- Is the biology of IBC at the time of its diagnosis the same biology that existed when the tumor consisted of as few as 100,000 cells? If not, what precipitates the change to an IBC phenotype? And at what time in the tumor’s growth?
- Does a wound healing environment transform non-IBC malignant mammary epithelial cells to an ibc genotype/phenotype? Does a wound healing environment play any role in the growth of IBC? Can breast compression for mammography result in a wound and subsequent wound healing environment? “Sudden outgrowth of tumor after wounding has been observed for a century.” Premenopausal status accelerates relapse in node positive breast cancer: hypothesis links angiogenesis, screening controversy, Retsky, M. et al., The role of extracellular matrix in postinflammatory wound healing and fibrosis, Raghow R. and Wounding from biopsy and breast-cancer progression, Retsky, M. et al.
- Is there an inherited genetic predisposition to IBC? What is the incidence of BRCA1 mutations in IBC patients? BRCA2?
- What is the evidence of epigenetic factors in IBC? “Our findings support the notion that hypermethylation of critical CpG island loci influences cancer development and produces distinct epigenetic signatures for particular tumor subtypes.” Dissecting complex epigenetic alterations in breast cancer using CpG island microarrays, Yan, PS et al.
- Does IBC occur as basal epithelial cell origin? as luminal epithelial origin? both? neither? Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications, Sorlie, T. et al. and Genes, chromatin, and breast cancer: an epigenetic tale, Mielnicki LM, et al.
- To what degree is the nonoxidative pentose phosphate pathway active in IBC tumors? Nonoxidative pentose phosphate pathways and their direct role in ribose synthesis in tumors: is cancer a disease of cellular glucose metabolism? , Boros, LG et al. and Thiamine supplementation to cancer patients: a double edged sword, Boros, LG et al.
