EcoRI polymorphism of the metastasis-suppressor gene NME1 in Mexican patients with breast cancer

Human breast cancer cells with high metastatic potential show reduced expression of the metastasis-suppressor gene NME1. There are two polymorphic sites for the restriction enzymes BglII and EcoRI, both detectable by Southern blot analysis. Although the BglII site has been analyzed for loss of heter...

Full description

Saved in:
Bibliographic Details
Published inBreast cancer research and treatment Vol. 96; no. 2; pp. 159 - 161
Main Authors Rubio, Susan Andrea Gutierrez, Martinez, Silvia Esperanza Flores, Corona, Jose Sanchez, Ruiz, Adriana Patricia Mendizabal, Rincon, Angel Emilio Suarez, Lagunas, Ignacio Arevalo, Camacho, Jose Gonzalo Vazquez, Moguel, Maria Cristina Moran
Format Journal Article
LanguageEnglish
Published Netherlands Springer Nature B.V 01.03.2006
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Human breast cancer cells with high metastatic potential show reduced expression of the metastasis-suppressor gene NME1. There are two polymorphic sites for the restriction enzymes BglII and EcoRI, both detectable by Southern blot analysis. Although the BglII site has been analyzed for loss of heterozygosity, the biallelic EcoRI site polymorphism has not been studied in association with breast cancer, complications or metastasis. We analyzed EcoRI site allele frequencies in Mexican patients with breast cancer, using polymerase chain reaction -restriction fragment length polymorphisms. The polymorphic allelic frequencies in the cases and reference groups were 0.4215 and 0.3375, respectively; this difference was not statistically significant (chi2=0.8687, p=0.3512). Thus, EcoR1 polymorphic site was not associated with breast cancer in this series, but could be analyzed in association with metastases and might be informative in the evaluation of loss of heterozygosity in women with breast cancer.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0167-6806
1573-7217
DOI:10.1007/s10549-005-9072-0