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Identification of frequent somatic mutations in inflammatory breast cancer

  • Clinical Trial
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Abstract

Purpose

Inflammatory breast cancer is an aggressive form of breast cancer that shows distinct clinical features from non-inflammatory breast cancer. Genomic understanding of inflammatory breast cancer will shed light on biological targets for this disease. Our objective was to identify targeted hotspot mutations using multiplex genome sequencing in inflammatory breast cancer and compare the findings with those for patients with non-inflammatory breast cancer to further recognize novel targets.

Methods

We studied 400 patients with metastatic breast cancer who had somatic hotspot mutation testing using a 46- or 50-gene multiplex platform from March 2012 to December 2014. Among this population, 24 patients had inflammatory breast cancer and 376 patients had non-inflammatory breast cancer. We tested a total of 26 samples from 24 patients with inflammatory breast cancer.

Results

The average number of mutations per patient was higher in inflammatory breast cancer than in non-inflammatory breast cancer (1.23 vs. 0.65, respectively). Identified somatic mutations in inflammatory breast cancer were TP53 (n = 18, 75%), PIK3CA (n = 10, 41.7%), and ERBB2 (n = 4, 16.7%). TP53 and ERBB2 mutations were significantly more prevalent in inflammatory breast cancer than in non-inflammatory breast cancer (P < 0.01). All patients with ERBB2 mutations had hormone receptor (HR)+ primary tumors.

Conclusions

TP53, PIK3CA, and ERBB2 were detected as three major somatic mutations in metastatic inflammatory breast cancer patients. While the inflammatory breast cancer TP53 and PIK3CA mutations mirrored previously reported data for metastatic non-inflammatory breast cancer, this is the first report of higher frequency of ERBB2 mutation in inflammatory breast cancer, especially in the HR+ subtype. Once validated in a larger cohort of inflammatory breast cancer patients, this novel finding could lead to development of treatments for HR+ inflammatory breast cancer.

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Acknowledgements

This work was supported in part by the Morgan Welch Inflammatory Breast Cancer Research Program; Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy; NIH/National Cancer Institute Grants 5T32 CA009599, U01 CA180964, and P30 CA016672 (MD Anderson’s Cancer Center Support Grant); NIH/National Center for Advancing Translational Sciences Grant UL1 TR000371 (Center for Clinical and Translational Sciences); the Nellie B. Connally Breast Cancer Research Endowment; the Bosarge Family Foundation; and a State of Texas Rare and Aggressive Breast Cancer Research Program Grant.

Author Contribution

SCP, Department of Scientific Publications at The University of Texas MD Anderson Cancer Center provided scientific editing services. Ms. Patterson was compensated for her contributions.

Role of the Funder/Sponsor

The Morgan Welch Inflammatory Breast Cancer Research Program and the State of Texas Rare and Aggressive Breast Cancer Research Program had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

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Authors and Affiliations

  1. Section of Translational Breast Cancer Research, Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Unit 1354, Houston, TX, 77030, USA

    Naoko Matsuda, Bora Lim, Ricardo H. Alvarez, Vicente Valero & Naoto T. Ueno

  2. Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Ying Wang

  3. Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Savitri Krishnamurthy

  4. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Wendy Woodward

  5. Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Anthony Lucci & Funda Meric-Bernstam

  6. Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    James M. Reuben

  7. Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, 1400 Holcombe Blvd., Unit 455, Houston, TX, 77030, USA

    Funda Meric-Bernstam

  8. Morgan Welch Inflammatory Breast Cancer Research Program and Clinic, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Naoko Matsuda, Bora Lim, Savitri Krishnamurthy, Wendy Woodward, Ricardo H. Alvarez, Anthony Lucci, Vicente Valero, James M. Reuben & Naoto T. Ueno

  9. Department of Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA

    Funda Meric-Bernstam

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  1. Naoko Matsuda
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  2. Bora Lim
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  3. Ying Wang
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  4. Savitri Krishnamurthy
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  5. Wendy Woodward
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  6. Ricardo H. Alvarez
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  7. Anthony Lucci
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  8. Vicente Valero
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  9. James M. Reuben
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  10. Funda Meric-Bernstam
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  11. Naoto T. Ueno
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Correspondence to Funda Meric-Bernstam or Naoto T. Ueno.

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Matsuda, N., Lim, B., Wang, Y. et al. Identification of frequent somatic mutations in inflammatory breast cancer. Breast Cancer Res Treat 163, 263–272 (2017). https://doi.org/10.1007/s10549-017-4165-0

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