The LCC15-MB cell line was established from a femoral bone metastasis that
arose in a 29-year-old woman initially diagnosed with an infiltrating ducta
l mammary adenocarcinoma. The tumor had a relatively high (8%) S-phase frac
tion and 1/23 positive lymph nodes (LN). Both the primary tumor and LN meta
stasis were positive for estrogen receptor (ER) and progesterone receptor (
PgR), but lacked erbB(2) expression. Approximately one year later, the pati
ent presented with a 0.8 cm comedo-type intraductal mammary adenocarcinoma
in the left breast that was negative for ER and PgR, but positive for erbB(
2). Thirty-five months after the initial diagnosis she was treated for acut
e skeletal metastasis, and stabilized with a hip replacement. At this time,
tumor cells were removed from surplus involved bone, inoculated into cell
culture, and developed into the LCC15-MB cell line. The bone metastasis was
a poorly differentiated adenocarcinoma lacking ER, PgR, and erbB(2), chara
cteristics shared by the LCC15-MB cells, although ER can be re-expressed by
treatment of the LCC15-MB cells for 5 days with 75 mu M 5-aza-2'-deoxycyti
dine. The LCC15-MB cell line is tumorigenic when implanted subcutaneously i
n NCr nu/nu mice and produces long-bone metastases after intracardiac injec
tion. Although the bone metastasis from which the LCC15-MB cell line was de
rived lacked vimentin (VIM) expression, the original primary tumor and lymp
h node metastasis were strongly VIM positive, as are LCC15-MB cells in vitr
o and in nude mice. The karyotype and isozyme profiles of LCC15-MB cells ar
e consistent with its origin from a human female, with most chromosome coun
ts in the hypertriploid range. Thirty-two marker chromosomes are present. T
hese cells provide an in vitro/in vivo model in which to study the inter-re
lationships between ER, VIM, and bone metastasis in human breast cancer.