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. 2020 Mar 23;20:244. doi: 10.1186/s12885-020-06724-5

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Molecular subtypes of the PABC, breast cancer other than PABC, PABC developed in women’s first pregnancy and non-first pregnancy. a Molecular subtypes of the PABC, n = 203. b Molecular subtypes of breast cancer other than PABC (non-PABC), n = 43,721. c Molecular subtypes of the PABC developed in women’s first pregnancy (First-Pregnancy subgroup), n = 79. d Molecular subtypes of the PABC not developed in women’s first pregnancy (Non-First-Pregnancy subgroup), n = 124. The P value was less than 0.001, by using Pearson Chi-square tests to compare the distribution of molecular subtypes in PABC patients (a) and non-PABC patients (b), demonstrating a difference. The P value was 0.554, by using Pearson Chi-square tests to compare the distribution of molecular subtypes in First-pregnancy group (c) and Non-first-pregnancy group (d), demonstrating no statistical significance. PABC=Pregnancy-associated breast cancer; ER = Estrogen Receptor; PR = Progesterone Receptor; HER-2 = Human Epidermal Growth Factor Receptor-2, HR (Hormone Receptor) +: Either ER or PR+. Luminal A: ER+, PR+, HER-2 (−), Ki-67 < 14%; Luminal B: HR+, Ki-67 ≥ 14%; HR+, HER-2(+); ER+, PR-; Her-2 overexpression: HR (−), HER-2 (+); TNBC (Triple negative breast cancer): ER (−), PR (−), HER-2 (−)