Evidence map›Paper›PMID 30806788›Full record

ArticleJournal of cancer research and clinical oncology2019

Co-mutation of TP53 and PIK3CA in residual disease after neoadjuvant chemotherapy is associated with poor survival in breast cancer.

Xinyi Chen, Yonghai Guo, Tao Ouyang, Jinfeng Li, Tianfeng Wang, Zhaoqing Fan, Tie Fan, Benyao Lin, Ye Xu, Yuntao Xie

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  4. ConcomitantJournal of breast cancer · 2023
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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

10 authors at 1 institution in 2 countries.

Xinyi ChenKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Yonghai GuoKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Tao OuyangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Jinfeng LiKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Tianfeng WangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Zhaoqing FanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Tie FanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Benyao LinKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China.
Ye XuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China. xuye@bjmu.edu.cn.
Yuntao XieKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Breast Center, Beijing Cancer Hospital and Institute, Peking University Cancer Hospital, Beijing, 100142, People's Republic of China. zlxyt2@bjmu.edu.cn.ORCID http://orcid.org/0000-0003-1151-8107
Peking University · CN

Funding

973 Project 2013CB911004the Science Foundation of Peking University Cancer Hospital 2017-8
6 · The paper itself

Abstract

purposeThe prevalence and clinical relevance of TP53 and PIK3CA mutations in pretreatment breast cancer have been previously reported. However, little is known regarding these mutations in residual tumor tissues after neoadjuvant chemotherapy. Here, we investigated the association between TP53 and PIK3CA mutations in residual disease and survival of breast cancers.

methodsTP53 and PIK3CA somatic mutations were examined in 353 post-neoadjuvant chemotherapy residual tumor tissues by Sanger sequencing. Survival curves of patients with TP53 and PIK3CA mutations were compared using the Kaplan-Meier method.

resultsFifty-six (15.9%) of the 353 patients carried a TP53 somatic mutation and 79 patients (22.4%) carried a PIK3CA somatic mutation. A total of 18 patients carried co-mutation of TP53 and PIK3CA. Patients with somatic co-mutation were more likely to have high-grade tumors (35.3% vs. 10.6%, P = 0.010), estrogen receptor-negative tumors (55.6% vs. 26.7%, P = 0.009), progesterone receptor-negative tumors (61.1% vs. 30.5%, P = 0.008) and triple-negative tumors (35.3% vs. 13.3%, P = 0.025) compared with non-carriers. More importantly, co-mutation of TP53 and PIK3CA carriers had a significantly worse disease-free survival (DFS) and distant disease-free survival (DDFS) than non-carriers (5-year DFS: 58.0% vs. 83.2%, P < 0.001; 5-year DDFS: 70.3% vs. 86.4%, P = 0.024). Furthermore, in multivariate regression analysis, TP53 and PIK3CA co-mutation carriers showed a significantly worse DFS (adjusted hazard ratio = 3.70; 95% confidence interval, 1.79-7.63; P < 0.001).

conclusionsPatients with somatic co-mutation of TP53 and PIK3CA were associated with unfavorable survival compared with non-carriers. Co-mutation of TP53 and PIK3CA could be used as a potential prognosis marker in post-neoadjuvant chemotherapy breast cancer patients.

Indexed as

MutationAdultAgedAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBreast NeoplasmsChemotherapy, AdjuvantClass I Phosphatidylinositol 3-KinasesFemaleHumansKaplan-Meier EstimateMiddle AgedNeoplasm GradingNeoplasm StagingPrognosisTreatment OutcomeBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humanTumor Suppressor Protein p53Breast cancerPIK3CAPost-neoadjuvant chemotherapySurvivalTP53

Identifiers

PMID30806788
PMCPMC11810230
OpenAlexW2916258951

What OpenQuestion holds

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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.