Evidence map›Paper›PMID 35462552›Full record

ArticleBMC medicine2022

Immune microenvironment, homologous recombination deficiency, and therapeutic response to neoadjuvant chemotherapy in triple-negative breast cancer: Japan Breast Cancer Research Group (JBCRG)22 TR.

Takayuki Ueno, Shigehisa Kitano, Norikazu Masuda, Daiki Ikarashi, Makiko Yamashita, Tomohiro Chiba, Takayuki Kadoya, Hiroko Bando, Takashi Yamanaka, Shoichiro Ohtani and 11 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in BMC medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

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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

21 authors at 12 institutions in 1 country.

Takayuki UenoBreast Surgical Oncology, The Cancer Institute Hospital of JFCR, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan. takayuki.ueno@jfcr.or.jp.ORCID 0000-0002-9080-9377
Shigehisa KitanoDivision of Cancer Immunotherapy Development, Advanced Medical Development Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Norikazu MasudaDepartment of Breast and Endocrine Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0002-7302-0278
Daiki IkarashiDivision of Cancer Immunotherapy Development, Advanced Medical Development Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Makiko YamashitaDivision of Cancer Immunotherapy Development, Advanced Medical Development Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Tomohiro ChibaDivision of Pathology, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Takayuki KadoyaDepartment of Breast Surgery, Hiroshima University Hospital, Hiroshima University, Hiroshima, Japan.
Hiroko BandoBreast and Endocrine Surgery, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Takashi YamanakaDepartment of Breast and Endocrine Surgery, Kanagawa Cancer Center, Yokohama, Japan.
Shoichiro OhtaniDepartment of Breast Surgery, Hiroshima City Hiroshima Citizens Hospital, Hiroshima, Japan.
Shigenori NagaiDivision of Breast Oncology, Saitama Cancer Center, Saitama, Japan.
Takahiro NakayamaDepartment of Breast and Endocrine Surgery, Osaka International Cancer Institute, Osako, Japan.
Masato TakahashiDepartment of Breast Surgery, NHO Hokkaido Cancer Center, Sapporo, Japan.
Shigehira SajiDepartment of Medical Oncology, Fukushima Medical University Hospital, Fukushima, Japan.
Kenjiro AogiDepartment of Breast Oncology, National Hospital Organization Shikoku Cancer Center, Matsuyama, Ehime, Japan.
Ravi VelagaDepartment of Breast Surgery, Kyoto University Hospital, Kyoto, Japan.
Kosuke KawaguchiDepartment of Breast Surgery, Kyoto University Hospital, Kyoto, Japan.
Satoshi MoritaDepartment of Biomedical Statistics and Bioinformatics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hironori HagaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Shinji OhnoBreast Oncology Center, The Cancer Institute Hospital of JFCR, Tokyo, Japan.
Masakazu ToiDepartment of Breast Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
The Cancer Institute Hospital · JPKyoto University Hospital · JPKyoto University · JPFukushima Medical University Hospital · JPHiroshima City Asa Citizens Hospital · JPHiroshima University Hospital · JPKanagawa Prefectural Hospital Organization · JPNagoya University · JPOsaka International Cancer Institute · JPSaitama Cancer Center · JPShikoku Cancer Center · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTriple-negative breast cancer (TNBC) is a biologically diverse disease, with characteristics such as homologous recombination deficiency (HRD), gene mutation, and immune reactions. Japan Breast Cancer Research Group 22 is a multicenter trial examining TNBC's response to neoadjuvant chemotherapy (NAC) according to the HRD status. This translational research investigated the clinical significance of the immune microenvironment of TNBC in association with HRD, tumor BRCA1/2 (tBRCA1/2) mutation, and response to NAC.

methodsPatients aged below 65 years with high HRD or germline BRCA1/2 (gBRCA1/2) mutation randomly received paclitaxel + carboplatin (group A1) or eribulin + carboplatin (A2), followed by anthracycline. Patients aged below 65 years with low HRD or those aged 65 years or older without gBRCA1/2 mutation randomly received eribulin + cyclophosphamide (B1) or eribulin + capecitabine (B2); nonresponders to the first four cycles of the therapy received anthracycline. A pathological complete response (pCR) was defined as the absence of residual cancer cells in the tissues. Pretreatment biopsy specimens were stained by multiplexed fluorescent immunohistochemistry using antibodies against CD3, CD4, CD8, Foxp3, CD204, and pan-cytokeratin. Immune cells with specific phenotypes were counted per mm

resultsThis study analyzed 66 samples. T1 tumors had a significantly higher density of intratumoral CD8

conclusionsIntratumoral and stromal CD4

trial registrationUMIN000023162.

Indexed as

Triple Negative Breast NeoplasmsAnthracyclinesAntineoplastic Combined Chemotherapy ProtocolsCarboplatinCD8-Positive T-LymphocytesHomologous RecombinationHumansJapanNeoadjuvant TherapyPaclitaxelTumor MicroenvironmentAnthracyclinesCarboplatinPaclitaxelBRCA1/2EribulinHomologous recombination deficiency (HRD)Immune microenvironmentNeoadjuvant chemotherapyPlatinumTriple-negative breast cancer

Identifiers

PMID35462552
PMCPMC9036790
OpenAlexW4224325677

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.