TY - JOUR
T1 - Comparison of molecular profile in triple-negative inflammatory and non-inflammatory breast cancer not of mesenchymal stem-like subtype
AU - Funakoshi, Yohei
AU - Wang, Ying
AU - Semba, Takashi
AU - Masuda, Hiroko
AU - Hout, David
AU - Ueno, Naoto T.
AU - Wang, Xiaoping
N1 - Funding Information:
This work was supported by National Institutes of Health grant 1R01CA205043-01A1 (Dr. Ueno), Breast Cancer Research Foundation grant BCRF-18-164 (Dr. Ueno), the Morgan Welch Inflammatory Breast Cancer Research Program, a State of Texas Rare and Aggressive Breast Cancer Research Program grant (Dr. Ueno), and National Cancer Institute award P30CA016672, which supports the MD Anderson Cancer Center Clinical Trials Support Resource. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© 2019 Funakoshi 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.
PY - 2019/9/1
Y1 - 2019/9/1
N2 - Background Inflammatory breast cancer (IBC) is an aggressive form of breast cancer. The triple-negative subtype of IBC (TN-IBC) is particularly aggressive. Identification of molecular differences between TN-IBC and TN-non-IBC may help clarify the unique clinical behaviors of TN-IBC. However, our previous study comparing gene expression between TN-IBC and TN-non-IBC did not identify any TN-IBC-specific molecular signature. Lehmann et al recently reported that the mesenchymal stem-like (MSL) TNBC subtype consisted of infiltrating tumor-associated stromal cells but not cancer cells. Therefore, we compared the gene expression profiles between TN-IBC and TN-non-IBC patient samples not of the MSL subtype. Methods We classified 88 TNBC samples from the World IBC Consortium into subtypes according to the Vanderbilt classification and Insight TNBCtype, removed samples of MSL and unstable subtype, and compared gene expression profiles between the remaining TN-IBC and TN-non-IBC samples. Results In the Vanderbilt analysis, we identified 75 genes significantly differentially expressed between TN-IBC and TN-non-IBC at an FDR of 0.2. In the Insight TNBCtype analysis, we identified 81 genes significantly differentially expressed between TN-IBC and TN-non-IBC at an FDR of 0.4. In both analyses, the top canonical pathway was “Fc Receptor-mediated Phagocytosis in Macrophages and Monocytes”, and the top 10 differentially regulated genes included PADI3 and MCTP1, which were up-regulated, and CDC42EP3, SSR1, RSBN1, and ZC3H13, which were downregulated. Conclusions Our data suggest that the activity of macrophages might be enhanced in TN-IBC compared with TN-non-IBC. Further clinical and preclinical studies are needed to determine the crosstalk between macrophages and IBC cells.
AB - Background Inflammatory breast cancer (IBC) is an aggressive form of breast cancer. The triple-negative subtype of IBC (TN-IBC) is particularly aggressive. Identification of molecular differences between TN-IBC and TN-non-IBC may help clarify the unique clinical behaviors of TN-IBC. However, our previous study comparing gene expression between TN-IBC and TN-non-IBC did not identify any TN-IBC-specific molecular signature. Lehmann et al recently reported that the mesenchymal stem-like (MSL) TNBC subtype consisted of infiltrating tumor-associated stromal cells but not cancer cells. Therefore, we compared the gene expression profiles between TN-IBC and TN-non-IBC patient samples not of the MSL subtype. Methods We classified 88 TNBC samples from the World IBC Consortium into subtypes according to the Vanderbilt classification and Insight TNBCtype, removed samples of MSL and unstable subtype, and compared gene expression profiles between the remaining TN-IBC and TN-non-IBC samples. Results In the Vanderbilt analysis, we identified 75 genes significantly differentially expressed between TN-IBC and TN-non-IBC at an FDR of 0.2. In the Insight TNBCtype analysis, we identified 81 genes significantly differentially expressed between TN-IBC and TN-non-IBC at an FDR of 0.4. In both analyses, the top canonical pathway was “Fc Receptor-mediated Phagocytosis in Macrophages and Monocytes”, and the top 10 differentially regulated genes included PADI3 and MCTP1, which were up-regulated, and CDC42EP3, SSR1, RSBN1, and ZC3H13, which were downregulated. Conclusions Our data suggest that the activity of macrophages might be enhanced in TN-IBC compared with TN-non-IBC. Further clinical and preclinical studies are needed to determine the crosstalk between macrophages and IBC cells.
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U2 - 10.1371/journal.pone.0222336
DO - 10.1371/journal.pone.0222336
M3 - Article
C2 - 31532791
AN - SCOPUS:85072320410
SN - 1932-6203
VL - 14
JO - PloS one
JF - PloS one
IS - 9
M1 - e0222336
ER -