Evidence map›Paper›PMID 39375938›Full record

ArticleCancer science2024

Genomic and transcriptomic profiling of pre- and postneoadjuvant chemotherapy triple negative breast cancer tumors.

Tomomi Nishimura, Ravi Velaga, Norikazu Masuda, Kosuke Kawaguchi, Shuji Kawaguchi, Masahiro Takada, Yurina Maeshima, Sunao Tanaka, Yuichiro Kikawa, Takayuki Kadoya and 12 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. 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

22 authors.

Tomomi NishimuraDepartment of Next-generation Clinical Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Ravi VelagaDepartment of Breast and Endocrine Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0009-0002-5962-0266
Norikazu MasudaDepartment of Breast and Endocrine Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-7302-0278
Kosuke KawaguchiDepartment of Breast Surgery, Kyoto University Hospital, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-3161-7981
Shuji KawaguchiCenter for Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masahiro TakadaDepartment of Breast Surgery, Kyoto University Hospital, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-5954-1296
Yurina MaeshimaDepartment of Breast Surgery, Kyoto University Hospital, Kyoto University, Kyoto, Japan.
Sunao TanakaDepartment of Breast Surgery, Kyoto University Hospital, Kyoto University, Kyoto, Japan.
Yuichiro KikawaDepartment of Breast Surgery, Kobe City Medical Center General Hospital, Kobe, Japan.
Takayuki KadoyaBreast Center, Shimane University Hospital, Izumo, Japan.
Hiroko BandoBreast and Endocrine Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Rikiya NakamuraDepartment of Breast Surgery, Chiba Cancer Center, Chiba, Japan.
Yutaka YamamotoDepartment of Breast and Endocrine Surgery, Kumamoto University, Graduate School of Medical Sciences, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-6147-6828
Takayuki UenoBreast Oncology Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.ORCID https://orcid.org/0000-0002-9080-9377
Hiroyuki YasojimaDepartment of Surgery, Breast Oncology, NHO Osaka National Hospital, Osaka, Japan.
Hiroshi IshiguroBreast Oncology Service, Saitama Medical University International Medical Center, Saitama, Japan.
Satoshi MoritaDepartment of Biomedical Statistics and Bioinformatics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shinji OhnoBreast Oncology Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Hironori HagaDiagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Fumihiko MatsudaCenter for Genomic Medicine (Human Biosciences), Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University, Graduate School of Medicine, Kyoto, Japan.
Masakazu ToiTokyo Metropolitan Cancer and Infectious Disease Center, Komagome Hospital, Bunkyo-ku, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1488-9958

Funding

Eisai Co., Ltd
6 · The paper itself

Abstract

Our understanding of neoadjuvant treatment with microtubule inhibitors (MTIs) for triple negative breast cancer (TNBC) remains limited. To advance our understanding of the role of breast cancer driver genes' mutational status with pathological complete response (pCR; ypT0/isypN0) prediction and to identify distinct gene sets for MTIs like eribulin and paclitaxel, we carried out targeted genomic (n = 50) and whole transcriptomic profiling (n = 64) of TNBC tumor samples from the Japan Breast Cancer Research Group 22 (JBCRG-22) clinical trial. Lower PIK3CA, PTEN, and HRAS mutations were found in homologous recombination deficiency (HRD)-high (HRD score ≥ 42) tumors with higher pCR rates. When HRD-high tumors were stratified by tumor BRCA mutation status, the pCR rates in BRCA2-mutated tumors were higher (83% vs. 36%). Transcriptomic profiling of TP53-positive tumors identified downregulation of FGFR2 (false discovery rate p value = 2.07e-7), which was also the only common gene between HRD-high and -low tumors with pCR/quasi-pCR treated with paclitaxel and eribulin combined with carboplatin, respectively. Differential enrichment analysis of the HRD-high group posttreatment tumors revealed significant correlation (p = 0.006) of the glycan degradation pathway. FGFR2 expression and the differentially enriched pathways play a role in the response and resistance to MTIs containing carboplatin treatment in TNBC patients.

Indexed as

Gene Expression ProfilingMutationNeoadjuvant TherapyPaclitaxelTriple Negative Breast NeoplasmsAdultAgedAntineoplastic Combined Chemotherapy ProtocolsBRCA2 ProteinCarboplatinClass I Phosphatidylinositol 3-KinasesFemaleFuransGene Expression Regulation, NeoplasticGenomicsHumansBRCA2 ProteinBRCA2 protein, humanCarboplatinClass I Phosphatidylinositol 3-KinaseseribulinFuransHRAS protein, humanKetonesPaclitaxelPIK3CA protein, humanPolyether PolyketidesProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Protein p53eribulinFGFR2HRDmicrotubule inhibitortriple negative breast cancer

Identifiers

PMID39375938
PMCPMC11611771

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.