Evidence map›Paper›PMID 38539256›Full record

ArticleDiagnostic pathology2024

Concurrent KRAS p.G12C mutation and ANK3::RET fusion in a patient with metastatic colorectal cancer: a case report.

Tillmann Bedau, Carina Heydt, Udo Siebolts, Thomas Zander, Max Kraemer, Heike Loeser, Reinhard Buettner, Alexander Quaas

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Diagnostic pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 1 country.

Tillmann BedauDepartment of Pathology, University Hospital Cologne, Cologne, Germany. tillmann.bedau@uk-koeln.de.
Carina HeydtDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
Udo SieboltsDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
Thomas ZanderDepartment I of Internal Medicine, Center for Integrated Oncology (CIO), University of Cologne, Cologne, Germany.
Max KraemerDepartment I of Internal Medicine, Center for Integrated Oncology (CIO), University of Cologne, Cologne, Germany.
Heike LoeserInstitut für Pathologie Köln-Deutz, Cologne, Germany.
Reinhard BuettnerDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
Alexander QuaasDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
University Hospital Cologne · DEUniversity of Cologne · DEDeutz (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) frequently involves mutations in the KRAS gene, impacting therapeutic strategies and prognosis. The occurrence of KRAS mutations typically precludes the presence of RET fusions, with current medical literature suggesting a mutual exclusivity between these two genetic alterations. We present a unique case that challenges this notion. CASE PRESENTATION: An 85-year-old female with metastatic CRC was found to have a combination of genetic anomalies that is to the best of our knowledge not yet described in the medical literature: a KRAS p.G12C mutation, associated with oncogenesis and treatment resistance, and an ANK3::RET fusion, an infrequent but targetable mutation in CRC. This molecular profile was uncovered through comprehensive genomic sequencing after the patient experienced metachronous tumor dissemination. The presence of both genetic events complicates the treatment approach.

conclusionsThe identification of both a KRAS p.G12C mutation and an ANK3::RET fusion in the same CRC patient adds a new layer to the oncogenic landscape and treatment considerations for CRC. It highlights the intricate decision-making required in the era of precision medicine, where targeted therapies must be carefully chosen and potentially combined to combat complex genetic profiles. The case emphasizes the urgency of investigating the clinical effects of concurrent or sequential use of KRAS p.G12C and RET inhibitors to inform future therapeutic guidelines and improve patient outcomes in similar cases.

Indexed as

Colonic NeoplasmsProto-Oncogene Proteins p21(ras)Aged, 80 and overAnkyrinsCarcinogenesisCell Transformation, NeoplasticFemaleHumansMutationProto-Oncogene Proteins c-retANK3 protein, humanAnkyrinsKRAS protein, humanProto-Oncogene Proteins c-retProto-Oncogene Proteins p21(ras)RET protein, humanANK3::RET fusion.Genetic profilingKRAS inhibitorsKRAS p.G12C mutationMetastatic colorectal cancerMolecular diagnosticsNovel therapeutic strategiesPrecision oncologyRET kinase inhibitorsTargeted therapy

Identifiers

PMID38539256
PMCPMC10976695
OpenAlexW4393223650

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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.