11p Deletions and breakpoints in squamous cell carcinoma: Association with altered reactivity with the UM‐E7 antibody

Carol R. Bradford, Kathryn A. Kimmel, Daniel L. Van Dyke, Maria J. Worsham, Barbara J. Tilley, David Burk, Fernando Del Rosario, Stephen Lutz, Richard Tooley, Diana J.S. Hayashida, Thomas E. Carey

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


The UM‐E7 monoclonal antibody raised against the UM‐SCC‐I human squamous cell carcinoma (SCC) cell line identifies a cell surface antigen that is strongly expressed in normal tissues. The locus (MICI) controlling the expression of E7 and related cell surface antigens has been mapped to chromosome band I I p 13. This band has been identified as a region of cancer‐associated aberrations and as the probable locus of a tumor suppressor gene. Although E7 antigen expression is strong in normal keratinocytes, it varies among squamous carcinoma cell lines. Some SCC lines (12/26) exhibit weak expression of the E7 antigen, whereas other SCC cell lines (14/26) and 21 cell lines from other tumor types express the antigen strongly. On the basis of these observations and of mapping data, we postulated that low E7 antigen expression in a subset of SCC cell lines might be associated with chromosomal rearrangement or deletion involving the E7 locus on 11p. Fully evaluable karyotypes were prepared from 19 SCC cell lines, including I I with weak and eight with strong E7 expression. Eight of the I I lines with weak E7 expression had I I p abnormalities. Four of these contained I I p deletions, and four others had a breakpoint in 11p. In contrast, none of the cell lines in the group with strong E7 expression had an I I p deletion, although one had a rearrangement with an 11p breakpoint. In the four tumors with visible 11p deletions, the smallest region of overlap corresponded to the 11p13‐p14 region. The mean log10 50% endpoint E7 titer in the group with 11p deletions or breakpoints was nearly two orders of magnitude lower than that of the lines with no 11p abnormality (1.95 ± 0.53) (P < 0.02). Our results indicate that the UM‐E7 antibody identifies tumors with 11p 13‐p 14 deletions and other 11p rearrangements and that the 11p region is a site of nonrandom chromosome rearrangement in a subset of human squamous cancers. The strong association of loss of antigen expression with visible 11 p deletion or rearrangement in some tumors suggests that other tumors with this phenotype may contain submicroscopic lesions of 11 p 13‐p 14.

Original languageEnglish (US)
Pages (from-to)272-282
Number of pages11
JournalGenes, Chromosomes and Cancer
Issue number4
StatePublished - Jul 1991

ASJC Scopus subject areas

  • Genetics
  • Cancer Research


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