pages6
JournalJournal of Neuro-Oncology
Volume31
Issue number1-2
StatePublished - 1997
Externally publishedYes

Keywords

  • Chromosome 1q
  • Cytogenetics
  • Ewing
  • Neural differentiation
  • der(16)t(1;16)
  • pPNET

Fingerprint

Dive into the research topics of 'Additional chromosome 1q aberrations and der(16)t(1;16), correlation to the phenotypic expression and clinical behavior of the Ewing family of tumors'. Together they form a unique fingerprint.

Cite this