Evidence map›Paper›PMID 42277259›Full record

ArticleNature genetics2026

Dynamic transitioning between MAPK-driven and WNT-driven cell states drives intestinal cancer and shapes therapy response.

Amanda R Moore, Brian Biehs, Noelyn Kljavin, Thi Thu Thao Nguyen, Akansha Shah, Jeremy Burton, Honglin Jiang, Jenille Tan, Deepankar Chakroborty, Lisa Wang and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Amanda R MooreDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0003-3864-6387
Brian BiehsDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.
Noelyn KljavinDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.
Thi Thu Thao NguyenComputational Sciences Center of Excellence, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0003-0270-4581
Akansha ShahDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-6902-106X
Jeremy BurtonDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.
Honglin JiangDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.
Jenille TanDepartment of Discovery Oncology, Genentech, South San Francisco, CA, USA.
Deepankar ChakrobortyDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-3458-0205
Lisa WangDepartment of Real World Data Science, Genentech, South San Francisco, CA, USA.
Nayan ChaudharyDepartment of Real World Data Science, Genentech, South San Francisco, CA, USA.
Dongze HeComputational Sciences Center of Excellence, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-8259-7434
William LinDepartment of Research Pathology, Genentech, South San Francisco, CA, USA.
Kathryn MeshDepartment of Research Pathology, Genentech, South San Francisco, CA, USA.
Xin YeDepartment of Discovery Oncology, Genentech, South San Francisco, CA, USA.
Kamakoti P BhatDepartment of Discovery Oncology, Genentech, South San Francisco, CA, USA.
Lisa TaiDepartment of Research Pathology, Genentech, South San Francisco, CA, USA.
Shiqi XieDepartment of Discovery Oncology, Genentech, South San Francisco, CA, USA.
Weilan YeDepartment of Research Oncology, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-6219-3982
Lisa McGinnisDepartment of Research Pathology, Genentech, South San Francisco, CA, USA.
Shiva MalekDepartment of Discovery Oncology, Genentech, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-9526-7968
Sandra P MeloDepartment of Research Oncology, Genentech, South San Francisco, CA, USA. melo-carlos.sandra@gene.com.ORCID http://orcid.org/0009-0000-8143-5417
Frederic J de SauvageDepartment of Research Oncology, Genentech, South San Francisco, CA, USA. desauvage.fred@gene.com.ORCID http://orcid.org/0000-0002-5275-2584

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) frequently harbors activating mutations in the WNT and MAPK pathways. While KRAS mutations alone can drive tumor initiation in many tissues, they are insufficient in the intestine. Leveraging allele-specific properties of RAS, we developed a mouse model to investigate MAPK hyperactivation. Here we show that KRAS mutations drive a regenerative state while antagonizing the Lgr5

Indexed as

Colorectal NeoplasmsIntestinal NeoplasmsMAP Kinase Signaling SystemWnt Signaling PathwayAnimalsCarcinogenesisHumansMiceMutationNeoplastic Stem CellsProto-Oncogene Proteins p21(ras)Receptors, G-Protein-CoupledHras protein, mouseLgr5 protein, mouseProto-Oncogene Proteins p21(ras)Receptors, G-Protein-Coupled

Identifiers

PMID42277259

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.