This finding may indicate why breast tumors have a preference for skeletal metastases, and these genes may have a potential as metastasis markers.
Our observation that Cost can reduce detyrosinated tubulin similarly to Parth may indicate that breast cancer cell lines with increased detyrosination levels are more susceptible to inhibition, or that extending treatment beyond two hours is required to realize the inhibitory action of Cost [see Additional file 1: Figure S1].
This may indicate that some breast tumors have a high ratio of cancer stem cells, and may require specific and aggressive treatment.
This association with histological grade may indicate that these female breast tumors possess the required degree of differentiation to synthesize the protein.
We propose that this independently validated protein biomarker panel may indicate a HER2-enriched breast cancer subtype with poor prognosis, and that measurement of S100P, in particular, may be valuable both in the classification of breast cancer and as a possible target for treatment.
Reports of differences in methylation pattern between primary and metastatic breast cancer [ 18] may indicate that therapeutic targets in primary breast cancer are not be the same as targets in metastatic sites.
Circulating IGFBP-3 may avert breast cancer development, with the clinical paradox that increasing IGFBP-3 levels in breast tumours may indicate adverse prognostic cancers [ 2, 23- 26].
The finding of the additional TP53 mutation in one patient, 1 year post breast biopsy, may indicate the worsening and progression of the disease.
The change over time to more mammography detected and lower stage breast cancer may indicate movement towards the achievement of mammography screening goals.
Increasing IGFBP-3 levels in breast tumours may indicate adverse prognostic cancers, with contradictory implications on patient outcomes[ B24, 25] to reflect the complexity of IGFBP-3 effects on cell proliferation[ B27, 28, 30].
