Evidence map›Paper›PMID 23456389›Full record

Trial reportAnnals of surgical oncology2013

Mutations in specific codons of the KRAS oncogene are associated with variable resistance to neoadjuvant chemoradiation therapy in patients with rectal adenocarcinoma.

Marjun P Duldulao, Wendy Lee, Rebecca A Nelson, Wenyan Li, Zhenbin Chen, Joseph Kim, Julio Garcia-Aguilar

Abstract readClinical Trial, Phase IIClinical Trial, Phase IIIMulticenter Study
In one paragraph

Trial report in Annals of surgical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 3 pooled it
3.6field-weighted citation impact, top 6% of its field
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

62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. KRASCellular & molecular biology letters · 2026
    Article
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  12. Unveiling radiobiological traits and therapeutic responses of BRAFJournal of experimental & clinical cancer research : CR · 2025
    Article
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  15. Review
  16. YB-1 activating cascades as potential targets in KRAS-mutated tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  17. Targeting oncogenicMolecular therapy. Nucleic acids · 2023
    Article
  18. Review
  19. Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Marjun P DuldulaoDepartment of Surgery, City of Hope, Duarte, CA, USA.
Wendy Lee
Rebecca A Nelson
Wenyan Li
Zhenbin Chen
Joseph Kim
Julio Garcia-Aguilar
City of Hope · USCity Of Hope National Medical Center · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Timing of Rectal Cancer Response to ChemoradiationR01CA090559 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GARCIA-AGUILAR, JULIO · 2003 to 2009
$3.9M
NCI NIH HHS CA090559NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA090559
6 · The paper itself

Abstract

backgroundMutations in KRAS and TP53 are common in colorectal carcinogenesis and are associated with resistance to therapy. Rectal cancers carrying both mutations are less likely to respond to neoadjuvant chemoradiation therapy (CRT) compared with wild-type tumors. Codon-specific KRAS mutations are associated with variable resistance to targeted therapies, but their association with rectal cancer response to CRT remains unclear. Our objective was to establish a correlation between specific KRAS mutations and rectal cancer response to CRT and to investigate if the correlation was related to a different association between KRAS and TP53 mutations.

methodsA total of 148 stage II-III rectal cancer patients underwent preoperative CRT followed by surgery. DNA was extracted from pretreatment tumor biopsies and paired normal surgical tissues and KRAS and TP53 genotyping was performed. Specific KRAS mutations were then correlated with tumor response and with concurrent TP53 mutation.

resultsA total of 60 patients had KRAS mutation, 12 in codon 13 and 48 in other locations. Also, 80 patients had TP53 mutation; 27 had concurrent KRAS/TP53 mutations. Tumors with any KRAS mutation were less likely to have a pCR compared with wild-type KRAS (p = 0.006). Specifically, no tumors with KRAS codon 13 mutations had a pCR (p = 0.03). Tumors with KRAS codon 13 mutations also had a higher incidence of concurrent TP53 mutation compared with tumors with other KRAS mutations (p = 0.02).

conclusionsMutations in different KRAS codons may have different effects on rectal cancer resistance to CRT. This variable resistance may be related to a different frequency of TP53 mutations in KRAS mutant tumors.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overChemoradiotherapy, AdjuvantCodonFemaleGenotypeHumansMaleMiddle AgedMutationNeoadjuvant TherapyProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsCodonKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTumor Suppressor Protein p53

Identifiers

PMID23456389
PMCPMC5584556
OpenAlexW1981346090

What OpenQuestion holds

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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 OpenQuestion graph.