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6 slides generated from the cancer page, with a quiz from the open benchmark and speaker notes that cite the sources. Arrow keys move between slides; Print gives one slide per page.
Mesenchymal triple-negative breast cancers have switched on the programme cells use to migrate (epithelial-to-mesenchymal transition). They overlap with claudin-low and metaplastic tumours, respond to chemotherapy less well than basal-like 1 tumours, and are the subtype the parent page names as resisting every drug class.
The mesenchymal (M) and mesenchymal stem-like (MSL) subtypes were enriched for epithelial-to-mesenchymal transition and growth factor pathway genes, and their cell lines responded to a PI3K/mTOR inhibitor and to dasatinib in the defining study (Lehmann 2011). In the 2016 refinement the stem-like signal proved to come from tumour-associated stromal cells, leaving M as the tumour-intrinsic mesenchymal subtype (Lehmann 2016). Burstein's mesenchymal (MES) subtype carries growth factor receptor targets (PDGFR alpha, c-KIT) (Burstein 2015). The claudin-low intrinsic subtype describes much of the same biology from the whole-breast-cancer side: low luminal differentiation markers, high epithelial-to-mesenchymal transition and stem-cell features, mostly triple-negative invasive carcinomas with frequent metaplastic and medullary differentiation, and a preoperative chemotherapy response between basal-like and luminal tumours (Prat 2010); a 2020 re-analysis found claudin-low is better understood as a phenotype with low genomic instability, low proliferation and high immune and stromal infiltration that can overlay any intrinsic subtype (Fougner 2020). Metaplastic carcinoma, the histological type most often mesenchymal, is on its own page.
A research classification by gene expression (Lehmann 2011, refined 2016), not a test the NHS runs; treatment follows the triple-negative rows on the parent page.
| Setting | Approach | Guideline |
|---|---|---|
| Stage II to III and metastatic | As for triple-negative disease; no mesenchymal-specific treatment is approved. PI3K/mTOR inhibitors and dasatinib were active in cell lines only. | not mapped |