Mesenchymal-like (MES-like) state
Also known as: MES-like · mesenchymal-like · MES
One of four recurrent malignant cell states of glioblastoma described by Neftel et al. (2019), alongside NPC-like, OPC-like and AC-like. Studies in the library link transitions toward MES-like or mesenchymal programs to cancer–immune cell interactions, BRD2 and recurrence after therapy. VC0059 VC0066 VC0095 VC0069
Review pending Version 0.1.0 · status: draft · last expert review: not yet reviewed
Relations
| Subject | Relation | Object | Confidence | Evidence (role) |
|---|---|---|---|---|
| NF1 | associated with | Mesenchymal-like state | high | VC0059 supports |
| BRD2 | promotes | Mesenchymal-like state | high | VC0095 supports Evidence is from patient-derived xenograft and cell models: PTEN loss recruited BRD2 to MES gene promoters and bromodomain ablation reversed the MES transition. |
| AP-1 transcription factor complex | promotes | Mesenchymal-like state | medium | VC0069 supports Reported as mediating the mesenchymal shift in recurrent tumors; this is an observation at recurrence and does not show whether therapy induces or selects the state. |
| Neftel meta-modules | marks | Mesenchymal-like state | medium | VC0059 supports Signature-score calls from the Neftel meta-modules are not ground truth; the signatures used in GlioState’s re-analysis were an unverified third-party transcription. |
| PTEN | suppresses | Mesenchymal-like state | low | VC0095 supports Inferred from loss-of-function wording only (“PTEN loss recruited BRD2 to MES gene promoters”); the library text does not state that intact PTEN suppresses the MES-like state. Needs review. |
| NF-κB signalling | associated with | Mesenchymal-like state | low | VC0095 supports Taken from the topic summary (“BRD2/NF-κB signalling”); the specific NF-κB statement was not independently re-checked against the paper. Needs review. |
| Hypoxia | associated with | Mesenchymal-like state | low | VC0061 supports VC0094 supports The library text says cell-state layers appear driven by hypoxia; it does not tie hypoxia to MES-like specifically. Needs review. |
| Radiotherapy | associated with | Mesenchymal-like state | low | VC0069 supports Recurrent GBM shows a mesenchymal shift after therapy, but whether therapy induces or selects MES-like cells is unresolved. |
| Neural-progenitor-like state | transitions to | Mesenchymal-like state | low | VC0066 supports VC0059 supports The library states that cancer–immune interactions drive transitions toward MES-like states and that cells can move between Neftel states, but does not name the source state; applied to all three non-MES states for review. |
| Oligodendrocyte-progenitor-like state | transitions to | Mesenchymal-like state | low | VC0066 supports VC0059 supports The library states that cancer–immune interactions drive transitions toward MES-like states and that cells can move between Neftel states, but does not name the source state; applied to all three non-MES states for review. |
| Astrocyte-like state | transitions to | Mesenchymal-like state | low | VC0066 supports VC0059 supports The library states that cancer–immune interactions drive transitions toward MES-like states and that cells can move between Neftel states, but does not name the source state; applied to all three non-MES states for review. |
Appears in research topics
Appears in library items (4)
Items whose title, tags or one-line summary match this entity (derived from the data), plus the items cited as evidence for the description.
- VC0095 BRD2 bromodomain-mediated regulation of cell state plasticity modulates therapy response in glioblastoma. — Vadla R et al., Neuro-oncology, 2025
- VC0066 Interactions between cancer cells and immune cells drive transitions to mesenchymal-like states in glioblastoma. — Hara T et al., Cancer cell, 2025
- VC0069 A single-cell atlas of glioblastoma evolution under therapy reveals cell-intrinsic and cell-extrinsic therapeutic targets. — Wang L, Jung J, Babikir H, Shamardani K, Jain S, Feng X, Gupta N, Rosi S, Chang S, Raleigh D, Solomon D, Phillips JJ, Diaz AA., Nature cancer, 2022
- VC0059 An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma. — Neftel C et al., Cell, 2019
For research and education only. Not medical advice and not a recommendation of any diagnosis, treatment or product. Patients should consult their own physicians.