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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.
Immunomodulatory triple-negative breast cancers are the ones packed with immune cells. The 2016 re-analysis showed the signature comes from those lymphocytes rather than the tumour, so today the same idea is captured by counting tumour-infiltrating lymphocytes on the biopsy, which predicts a better outcome and is used to test whether some small tumours need less treatment.
The immunomodulatory (IM) subtype was enriched for immune cell processes, cytokine and antigen-processing pathways and immune signal transduction (Lehmann 2011). Laser-capture microdissection then showed those transcripts were contributed by infiltrating lymphocytes, so IM was removed as a tumour-intrinsic subtype in the four-way refinement (Lehmann 2016). Burstein's basal-like immune-activated (BLIA) subtype, defined by Stat signalling and cytokine expression, had the best disease-free and disease-specific survival of the four Burstein subtypes, and basal-like immunosuppressed (BLIS), marked by the immunosuppressing molecule VTCN1, the worst (Burstein 2015). In clinical practice the equivalent measurement is stromal tumour-infiltrating lymphocytes, and the parent page's biomarker and stage I rows carry the de-escalation cohorts; PD-L1 expression on immune cells is the treatment-selecting marker in metastatic disease (the glossary term for CPS 10 has the figures).
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 |
|---|---|---|
| Metastatic, PD-L1 CPS 10 or more | Pembrolizumab with chemotherapy (KEYNOTE-355; NICE TA801) or with sacituzumab govitecan (ASCENT-04); the rows on the parent page. | not mapped |