Related Experiment Video
Updated: Aug 8, 2026
Colorectal Cancer Cell Surface Protein Profiling Using an Antibody Microarray and Fluorescence Multiplexing
Published on: September 25, 2011
The E7-associated cell-surface antigen: a marker for the 11p13 chromosomal deletion associated with aniridia-Wilms
Insights
Researchers mapped the E7 cell-surface antigen to chromosome 11p13, a region linked to Wilms tumor and aniridia. This antigen may serve as a marker for this specific chromosome abnormality.
Area of Science:
- Genetics
- Molecular Biology
- Oncology
Background:
- Interstitial deletions in chromosome 11p13 are associated with Wilms tumor, aniridia, and other developmental abnormalities.
- Previous studies localized the E7 cell-surface antigen to the 11p1300-11p15.1 region using somatic cell hybrids.
Purpose of the Study:
- To further refine the localization of the E7 cell-surface antigen on chromosome 11p.
- To investigate the E7 antigen as a potential marker for chromosome 11 abnormalities associated with Wilms tumor and aniridia.
Main Methods:
- Generation of new somatic cell hybrids from a patient with a distinct 11p deletion and Wilms tumor/aniridia.
- Distinguishing between normal and deleted chromosome 11 using beta-globin gene restriction fragment length polymorphism.
- Assessing E7 antigen expression via complement-mediated cell killing in the presence of E7 monoclonal antibody.
Main Results:
- The E7 cell-surface antigen was successfully mapped to the 11p13 region.
- Hybrid cells with the deleted chromosome 11 (lacking E7 expression) survived, while those with the normal chromosome 11 (expressing E7) were eliminated.
Conclusions:
- The E7 cell-surface antigen expression is localized to the 11p13 region.
- The E7 antigen serves as a potential molecular marker for the chromosomal abnormality linked to aniridia and Wilms tumor.
Abstract:
Unbalanced interstitial deletions of the p13 region of human chromosome 11 have been associated with congenital hypoplasia or aplasia of the iris, mental retardation, ambiguous genitalia, and predisposition to Wilms tumor of the kidney. Utilizing somatic cell hybrids containing either the normal or abnormal chromosome 11 from a child with Wilms tumor and aniridia, we previously mapped the E7 cell-surface antigen to the 11p1300-to-11p15.1 region. To localize even further the site of this antigen on chromosome arm 11p, we have produced somatic cell hybrids from the fibroblasts of a second child with Wilms tumor and aniridia and a different deletion of 11p [46,XY, del (11)(pter----p14.1::p11.2----qter)]. Furthermore, the normal and deleted chromosome 11 could also be distinguished on the basis of a restriction fragment length polymorphism for the beta-globin gene. Hybrid cells containing the deleted chromosome were not killed in the presence of complement and the E7 monoclonal antibody (which recognizes E7 cell surface antigen), while hybrid cells containing the patient's normal chromosome 11 were killed. Thus, expression of the E7-associated cell-surface antigen can be mapped to the 11p13 region, and it appears to be a potential marker of the chromosome abnormality associated with aniridia-Wilms tumor.
Related Concept Videos
02:23Abnormal Proliferation
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
01:22Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal