Evidence map›Paper›PMID 37434969›Full record

ArticleFrontiers in oncology2023

Case Report: Longitudinal monitoring of clonal evolution by circulating tumor DNA for resistance to anti-EGFR antibody in a case of metastatic colorectal cancer.

Tamotsu Sagawa, Yasushi Sato, Masahiro Hirakawa, Kyoko Hamaguchi, Fumito Tamura, Hiroyuki Nagashima, Koshi Fujikawa, Koichi Okamoto, Yutaka Kawano, Masahiro Sogabe and 2 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
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

12 authors at 2 institutions in 1 country.

Tamotsu SagawaDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Yasushi SatoDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masahiro HirakawaDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Kyoko HamaguchiDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Fumito TamuraDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Hiroyuki NagashimaDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Koshi FujikawaDepartment of Gastroenterology, Hokkaido Cancer Center, Sapporo, Hokkaido, Japan.
Koichi OkamotoDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Yutaka KawanoDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masahiro SogabeDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Hiroshi MiyamotoDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Tetsuji TakayamaDepartment of Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Hokkaido University Hospital · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Treatment with anti-EGFR antibody has been shown to prolong survival in patients with RAS wild-type metastatic colorectal cancer (mCRC). However, even patients who initially respond to anti-EGFR antibody therapy, almost without exception, develop resistance to the therapy and then fail to respond. Secondary mutations in the mitogen-activated protein (MAPK) signaling pathway (mainly in NRAS and BRAF) have been implicated in anti-EGFR resistance. However, the process by which resistant clones develop during therapy has not been elucidated, and considerable intrapatient and interpatient heterogeneity exists. Circulating tumor DNA (ctDNA) testing has recently allowed the noninvasive detection of heterogeneous molecular alterations that underlie the evolution of resistance to anti-EGFR. In this report, we describe our observation of genomic alterations in Case presentation: A 54-year-old woman was initially diagnosed with sigmoid colon cancer with multiple liver metastases. After receiving first-line mFOLFOX + cetuximab, second-line FOLFIRI + ramucirumab, third-line trifluridine/tipiracil + bevacizumab, fourth-line regorafenib, and fifth-line CAPOX + bevacizumab, she was rechallenged with CPT-11 + cetuximab. The best response to anti-EGFR rechallenge therapy was a partial response. Conclusion: In this report, tracking of ctDNA allowed us to describe clonal evolution in a case in which we observed genomic alterations in

Indexed as

anti-EGFR antibodyclonal evolutionctDNAmetastatic colorectal cancerresistance

Identifiers

PMID37434969
PMCPMC10332633
OpenAlexW4382133793

What OpenQuestion holds

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LicenceCC BY
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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.