I’m attending American Association of Cancer Research annual meeting in Washington DC right now. I’m enjoying meeting so far and planning to share with you some of my brief notes – quotes (tweet-like style) that I took during cancer stem cell sessions yesterday and today.
– 2 theories (clonal evolution and cancer stem cells) are not mutually exclusive and likely act concurrently;
– cancer stem cell (CSC) are functionally definded by self-renewal, susteained proliferation and tumor initiation -propagation ability;
– CSC act not in cell autonomous manner
– other proposed functional characteristics of CSC – evasion-metastasis, immune evasion, relation to niche, angiogenesis;
– cell lines fail to replicate original heterogeneity.
– tumorigeneity is very much assay-dependent;
– surface markers (CD133 for instance) frequently does not distinguish tumorigenuc vs. non-tumorigenic populations;
– cancers need to be hierarchycally organized in order to be heterogeneous;
– heterogeneity is driven by reversible phenotypically changes and irreversible genetic changes;
– no xenotransplant assay recapitulates the immune response that occurs in some patients;
– immunocompetence should be tested with mouse models of cancer transplanted into histocompatible recipients;
– tumor genotype can have an impact to tumorigeneity assays and frequency of SCS;
– the potential of cancer cells to proliferate extensevely is context dependent.
– natural selection should lead to neoplasms dominated almost completely by cancer stem cells but we don’t see that;
– hierarchy of CSC is an assumption which should be tested further;
– current assays confound engraftment with stemness;
– non-CSC have fitness effect on CSC, such as: niche-stroma and supression of competitors, they must co-exist.
and the last point for today, but very important:
– non-tumorigeneic is mean able to survive in mice for few months without tumor formation.