A comparison of PAM50 intrinsic subtyping with immunohistochemistry and clinical prognostic factors in tamoxifen-treated estrogen receptor-positive breast cancer
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Nielsen, Torsten O, et al. A Comparison of Pam50 Intrinsic Subtyping with Immunohistochemistry and Clinical Prognostic Factors In Tamoxifen-treated Estrogen Receptor-positive Breast Cancer. 2010. https://doi.org/10.17615/fc4v-bc57APA
Nielsen, T., Parker, J., Leung, S., Voduc, D., Ebbert, M., Vickery, T., Davies, S., Snider, J., Stijleman, I., Reed, J., Cheang, M., Mardis, E., Perou, C., Bernard, P., & Ellis, M. (2010). A comparison of PAM50 intrinsic subtyping with immunohistochemistry and clinical prognostic factors in tamoxifen-treated estrogen receptor-positive breast cancer. https://doi.org/10.17615/fc4v-bc57Chicago
Nielsen, Torsten O., Joel Parker, Samuel Leung, David Voduc, Mark Ebbert, Tammi Vickery, Sherri R Davies et al. 2010. A Comparison of Pam50 Intrinsic Subtyping with Immunohistochemistry and Clinical Prognostic Factors In Tamoxifen-Treated Estrogen Receptor-Positive Breast Cancer. https://doi.org/10.17615/fc4v-bc57- Creator
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Nielsen, Torsten O.
- Other Affiliation: Genetic Pathology Evaluation Centre, Vancouver Coastal Health Research Institute, British Columbia Cancer Agency, and University of British Columbia, Vancouver, British Columbia, Canada
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Parker, Joel
- Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
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Leung, Samuel
- Other Affiliation: Genetic Pathology Evaluation Centre, Vancouver Coastal Health Research Institute, British Columbia Cancer Agency, and University of British Columbia, Vancouver, British Columbia, Canada
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Voduc, David
- Other Affiliation: Genetic Pathology Evaluation Centre, Vancouver Coastal Health Research Institute, British Columbia Cancer Agency, and University of British Columbia, Vancouver, British Columbia, Canada
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Ebbert, Mark
- Other Affiliation: Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah
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Vickery, Tammi
- Other Affiliation: Department of Genetics, The Genome Center, Washington University School of Medicine, St Louis, Missouri
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Davies, Sherri R.
- Other Affiliation: Department of Medicine, Division of Oncology, Washington University School of Medicine, St Louis, Missouri
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Snider, Jacqueline
- Other Affiliation: Department of Medicine, Division of Oncology, Washington University School of Medicine, St Louis, Missouri
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Stijleman, Inge J.
- Other Affiliation: Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah
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Reed, Jerry
- Other Affiliation: Department of Genetics, The Genome Center, Washington University School of Medicine, St Louis, Missouri
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Cheang, Maggie C.U.
- Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
- Other Affiliation: Genetic Pathology Evaluation Centre, Vancouver Coastal Health Research Institute, British Columbia Cancer Agency, and University of British Columbia, Vancouver, British Columbia, Canada
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Mardis, Elaine R.
- Other Affiliation: Department of Genetics, The Genome Center, Washington University School of Medicine, St Louis, Missouri; Siteman Comprehensive Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital, St Louis, Missouri
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Perou, Charles
- ORCID: https://orcid.org/0000-0001-9827-2247
- Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
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Bernard, Philip S.
- Other Affiliation: Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah
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Ellis, Matthew J.
- Other Affiliation: Department of Medicine, Division of Oncology, Washington University School of Medicine, St Louis, Missouri; Siteman Comprehensive Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital, St Louis, Missouri
- Abstract
- Purpose: To compare clinical, immunohistochemical (IHC), and gene expression models of prognosis applicable to formalin-fixed, paraffin-embedded blocks in a large series of estrogen receptor (ER)–positive breast cancers from patients uniformly treated with adjuvant tamoxifen. Experimental Design: Quantitative real-time reverse transcription-PCR (qRT-PCR) assays for 50 genes identifying intrinsic breast cancer subtypes were completed on 786 specimens linked to clinical (median follow-up, 11.7 years) and IHC [ER, progesterone receptor (PR), HER2, and Ki67] data. Performance of predefined intrinsic subtype and risk-of-relapse scores was assessed using multivariable Cox models and Kaplan-Meier analysis. Harrell's C-index was used to compare fixed models trained in independent data sets, including proliferation signatures. Results: Despite clinical ER positivity, 10% of cases were assigned to nonluminal subtypes. qRT-PCR signatures for proliferation genes gave more prognostic information than clinical assays for hormone receptors or Ki67. In Cox models incorporating standard prognostic variables, hazard ratios for breast cancer disease-specific survival over the first 5 years of follow-up, relative to the most common luminal A subtype, are 1.99 [95% confidence interval (CI), 1.09-3.64] for luminal B, 3.65 (95% CI, 1.64-8.16) for HER2-enriched subtype, and 17.71 (95% CI, 1.71-183.33) for the basal-like subtype. For node-negative disease, PAM50 qRT-PCR–based risk assignment weighted for tumor size and proliferation identifies a group with >95% 10-year survival without chemotherapy. In node-positive disease, PAM50-based prognostic models were also superior. Conclusion: The PAM50 gene expression test for intrinsic biological subtype can be applied to large series of formalin-fixed, paraffin-embedded breast cancers, and gives more prognostic information than clinical factors and IHC using standard cut points.
- Date of publication
- 2010
- DOI
- Identifier
- 2-s2.0-78049453780
- https://doi.org/10.1158/1078-0432.CCR-10-1282
- Related resource URL
- Resource type
- Article
- Rights statement
- In Copyright
- Journal title
- Clinical Cancer Research
- Journal volume
- 16
- Journal issue
- 21
- Page start
- 5222
- Page end
- 5232
- Language
- English
- Version
- Postprint
- ISSN
- 1078-0432
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