Colorectal cancer residual disease at maximal response to EGFR blockade displays a druggable Paneth cell-like phenotype.

doi:10.1126/scitranslmed.aax8313

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Colorectal cancer residual disease at maximal response to EGFR blockade displays a druggable Paneth cell-like phenotype.

Science translational medicine - 5 Aug 2020

Lupo Barbara, Sassi Francesco, Pinnelli Marika, Galimi Francesco, Zanella Eugenia R, Vurchio Valentina, Migliardi Giorgia, Gagliardi Paolo Armando, Puliafito Alberto, Manganaro Daria, Luraghi Paolo, Kragh Michael, Pedersen Mikkel W, Horak Ivan D, Boccaccio Carla, Medico Enzo, Primo Luca, Nichol Daniel, Spiteri Inmaculada, Heide Timon, Vatsiou Alexandra, Graham Trevor A, Élez Elena, Argiles Guillem, Nuciforo Paolo, Sottoriva Andrea, Dienstmann Rodrigo, Pasini Diego, Grassi Elena, Isella Claudio, Bertotti Andrea, Trusolino Livio

Abstract excerpt

Blockade of epidermal growth factor receptor (EGFR) causes tumor regression in some patients with metastatic colorectal cancer (mCRC). However, residual disease reservoirs typically remain even after maximal response to therapy, leading to relapse. Using patient-derived xenografts (PDXs), we observed that mCRC cells surviving EGFR inhibition exhibited gene expression patterns similar to those of a quiescent...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Colorectal Neoplasms

Share to ErbB Receptors

Share to Neoplasm Recurrence, Local

Share to Neoplasm, Residual

Share to Paneth Cells

Share to Phenotype

Share to Phosphatidylinositol 3-Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 32759276
DOI: 10.1126/scitranslmed.aax8313
PMCID: PMC7617202

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Colorectal cancer residual disease at maximal response to EGFR blockade displays a druggable Paneth cell-like phenotype.PMID 32759276Read ↗

Paneth-like transition drives resistance to dual targeting of KRAS and EGFR in colorectal cancer.Semantic proximity Read ↗

Plastic persisters: revival stem cells in colorectal cancerSemantic proximity Read ↗

A small natural molecule CADPE kills residual colorectal cancer cells by inhibiting key transcription factors and translation initiation factorsSemantic proximity Read ↗

RNA-Sequencing of Long-Term Label-Retaining Colon Cancer Stem Cells Identifies Novel Regulators of QuiescenceSemantic proximity Read ↗

LGR5‐Positive Colon Cancer Stem Cells Interconvert with Drug‐Resistant LGR5‐Negative cells and are Capable of Tumor ReconstitutionSemantic proximity Read ↗

Dormant Cancer Cells Contribute to Residual Disease in a Model of Reversible Pancreatic CancerSemantic proximity Read ↗

Cellular dormancy in minimal residual disease following targeted therapySemantic proximity Read ↗

LRIG1 is a triple threat: ERBB negative regulator, intestinal stem cell marker and tumour suppressorSemantic proximity Read ↗

Secondary resistance to anti-EGFR therapy by transcriptional reprogramming in patient-derived colorectal cancer models.Semantic proximity Read ↗

A pre-existing population of ZEB2+ quiescent cells with stemness and mesenchymal features dictate chemoresistance in colorectal cancerSemantic proximity Read ↗

Clusterin: a marker and mediator of chemoresistance in colorectal cancerSemantic proximity Read ↗

Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.