Evidence map›Paper›PMID 42330962›Full record

ArticleCell stem cell2026

Lineage plasticity driven by GATA6 loss fuels colorectal cancer metastasis.

Saori Goto, Vikram Deshpande, Ömer H Yilmaz, Norihiro Goto

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell stem cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Saori GotoJoan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Biology, The David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Vikram DeshpandeDepartment of Pathology, Beth Israel Deaconess Hospital and Harvard Medical School, Boston, MA 02114, USA.
Ömer H YilmazDepartment of Biology, The David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Department of Pathology, Beth Israel Deaconess Hospital and Harvard Medical School, Boston, MA 02114, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: ohyilmaz@gmail.com.
Norihiro GotoJoan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Cell and Developmental Biology, Weill Cornell Medicine, New York, NY, USA. Electronic address: nog4004@med.cornell.edu.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Jacqueline A. Lees · 1985 to 2026
$93.9M
Effects of inflammaging on intestinal epithelial cells and aspirin chemoprevention.R01CA257523 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CHAN, ANDREW T, STAPPENBECK, THADDEUS S · 2021 to 2025
$3.7M
Immunometabolic regulation of CD8+ T cell mediated intestinal epithelial cell death in people with HIV (PWH)R01DK133919 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Douglas Kwon, Omer Yilmaz · 2022 to 2026
$3.5M
Development of a novel therapy targeting the tumor microenvironment in inflammatory breast cancerR01CA258523 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI UENO, NAOTO T. · 2022 to 2025
$3.2M
Developing high-throughput genetic perturbation strategies for single cells in cancer organoidsU01CA250554 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BERGER, BONNIE, YILMAZ, OMER · 2020 to 2022
$2.8M
The lysosomal fasting response in intestinal stem cells and cancerR01DK140310 · NIDDK · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Omer Yilmaz · 2024 to 2026
$2.4M
Impact of fasting on intestinal stem cells and cancerR01CA245314 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Omer Yilmaz · 2020 to 2026
$2.3M
PROSPECT - Stem cell modelsOT2CA297570 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Omer Yilmaz · 2024 to 2026
$1.4M
Targeting a human gut bacterial genotoxin via engineered commensal bacteriaR01CA299955 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jiahe Li, Omer Yilmaz · 2025 to 2026
$1.2M
Understanding the role of the stromal cell niche in intestinal stem cell agingR00AG076987 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI Norihiro Goto · 2025 to 2026
$493k
Optimizing Gram-positive bacteria as a candidate for targeted anti-tumor therapyF32CA254314 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SHUSTER, BENTLEY M. · 2020 to 2022
$151k
NCI NIH HHS F32 CA254314NCI NIH HHS OT2 CA297570NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA245314NCI NIH HHS R01 CA257523NCI NIH HHS R01 CA258523NCI NIH HHS R01 CA299955NCI NIH HHS U01 CA250554NIA NIH HHS R00 AG076987NIDDK NIH HHS R01 DK133919NIDDK NIH HHS R01 DK140310
6 · The paper itself

Abstract

Colorectal cancer (CRC) liver metastases are the leading cause of CRC-related mortality, yet the genetic and epigenetic drivers underlying this process remain poorly understood. Here, we established a pro-metastatic CRC organoid library through serial orthotopic transplantation of liver metastasis-derived organoids. Integrative RNA sequencing (RNA-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) analyses identified a pro-metastatic signature characterized by multilineage plasticity, including fetal-like and basal-like/squamous transcriptional programs. Motif and transcription factor activity analyses identified GATA6 as a key regulator of these epigenetic alterations. GATA6 expression is downregulated in liver metastases, and its genetic ablation enhances liver metastasis with minimal effects on primary tumor growth. Mechanistically, GATA6 loss triggers pro-metastatic transcriptional programs, including fetal-like and basal-like/squamous states, accompanied by LGR5

Indexed as

Cell LineageCell PlasticityColorectal NeoplasmsGATA6 Transcription FactorLiver NeoplasmsAnimalsCell Line, TumorEpigenesis, GeneticGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 4HMGB ProteinsHumansMiceNeoplasm MetastasisOrganoidsSOXF Transcription FactorsGATA6 protein, humanGata6 protein, mouseGATA6 Transcription FactorHepatocyte Nuclear Factor 4HMGB ProteinsSox17 protein, mouseSOXF Transcription Factorscolorectal cancermetastasisorganoid

Identifiers

PMID42330962
PMCPMC13499791

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.