A new approach, based on the competitive amplification of wild-type an
d exon deleted estrogen receptor (ER) variant cDNAs, was used to scree
n 100 human breast tumors for the presence of ER variants. Already des
cribed exon 4-deleted ER mRNA was preferentially detected in tumors wi
th lower grades (P < 0.05) or higher progesterone receptor levels (P <
0.01), whereas new ER variants, deleted in exons 2-4 or in regions wi
thin exons 3-7 were associated with higher grades (P < 0.025) and high
er ERs (P < 0.001), This approach allows investigation of the expressi
on of multiple ER variant mRNAs and may implicate them as new prognost
ic markers and as possible contributors to tumor progression.