Evidence map›Paper›PMID 42167227›Full record

ArticleCancer cell2026

Concurrent genetic and non-genetic resistance mechanisms to KRAS inhibition in colorectal cancer.

Salvador Alonso, Kevan Chu, Elizabeth Granowsky, Valeria Saraiba Rabanales, Marie J Parsons, Himari Gunasinghe, Jinru Shia, Rona Yaeger, Lukas E Dow

Abstract read
In one paragraph

Article in Cancer 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. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Salvador AlonsoSandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA; Department of Gastrointestinal Medical Oncology, Division of Cancer Medicine, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: salonso1@mdanderson.org.
Kevan ChuSandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA; Weill Cornell Graduate School and Medical Sciences, Weill Cornell Medicine, New York, NY, USA.
Elizabeth GranowskySandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Valeria Saraiba RabanalesDepartment of Gastrointestinal Medical Oncology, Division of Cancer Medicine, MD Anderson Cancer Center, Houston, TX, USA.
Marie J ParsonsSandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Himari GunasingheSandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Jinru ShiaDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Rona YaegerDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Lukas E DowSandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA; Weill Cornell Graduate School and Medical Sciences, Weill Cornell Medicine, New York, NY, USA; Department of Biochemistry, Weill Cornell Medicine, New York, NY, USA; Department of Medicine, Weill Cornell Medicine, New York, NY, USA. Electronic address: lud2005@med.cornell.edu.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
MSK Paul Calabresi Career Development Award for Clinical OncologyK12CA184746 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Omar Abdel-Wahab, Simon N. Powell · 2015 to 2026
$8.3M
Mechanisms of genetic and non-genetic resistance to KRAS inhibitionR01CA297721 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LUKAS Edward DOW · 2025 to 2026
$1.2M
Targeting regenerative reprogramming in colorectal cancerK08CA279499 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Salvador Alonso Martinez · 2023 to 2026
$1.2M
Targeting Chromosomal Instability in the Evolution of Resistance to Matched Therapies Against Colorectal Cancer to Extend Treatment ResponseR21CA292178 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Rona Yaeger · 2025 to 2026
$453k
NCI NIH HHS K08 CA279499NCI NIH HHS K12 CA184746NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA297721NCI NIH HHS R21 CA292178
6 · The paper itself

Abstract

KRAS is mutationally activated in 45%-50% of colorectal cancer (CRC) cases, and while KRAS-targeted therapies have shown clinical promise, drug resistance limits their efficacy. To explore the mechanisms underlying KRAS inhibitor resistance, we use targeted exome sequencing and spatial transcriptomics on patient-matched CRC biopsies following combined treatment with KRAS

Indexed as

Antineoplastic AgentsColorectal NeoplasmsDrug Resistance, NeoplasmProto-Oncogene Proteins p21(ras)AcetonitrilesAnimalsErbB ReceptorsExosomesFemaleHEK293 CellsHumansMiceMutationOrganoidsPiperazinesProtein Kinase InhibitorsAcetonitrilesadagrasibAntineoplastic AgentsErbB ReceptorsKRAS protein, humanPiperazinesProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)PyridinesPyrimidinessotorasibTBK1 protein, humanCRCinflammationKRASplasticityTBK1

Identifiers

PMID42167227
PMCPMC13417870

What OpenQuestion holds

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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 OpenQuestion graph.