Evidence map›Paper›PMID 37106324›Full record

ArticleBMC cancer2023

The impact of PIK3CA mutations and PTEN expression on the effect of neoadjuvant therapy for postmenopausal luminal breast cancer patients.

Shouko Hayama, Rikiya Nakamura, Takayuki Ishige, Takafumi Sangai, Masahiro Sakakibara, Hiroshi Fujimoto, Emi Ishigami, Takahito Masuda, Ayako Nakagawa, Ryotaro Teranaka and 5 more

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

Article in BMC cancer, 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
1.7field-weighted citation impact, top 16% 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, 11 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

15 authors at 6 institutions in 1 country.

Shouko HayamaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Rikiya NakamuraDepartment of Breast Surgery, Chiba Cancer Center, 666-2 Nitona, Chuo-Ku, Chiba-Shi, Chiba, 260-8717, Japan.
Takayuki IshigeDepartment of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Takafumi SangaiDepartment of Breast and Thyroid Surgery, Kitasato University School of Medicine, 1-15-1 Kitazato Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan. sangai@med.kitasato-u.ac.jp.
Masahiro SakakibaraDepartments of Breast Surgery, Toho University Sakura Medical Center, 564-1 Shimoshizu, Sakura, Chiba, 285-8741, Japan.
Hiroshi FujimotoDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Emi IshigamiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Takahito MasudaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Ayako NakagawaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Ryotaro TeranakaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Satoshi OtaDepartment of Pathology, Chiba University Hospital, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Sakae ItogaDepartment of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu Chiba, 292-0818, Japan.
Naohito YamamotoDepartment of Breast Surgery, Chiba Cancer Center, 666-2 Nitona, Chuo-Ku, Chiba-Shi, Chiba, 260-8717, Japan.
Takeshi NagashimaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Masayuki OtsukaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8677, Japan.
Chiba University · JPChiba Cancer Center · JPChiba University Hospital · JPKazusa DNA Research Institute · JPKitasato University · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is pressing needs to find the biomarker in the selection of neoadjuvant therapy in postmenopausal luminal breast cancer patients. We examined the hypothesis that PIK3CA mutations and low phosphatase and tensin homolog (PTEN) expression affect the response to neoadjuvant therapy and prognosis in postmenopausal luminal breast cancer patients.

methodsPostmenopausal patients with estrogen receptor-positive, human epidermal growth factor receptor 2-negative breast cancer, up to stage II, who underwent neoadjuvant chemotherapy (NAC; n = 60) or neoadjuvant endocrine therapy (NAE; n = 55) were selected. PIK3CA exon 9 and exon 20 mutations were screened by high resolution melting analysis and confirmed by Sanger sequence. PTEN expression was evaluated by immunohistochemistry. The relationships among PIK3CA mutations, PTEN expression, clinicopathological features, the pathological effect of neoadjuvant therapy, recurrence-free survival (RFS) and overall survival were analyzed.

resultsAmong 115 patients, PIK3CA mutations and low PTEN expression before treatment were detected in 35 patients (30.4%) and in 28 patients (24.3%), respectively. In the NAC group, tumor with PIK3CA mutations showed significantly poorer response than tumor with PIK3CA wild-type (p = 0.03). On the other hand, in the NAE group, there was no significant difference in pathological therapeutic effect between tumor with PIK3CA mutations and tumor with PIK3CA wild-type (p = 0.54). In the NAC group, the log-rank test showed no difference in RFS between patients with PIK3CA mutations and PIK3CA wild-type (p = 0.43), but patients with low PTEN expression showed significantly worse RFS compared to patients with high PTEN expression (5 year RFS 0.64 vs. 0.87, p = 0.01). In the Cox proportional hazards model for RFS, PTEN expression, progesterone receptor, and pathological therapeutic effect were predictive factors for time to recurrence (All p < 0.05).

conclusionsPIK3CA mutations are associated with resistance to NAC but do not affect the response to NAE. Low PTEN expression does not affect response to either NAC or NAE but correlates with shorter RFS in patients who received NAC. These biomarkers will be further evaluated for clinical use to treat postmenopausal luminal breast cancer patients.

Indexed as

Breast NeoplasmsBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesErb-b2 Receptor Tyrosine KinasesFemaleHumansMutationNeoadjuvant TherapyPostmenopausePTEN PhosphohydrolaseBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesErb-b2 Receptor Tyrosine KinasesPIK3CA protein, humanPTEN PhosphohydrolasePTEN protein, humanBreast neoplasmsNeoadjuvant therapyPhosphatidylinositol 3-Kinases/geneticsPrognosisPTEN Phosphohydrolase

Identifiers

PMID37106324
PMCPMC10134571
OpenAlexW4367182783

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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.