From:  Metabolic plasticity drives specific mechanisms of chemotherapy and targeted therapy resistance in metastatic colorectal cancer

 Transcriptomic characteristics in metastatic biopsies.

ReferencesM1 locationBulk transcriptomicsConcordance (primary and M1)
Laoukili et al. [8]
(n = 12)
Peritoneal*, &CMS4 (100%)92%
Lenos et al. [9]
(n = 52)
Peritoneal**, &CMS1 (6%), CMS2 (8%), CMS3 (2%), CMS4 (85%)63%
Piskol et al. [10]
(n = 130)
Not defined&CMS1 (17%), CMS2 (48%), CMS3 (8%), CMS4 (27%)60%
Kamal et al. [11]
(n = 257)
Lung, liver*M1 (86%) and CMS4 (85%); M2 (63%) and CMS2 (52%)NE
Eide et al. [12]
(n = 295)
Liver*, &CMS1 (6%), CMS2 (35%), CMS3 (2%), CMS4 (35%)33%
Chowdhury et al. [13]
(n = 10,776)
Multiple sitesCMS1 (10–16%), CMS2 (37–45%), CMS3 (11–13%), CMS4 (27–39%)NE
Pitroda et al. [14]
(n = 134)
Liver**, &Canonical (33%), immune (28%), stromal (39%)NE
Katipally et al. [15]
(n = 240)
Liver**, &Canonical (50%), immune (19%), stromal (31%)NE

*: Sample obtained from untreated patients; **: sample obtained from pretreated patients; &: sample obtained from resected metastatic biopsies; n: number of patients included in each cohort; M1: transcriptomic subtype characterized by inflammatory and T-cell infiltration; M2: transcriptomic subtype enriched in MYC and E2F targets. CMS: consensus molecular subtypes; NE: not evaluated.