These experiments do however show that a peptide, which shares antigenic determinants with human alpha-lactalbumin is present in some breast tumour tissues.
Analysis of expression of Harvey-ras related oncogenes in human malignant breast tumours and in their respective normal tissue has revealed a significant elevation of Harvey-ras transcripts in malignant as compared to normal tissue.
Structure of the human c-mos protooncogene in DNAs from breast tumors, leukemic cells, and lymphocytes from normal individuals was analyzed by restriction enzyme digestion and Southern blot.
Amplification of the human protooncogene c-erbB-2 was found in 12 of 36 human breast tumours and was associated with increased levels of expression of the c-erbB-2 protein, measured both by immunohistological staining and by western blotting.
In order to draw this conclusion we have used an EGF receptor gene-amplified human breast tumor cell line that is growth-inhibited by EGF, and exponentially growing normal human fibroblasts.
A rare EcoRI restriction fragment length polymorphism (RFLP) in the 3' end of the human c-mos locus has been identified in DNA from patients with breast tumors, esophageal carcinomas and leukemias.
Restriction fragment length polymorphism analysis of these DNAs further suggests that the most frequent loss of sequences in breast tumors occurs between the beta-globin and parathyroid hormone loci on the short arm of chromosome 11.
Expression of TGF alpha mRNA was detected in 70% of estrogen receptor positive and negative primary human breast tumors from 40 patients when examined by slot blot and Northern analysis.
Steady state mRNA levels for transforming growth factor beta, erbB2, c-myc, and Ha-ras in the normal cells were greater than or comparable to those in all of the breast tumor lines.
Initial studies in human breast cancer cell lines suggested a possible association between the absence of one allele and the absence of ER expression; subsequent analysis of allele distribution and frequency in 188 primary human breast tumor biopsies did indeed show a significant but not complete correlation between the absence of one allele and the failure to express ER.
We show here that a monoclonal antibody directed against the extracellular domain of p185HER2 specifically inhibits the growth of breast tumor-derived cell lines overexpressing the HER2/c-erbB-2 gene product and prevents HER2/c-erbB-2-transformed NIH 3T3 cells from forming colonies in soft agar.
Since sex steroid hormones and growth factors are known to modulate the proliferation of breast tumors, we have studied the effects of estrogen and progestin, their antagonists, and growth factors on the regulation of estrogen receptor (ER) mRNA and protein levels in T47D breast cancer cells, which contain low levels of ER, and in two sublines of MCF-7 cells which contain high ER levels.