Evidence map›Paper›PMID 39039804›Full record

ArticleCancer science2024

Clinicopathological, molecular, and prognostic features of colorectal carcinomas with KRAS c.34G>T (p.G12C) mutation.

Satoko Ugai, Qian Yao, Yasutoshi Takashima, Yuxue Zhong, Kosuke Matsuda, Hidetaka Kawamura, Yu Imamura, Kazuo Okadome, Kosuke Mima, Kota Arima and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Adagrasib in the treatment of colorectal cancer.Future oncology (London, England) · 2025
    Review
  4. Review
  5. 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

17 authors.

Satoko UgaiProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Qian YaoProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Yasutoshi TakashimaProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Yuxue ZhongProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Kosuke MatsudaProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Hidetaka KawamuraProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Yu ImamuraDepartment of Esophageal Surgery, The Cancer Institute Hospital of the Japanese Foundation of Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0036-0124
Kazuo OkadomeProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Kosuke MimaDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kota ArimaDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Keisuke KosumiDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Mingyang SongDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Jeffrey A MeyerhardtDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical, Boston, Massachusetts, USA.
Marios GiannakisDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical, Boston, Massachusetts, USA.
Jonathan A NowakProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
Tomotaka UgaiProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.ORCID https://orcid.org/0000-0003-0182-5269
Shuji OginoProgram in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.

Funding

Coffee and metabolites modulating the gut microbiome for improved colorectal cancer survivalR01CA263776 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Mingyang Song · 2022 to 2026
$3.3M
The Gut Microbiome, Lifestyle, and Colorectal NeoplasiaU01CA261961 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Mingyang Song · 2022 to 2026
$3.0M
Cancer Research UK 27140NCI NIH HHS R01 CA263776NCI NIH HHS U01 CA261961
6 · The paper itself

Abstract

Evidence indicates that combinations of anti-EGFR antibodies and KRAS p.G12C (c.34G>T) inhibitors can be an effective treatment strategy for advanced colorectal cancer. We hypothesized that KRAS c.34G>T (p.G12C)-mutated colorectal carcinoma might be a distinct tumor subtype. We utilized a prospective cohort incident tumor biobank (including 1347 colorectal carcinomas) and detected KRAS c.34G>T (p.G12C) mutation in 43 cases (3.2%) and other KRAS mutations (in codon 12, 13, 61, or 146) in 467 cases (35%). The CpG island methylator phenotype (CIMP)-low prevalence was similarly higher in KRAS c.34G>T mutants (52%) and other KRAS mutants (49%) than in KRAS-wild-type tumors (31%). KRAS c.34G>T mutants showed higher CIMP-high prevalence (14%) and lower CIMP-negative prevalence (33%) compared with other KRAS mutants (6% and 45%, respectively; p = 0.0036). Similar to other KRAS mutants, KRAS c.34G>T-mutated tumors were associated with cecal location, non-microsatellite instability (MSI)-high status, BRAF wild type, and PIK3CA mutation when compared with KRAS-wild-type tumors. Compared with BRAF-mutated tumors, KRAS c.34G>T mutants showed more frequent LINE-1 hypomethylation, a biomarker for early-onset colorectal carcinoma. KRAS c.34G>T mutants were not associated with other features, including the tumor tissue abundance of Fusobacterium nucleatum (F. animalis), pks

Indexed as

Colorectal NeoplasmsCpG IslandsDNA MethylationMutationProto-Oncogene Proteins p21(ras)AdultAgedAged, 80 and overClass I Phosphatidylinositol 3-KinasesFemaleHumansMaleMicrosatellite InstabilityMiddle AgedPrognosisProspective StudiesBRAF protein, humanClass I Phosphatidylinositol 3-KinasesKRAS protein, humanPIK3CA protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)adagrasibcolorectal tumorCpG island methylator phenotypeKRASsotorasib

Identifiers

PMID39039804
PMCPMC11448363

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Registered trials

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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.