Evidence map›Paper›PMID 35103835›Full record

ArticleMedical molecular morphology2022

The role of mineralocorticoids and glucocorticoids under the impact of 11β-hydroxysteroid dehydrogenase in human breast lesions.

Mingzhen Cai, Keely McNamara, Yuto Yamazaki, Narumi Harada, Minoru Miyashita, Hiroshi Tada, Takanori Ishida, Hironobu Sasano

Abstract read
PubMed Publisher
In one paragraph

Article in Medical molecular morphology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

8 authors at 1 institution in 1 country.

Mingzhen CaiDepartment of Breast and Endocrine Surgery, Tohoku University School of Medicine, Sendai, Japan.
Keely McNamaraDepartment of Anatomic Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yuto YamazakiDepartment of Anatomic Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Narumi HaradaDepartment of Breast and Endocrine Surgery, Tohoku University School of Medicine, Sendai, Japan.
Minoru MiyashitaDepartment of Breast and Endocrine Surgery, Tohoku University School of Medicine, Sendai, Japan.
Hiroshi TadaDepartment of Breast and Endocrine Surgery, Tohoku University School of Medicine, Sendai, Japan.
Takanori IshidaDepartment of Breast and Endocrine Surgery, Tohoku University School of Medicine, Sendai, Japan.
Hironobu SasanoDepartment of Anatomic Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan. hsasano@patholo2.med.tohoku.ac.jp.
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We attempted to explore the possible involvement of the in situ availability of mineralocorticoids and mineralocorticoid receptor (MR) in the pathogenesis of mammary ductal carcinoma. We also explored their individual profiles among different subtypes of invasive ductal carcinomas of no special type (IDC-NST) by evaluating the status of MR, Glucocorticoid receptor (GR), and 11β hydroxysteroid dehydrogenase (HSD) 1/2 at each stage of the putative cascade of the mammary ductal proliferative disorders. In this study, IDC-NST, ductal carcinoma in situ (DCIS), atypical ductal hyperplasia (ADH), and non-pathological breast tissues were all evaluated by immunohistochemistry. MR was significantly lower in ADH than in DCIS or IDC-NST. 11βHSD2 was significantly lower in ADH than normal breast tissue and 11βHSD1 was significantly higher in DCIS than normal, ADH, or IDC-NST. MR in progesterone receptor (PR)-positive IDC-NST cases tended to be associated with the Ki-67 labeling index. Results of the present study demonstrated that the status of MR and GR in conjunction with the 11βHSDs was correlated with the development of low-grade proliferative disorders in mammary glands. In addition, the potential crosstalk between MR and PR could also influence cell proliferation of breast carcinoma cells but further investigations are required for clarification.

Indexed as

Breast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, Intraductal, Noninfiltrating11-beta-Hydroxysteroid DehydrogenasesFemaleGlucocorticoidsHumansMineralocorticoids11-beta-Hydroxysteroid DehydrogenasesGlucocorticoidsMineralocorticoids11beta-hydroxysteroid dehydrogenasesBreast cancerBreast lesionGlucocorticoid receptorMineralocorticoid receptor

Identifiers

PMID35103835
OpenAlexW4210478143

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.