PMID- 36996051
OWN - NLM
STAT- MEDLINE
DCOM- 20230404
LR  - 20230417
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 18
IP  - 3
DP  - 2023
TI  - GATA-3 expression in breast cancer is related to intratumoral M2 macrophage 
      infiltration and tumor differentiation.
PG  - e0283003
LID - 10.1371/journal.pone.0283003 [doi]
LID - e0283003
AB  - Accumulating evidence indicates that tumor-associated macrophages promote tumor 
      progression and that high macrophage infiltration is correlated with advanced 
      tumor stages and poor prognosis in breast cancer. GATA binding protein 3 (GATA-3) 
      is a differentiation marker related to differentiated states in breast cancer. In 
      this study, we explore how the extent of MI relates to GATA-3 expression, 
      hormonal status, and the differentiation grade of breast cancer. To examine 
      breast cancer in early development, we selected 83 patients that were treated 
      with radical breast-conserving surgery (R0), without lymph node metastases (N0) 
      or distant metastases (M0), with and without postoperative radiotherapy. 
      Immunostaining of M2-macrophage-specific antigen CD163 was used to detect 
      tumor-associated macrophages, and macrophage infiltration was estimated 
      semi-quantitatively into no/low, moderate, and high infiltration. The macrophage 
      infiltration was compared to GATA-3, estrogen receptor (ER), progesterone 
      receptor (PR), human epidermal growth factor receptor 2 (HER-2), and Ki-67 
      expression in cancer cells. GATA-3 expression is associated with ER and PR 
      expression but inversely correlated to macrophage infiltration and Nottingham 
      histologic grade. High macrophage infiltration in advanced tumor grade was 
      associated with low GATA-3 expression. The disease-free survival is inversely 
      related to Nottingham histologic grade in patients having tumors with no/low 
      macrophage infiltration, a difference that is not found in patients with 
      moderate/high macrophage infiltration. These findings indicate that macrophage 
      infiltration might impact the differentiation, malignant behavior, and prognosis 
      of breast cancer, regardless of the morphological and hormonal states of the 
      cancer cells in the primary tumor.
CI  - Copyright: (c) 2023 Oda et al. This is an open access article distributed under the 
      terms of the Creative Commons Attribution License, which permits unrestricted 
      use, distribution, and reproduction in any medium, provided the original author 
      and source are credited.
FAU - Oda, Husam
AU  - Oda H
AD  - Institution of Medical Biosciences, Clinical Pathology, Umea University, Umea, 
      Sweden.
FAU - Hedayati, Elham
AU  - Hedayati E
AD  - Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
AD  - Department of Breast, Endocrine Tumors, and Sarcoma, Karolinska University 
      Hospital, Stockholm, Sweden.
FAU - Lindstrom, Annelie
AU  - Lindstrom A
AUID- ORCID: 0000-0003-2130-5375
AD  - Division of Cell Biology, Department of Biomedical and Clinical Sciences, Faculty 
      of Medicine and Health Sciences, Linkoping University, Linkoping, Sweden.
FAU - Shabo, Ivan
AU  - Shabo I
AUID- ORCID: 0000-0002-9866-4192
AD  - Department of Breast, Endocrine Tumors, and Sarcoma, Karolinska University 
      Hospital, Stockholm, Sweden.
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden.
LA  - eng
PT  - Journal Article
DEP - 20230330
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Biomarkers, Tumor)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
RN  - 0 (Receptors, Progesterone)
RN  - 0 (GATA3 protein, human)
SB  - IM
MH  - Female
MH  - Humans
MH  - Biomarkers, Tumor/metabolism
MH  - *Breast Neoplasms/pathology
MH  - Cell Differentiation
MH  - Disease-Free Survival
MH  - Macrophages/metabolism
MH  - Prognosis
MH  - Receptor, ErbB-2/metabolism
MH  - Receptors, Progesterone/metabolism
PMC - PMC10062580
COIS- NO authors have competing interests.
EDAT- 2023/03/31 06:00
MHDA- 2023/04/03 06:41
PMCR- 2023/03/30
CRDT- 2023/03/30 13:42
PHST- 2022/11/27 00:00 [received]
PHST- 2023/02/28 00:00 [accepted]
PHST- 2023/04/03 06:41 [medline]
PHST- 2023/03/30 13:42 [entrez]
PHST- 2023/03/31 06:00 [pubmed]
PHST- 2023/03/30 00:00 [pmc-release]
AID - PONE-D-22-32657 [pii]
AID - 10.1371/journal.pone.0283003 [doi]
PST - epublish
SO  - PLoS One. 2023 Mar 30;18(3):e0283003. doi: 10.1371/journal.pone.0283003. 
      eCollection 2023.