Diverse histomorphology of HER2-positive breast carcinomas based on differential ER expression.


Journal

Histopathology
ISSN: 1365-2559
Titre abrégé: Histopathology
Pays: England
ID NLM: 7704136

Informations de publication

Date de publication:
Mar 2020
Historique:
received: 29 03 2019
accepted: 22 09 2019
pubmed: 26 9 2019
medline: 2 12 2020
entrez: 26 9 2019
Statut: ppublish

Résumé

HER2-positive (HER2+) breast carcinoma (BC) cases are often treated similarly; however, they can be classified as either luminal B (LH) or non-luminal type (NLH) BC, which have different prognoses. In this study, we investigated the clinicohistomorphological features of each HER2+ BC subgroup. We classified 166 patients with HER2+ invasive BC into LH (n = 110, 66.3%) and NLH groups (n = 56, 33.7%). We further subclassified LH into patients with carcinomas expressing high levels of hormone receptors [LH-high; Allred score, oestrogen receptor (ER) and/or progesterone receptor (PgR) 4-8, n = 89, 53.6%] or low levels (LH-low; Allred score, ER and/or PgR 2 or 3, n = 21, 12.7%) for clinicohistomorphological characterisation. Morphological review showed that NLH included a percentage of patients with comedo necrosis, while LH patients had significantly more central scarring. In terms of immune responsiveness, NLH showed significantly higher rates of tumour-infiltrating lymphocytes and healing. The LH-high and NLH groups showed distinct characteristics (by both models, P < 0.05) and the LH-low group appeared to demonstrate intermediate characteristics according to multinomial analyses using covariates reflecting tumour morphology and immune response outcomes. These results support the classification of HER2+ BC into two major subgroups, LH-high and NLH, based on tumour morphology and immune response; LH-high proliferates via scirrhous and/or spiculated growth with a central scar, while the primary proliferation pattern of NLH is based on in-situ carcinomas containing comedo necrosis with noticeable TILs and healing.

Identifiants

pubmed: 31554015
doi: 10.1111/his.14003
doi:

Substances chimiques

Biomarkers, Tumor 0
Receptors, Estrogen 0
Receptors, Progesterone 0
ERBB2 protein, human EC 2.7.10.1
Receptor, ErbB-2 EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

560-571

Subventions

Organisme : JSPS KAKENHI
ID : JP17K08707

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Références

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Auteurs

Momoko Akashi (M)

Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Rin Yamaguchi (R)

Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Department of Pathology and Laboratory Medicine, Kurume University Medical Centre, Kurume, Fukuoka, Japan.

Hironori Kusano (H)

Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Hitoshi Obara (H)

Biostatistics Centre, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Miki Yamaguchi (M)

Department of Surgery, Japan Community Healthcare Organization Kurume General Hospital, Kurume, Fukuoka, Japan.

Uhi Toh (U)

Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Jun Akiba (J)

Department of Diagnostic Pathology, Kurume University Hospital, Kurume, Fukuoka, Japan.

Tatsuyuki Kakuma (T)

Biostatistics Centre, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Maki Tanaka (M)

Department of Surgery, Japan Community Healthcare Organization Kurume General Hospital, Kurume, Fukuoka, Japan.

Yoshito Akagi (Y)

Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

Hirohisa Yano (H)

Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan.

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