Comparative Effectiveness of an mTOR‐Based Systemic Therapy Regimen in Advanced, Metaplastic and Nonmetaplastic Triple‐Negative Breast Cancer
Background Triple‐negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different “targetable” molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR...
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| Published in | The oncologist (Dayton, Ohio) Vol. 23; no. 11; pp. 1300 - 1309 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.11.2018
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1083-7159 1549-490X 1549-490X |
| DOI | 10.1634/theoncologist.2017-0498 |
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| Abstract | Background
Triple‐negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different “targetable” molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR‐based chemotherapy regimen in MpBC. To determine if tumor subtype influences prognosis, we compared treatment outcomes of patients with MpBC with those of patients with nonmetaplastic TNBC receiving an mTOR‐based systemic therapy regimen.
Patients and Methods
Patients with advanced MpBC and nonmetaplastic TNBC were treated at our institution from April 16, 2009, through November 4, 2014, using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab (DAT/DAE). Median progression‐free survival (PFS) and overall survival (OS) were estimated by the Kaplan‐Meier method. Cox regression analyses were used to evaluate associations between tumor histology and outcomes. Multivariable models were adjusted for all covariates.
Results
Fourteen patients with nonmetaplastic TNBC and 59 patients with advanced MpBC were treated with DAT/DAE. MpBC patients were older (p = .002) and less likely to have a history of bevacizumab use (p = .023). Median PFS for the nonmetaplastic TNBC and MpBC patients was 2.5 months and 4.8 months, respectively. This difference in PFS was statistically significant on univariable (p = .006) but not multivariable analysis (p = .087). Median OS for the nonmetaplastic TNBC and MpBC patients was 3.7 months and 10.0 months, respectively (p = .0003). MpBC remained significantly associated with improved OS on multivariable analysis (p < .0001).
Conclusion
In our study, DAT/DAE appeared to be more effective in MpBC compared with nonmetaplastic TNBC. These data support patient selection for targeted therapy in TNBC.
Implications for Practice
Metaplastic breast cancers (MpBCs) represent <1% of all breast cancers, demonstrate mesenchymal differentiation, and are typically resistant to chemotherapy. Patients with advanced MpBC treated with an mTOR‐based systemic therapy regimen had better long‐term outcomes compared with patients with nonmetaplastic triple‐negative breast cancer treated with the same regimen, suggesting that metaplastic histology may predict benefit from agents targeting the PI3K/Akt/mTOR pathway.
摘要
背景。三阴性乳腺癌 (TNBC) 是一种异质性疾病,其亚型具有不同的“可靶向”分子畸变。化生性乳腺癌 (MpBC) 通常是 TNBC,并且 PI3K/Akt/mTOR 通路通常发生改变。我们之前报告了基于 mTOR 的化疗方案对 MpBC 的效果。为了确定肿瘤亚型是否影响预后,我们比较了 MpBC 患者与接受基于 mTOR 的系统治疗方案的非化生性 TNBC 患者的治疗效果。
患者和方法。2009 年 4 月 16 日至 2014 年 11 月 4 日,我们机构采用 mTOR 抑制剂(替西罗莫司或依维莫司)搭配脂质体多柔比星和贝伐珠单抗 (DAT/DAE) 对晚期 MpBC 和非化生性 TNBC 患者进行治疗。我们通过 Kaplan‐Meier 法估算了患者的中位无进展生存期 (PFS) 和总生存期 (OS)。我们采用 Cox 回归分析评估了肿瘤组织学与预
后之间的关系 并针对所有协变量调整了多变量模型。结果。14名非化生性 TNBC 患者与 59 名晚期 MpBC 患者接受了 DAT/DAE 的治疗。MpBC 患者年龄较大 (p = 0.002)和贝伐珠单抗使用史的较少 (p = 0.023)。非化生性 TNBC 和 MpBC 患者的中位 PFS 分别为 2.5 个月和 4.8 个月。PFS 的这种差异在单变量分析中具有统计学意义 (p = 0.006),但在多变量分析则不具有统计学意义 (p = 0.087)。非化生性 TNBC 患者和 MpBC 患者的中位 OS 分别为 3.7 个月和 10.0 个月 (p = 0.000 3)。在多变量分析 (p < 0.0001) 中,MpBC 始终与 OS 的改善关系密切。
结论。我们的研究显示,DAT/DAE 对 MpBC 的效果优于对非化生性 TNBC 的效果。这些数据可帮助 TNBC 患者选择靶向治疗方案。
对临床实践的提示: 化生性乳腺癌 (MpBC) 占所有乳腺癌的比例 <1%,表现出间质分化,并且通常对化疗具有耐药性。采用基于 mTOR 系统治疗方案的晚期 MpBC 患者的长期预后效果优于采用相同治疗方案的非化生三阴性乳腺癌患者的长期预后效果,表明化生组织可能预测针对 PI3K/Akt/mTOR通路的制剂的疗效
This article reports the results of a post hoc analysis of a clinical trial, comparing outcomes of 14 patients with advanced nonmetaplastic triple‐negative breast cancer and 59 patients with advanced metaplastic triple‐negative breast cancer treated with targeted therapy using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab. |
|---|---|
| AbstractList | Background
Triple‐negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different “targetable” molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR‐based chemotherapy regimen in MpBC. To determine if tumor subtype influences prognosis, we compared treatment outcomes of patients with MpBC with those of patients with nonmetaplastic TNBC receiving an mTOR‐based systemic therapy regimen.
Patients and Methods
Patients with advanced MpBC and nonmetaplastic TNBC were treated at our institution from April 16, 2009, through November 4, 2014, using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab (DAT/DAE). Median progression‐free survival (PFS) and overall survival (OS) were estimated by the Kaplan‐Meier method. Cox regression analyses were used to evaluate associations between tumor histology and outcomes. Multivariable models were adjusted for all covariates.
Results
Fourteen patients with nonmetaplastic TNBC and 59 patients with advanced MpBC were treated with DAT/DAE. MpBC patients were older (p = .002) and less likely to have a history of bevacizumab use (p = .023). Median PFS for the nonmetaplastic TNBC and MpBC patients was 2.5 months and 4.8 months, respectively. This difference in PFS was statistically significant on univariable (p = .006) but not multivariable analysis (p = .087). Median OS for the nonmetaplastic TNBC and MpBC patients was 3.7 months and 10.0 months, respectively (p = .0003). MpBC remained significantly associated with improved OS on multivariable analysis (p < .0001).
Conclusion
In our study, DAT/DAE appeared to be more effective in MpBC compared with nonmetaplastic TNBC. These data support patient selection for targeted therapy in TNBC.
Implications for Practice
Metaplastic breast cancers (MpBCs) represent <1% of all breast cancers, demonstrate mesenchymal differentiation, and are typically resistant to chemotherapy. Patients with advanced MpBC treated with an mTOR‐based systemic therapy regimen had better long‐term outcomes compared with patients with nonmetaplastic triple‐negative breast cancer treated with the same regimen, suggesting that metaplastic histology may predict benefit from agents targeting the PI3K/Akt/mTOR pathway.
摘要
背景。三阴性乳腺癌 (TNBC) 是一种异质性疾病,其亚型具有不同的“可靶向”分子畸变。化生性乳腺癌 (MpBC) 通常是 TNBC,并且 PI3K/Akt/mTOR 通路通常发生改变。我们之前报告了基于 mTOR 的化疗方案对 MpBC 的效果。为了确定肿瘤亚型是否影响预后,我们比较了 MpBC 患者与接受基于 mTOR 的系统治疗方案的非化生性 TNBC 患者的治疗效果。
患者和方法。2009 年 4 月 16 日至 2014 年 11 月 4 日,我们机构采用 mTOR 抑制剂(替西罗莫司或依维莫司)搭配脂质体多柔比星和贝伐珠单抗 (DAT/DAE) 对晚期 MpBC 和非化生性 TNBC 患者进行治疗。我们通过 Kaplan‐Meier 法估算了患者的中位无进展生存期 (PFS) 和总生存期 (OS)。我们采用 Cox 回归分析评估了肿瘤组织学与预
后之间的关系 并针对所有协变量调整了多变量模型。结果。14名非化生性 TNBC 患者与 59 名晚期 MpBC 患者接受了 DAT/DAE 的治疗。MpBC 患者年龄较大 (p = 0.002)和贝伐珠单抗使用史的较少 (p = 0.023)。非化生性 TNBC 和 MpBC 患者的中位 PFS 分别为 2.5 个月和 4.8 个月。PFS 的这种差异在单变量分析中具有统计学意义 (p = 0.006),但在多变量分析则不具有统计学意义 (p = 0.087)。非化生性 TNBC 患者和 MpBC 患者的中位 OS 分别为 3.7 个月和 10.0 个月 (p = 0.000 3)。在多变量分析 (p < 0.0001) 中,MpBC 始终与 OS 的改善关系密切。
结论。我们的研究显示,DAT/DAE 对 MpBC 的效果优于对非化生性 TNBC 的效果。这些数据可帮助 TNBC 患者选择靶向治疗方案。
对临床实践的提示: 化生性乳腺癌 (MpBC) 占所有乳腺癌的比例 <1%,表现出间质分化,并且通常对化疗具有耐药性。采用基于 mTOR 系统治疗方案的晚期 MpBC 患者的长期预后效果优于采用相同治疗方案的非化生三阴性乳腺癌患者的长期预后效果,表明化生组织可能预测针对 PI3K/Akt/mTOR通路的制剂的疗效
This article reports the results of a post hoc analysis of a clinical trial, comparing outcomes of 14 patients with advanced nonmetaplastic triple‐negative breast cancer and 59 patients with advanced metaplastic triple‐negative breast cancer treated with targeted therapy using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab. This article reports the results of a post hoc analysis of a clinical trial, comparing outcomes of 14 patients with advanced nonmetaplastic triple‐negative breast cancer and 59 patients with advanced metaplastic triple‐negative breast cancer treated with targeted therapy using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab. Triple-negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different "targetable" molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR-based chemotherapy regimen in MpBC. To determine if tumor subtype influences prognosis, we compared treatment outcomes of patients with MpBC with those of patients with nonmetaplastic TNBC receiving an mTOR-based systemic therapy regimen.BACKGROUNDTriple-negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different "targetable" molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR-based chemotherapy regimen in MpBC. To determine if tumor subtype influences prognosis, we compared treatment outcomes of patients with MpBC with those of patients with nonmetaplastic TNBC receiving an mTOR-based systemic therapy regimen.Patients with advanced MpBC and nonmetaplastic TNBC were treated at our institution from April 16, 2009, through November 4, 2014, using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab (DAT/DAE). Median progression-free survival (PFS) and overall survival (OS) were estimated by the Kaplan-Meier method. Cox regression analyses were used to evaluate associations between tumor histology and outcomes. Multivariable models were adjusted for all covariates.PATIENTS AND METHODSPatients with advanced MpBC and nonmetaplastic TNBC were treated at our institution from April 16, 2009, through November 4, 2014, using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab (DAT/DAE). Median progression-free survival (PFS) and overall survival (OS) were estimated by the Kaplan-Meier method. Cox regression analyses were used to evaluate associations between tumor histology and outcomes. Multivariable models were adjusted for all covariates.Fourteen patients with nonmetaplastic TNBC and 59 patients with advanced MpBC were treated with DAT/DAE. MpBC patients were older (p = .002) and less likely to have a history of bevacizumab use (p = .023). Median PFS for the nonmetaplastic TNBC and MpBC patients was 2.5 months and 4.8 months, respectively. This difference in PFS was statistically significant on univariable (p = .006) but not multivariable analysis (p = .087). Median OS for the nonmetaplastic TNBC and MpBC patients was 3.7 months and 10.0 months, respectively (p = .0003). MpBC remained significantly associated with improved OS on multivariable analysis (p < .0001).RESULTSFourteen patients with nonmetaplastic TNBC and 59 patients with advanced MpBC were treated with DAT/DAE. MpBC patients were older (p = .002) and less likely to have a history of bevacizumab use (p = .023). Median PFS for the nonmetaplastic TNBC and MpBC patients was 2.5 months and 4.8 months, respectively. This difference in PFS was statistically significant on univariable (p = .006) but not multivariable analysis (p = .087). Median OS for the nonmetaplastic TNBC and MpBC patients was 3.7 months and 10.0 months, respectively (p = .0003). MpBC remained significantly associated with improved OS on multivariable analysis (p < .0001).In our study, DAT/DAE appeared to be more effective in MpBC compared with nonmetaplastic TNBC. These data support patient selection for targeted therapy in TNBC.CONCLUSIONIn our study, DAT/DAE appeared to be more effective in MpBC compared with nonmetaplastic TNBC. These data support patient selection for targeted therapy in TNBC.Metaplastic breast cancers (MpBCs) represent <1% of all breast cancers, demonstrate mesenchymal differentiation, and are typically resistant to chemotherapy. Patients with advanced MpBC treated with an mTOR-based systemic therapy regimen had better long-term outcomes compared with patients with nonmetaplastic triple-negative breast cancer treated with the same regimen, suggesting that metaplastic histology may predict benefit from agents targeting the PI3K/Akt/mTOR pathway.IMPLICATIONS FOR PRACTICEMetaplastic breast cancers (MpBCs) represent <1% of all breast cancers, demonstrate mesenchymal differentiation, and are typically resistant to chemotherapy. Patients with advanced MpBC treated with an mTOR-based systemic therapy regimen had better long-term outcomes compared with patients with nonmetaplastic triple-negative breast cancer treated with the same regimen, suggesting that metaplastic histology may predict benefit from agents targeting the PI3K/Akt/mTOR pathway. Triple-negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different "targetable" molecular aberrations. Metaplastic breast cancers (MpBCs) are typically TNBCs and commonly have alterations in the PI3K/Akt/mTOR pathway. We previously reported efficacy for an mTOR-based chemotherapy regimen in MpBC. To determine if tumor subtype influences prognosis, we compared treatment outcomes of patients with MpBC with those of patients with nonmetaplastic TNBC receiving an mTOR-based systemic therapy regimen. Patients with advanced MpBC and nonmetaplastic TNBC were treated at our institution from April 16, 2009, through November 4, 2014, using mTOR inhibition (temsirolimus or everolimus) with liposomal doxorubicin and bevacizumab (DAT/DAE). Median progression-free survival (PFS) and overall survival (OS) were estimated by the Kaplan-Meier method. Cox regression analyses were used to evaluate associations between tumor histology and outcomes. Multivariable models were adjusted for all covariates. Fourteen patients with nonmetaplastic TNBC and 59 patients with advanced MpBC were treated with DAT/DAE. MpBC patients were older ( = .002) and less likely to have a history of bevacizumab use ( = .023). Median PFS for the nonmetaplastic TNBC and MpBC patients was 2.5 months and 4.8 months, respectively. This difference in PFS was statistically significant on univariable ( = .006) but not multivariable analysis ( = .087). Median OS for the nonmetaplastic TNBC and MpBC patients was 3.7 months and 10.0 months, respectively ( = .0003). MpBC remained significantly associated with improved OS on multivariable analysis ( < .0001). In our study, DAT/DAE appeared to be more effective in MpBC compared with nonmetaplastic TNBC. These data support patient selection for targeted therapy in TNBC. Metaplastic breast cancers (MpBCs) represent <1% of all breast cancers, demonstrate mesenchymal differentiation, and are typically resistant to chemotherapy. Patients with advanced MpBC treated with an mTOR-based systemic therapy regimen had better long-term outcomes compared with patients with nonmetaplastic triple-negative breast cancer treated with the same regimen, suggesting that metaplastic histology may predict benefit from agents targeting the PI3K/Akt/mTOR pathway. |
| Author | Murthy, Rashmi K. Hong, David Moulder, Stacy L. Helgason, Thorunn Meric‐Bernstam, Funda Yam, Clinton Litton, Jennifer K. Kurzrock, Razelle Hortobagyi, Gabriel N. Valero, Vicente Gilcrease, Michael Janku, Filip Chavez‐MacGregor, Mariana Albarracin, Constance Karp, Daniel D. Basho, Reva K. Hess, Kenneth R. |
| Author_xml | – sequence: 1 givenname: Reva K. surname: Basho fullname: Basho, Reva K. organization: Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center – sequence: 2 givenname: Clinton surname: Yam fullname: Yam, Clinton organization: Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center – sequence: 3 givenname: Michael surname: Gilcrease fullname: Gilcrease, Michael organization: Department of Pathology, The University of Texas MD Anderson Cancer Center – sequence: 4 givenname: Rashmi K. surname: Murthy fullname: Murthy, Rashmi K. organization: Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center – sequence: 5 givenname: Thorunn surname: Helgason fullname: Helgason, Thorunn organization: Department of Investigational Cancer Therapeutics (Phase I Trials Program), The University of Texas MD Anderson Cancer Center – sequence: 6 givenname: Daniel D. surname: Karp fullname: Karp, Daniel D. organization: Department of Investigational Cancer Therapeutics (Phase I Trials Program), The University of Texas MD Anderson Cancer Center – sequence: 7 givenname: Funda surname: Meric‐Bernstam fullname: Meric‐Bernstam, Funda organization: Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy, The University of Texas MD Anderson Cancer Center – sequence: 8 givenname: Kenneth R. surname: Hess fullname: Hess, Kenneth R. organization: Department of Biostatistics, The University of Texas MD Anderson Cancer Center – sequence: 9 givenname: Vicente surname: Valero fullname: Valero, Vicente organization: Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center – sequence: 10 givenname: Constance surname: Albarracin fullname: Albarracin, Constance organization: Department of Pathology, The University of Texas MD Anderson Cancer Center – sequence: 11 givenname: Jennifer K. surname: Litton fullname: Litton, Jennifer K. organization: Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center – sequence: 12 givenname: Mariana surname: Chavez‐MacGregor fullname: Chavez‐MacGregor, Mariana organization: Department of Health Services Research, The University of Texas MD Anderson Cancer Center – sequence: 13 givenname: David surname: Hong fullname: Hong, David organization: Department of Investigational Cancer Therapeutics (Phase I Trials Program), The University of Texas MD Anderson Cancer Center – sequence: 14 givenname: Razelle surname: Kurzrock fullname: Kurzrock, Razelle organization: Division of Hematology and Oncology, The University of California San Diego Moores Cancer Center – sequence: 15 givenname: Gabriel N. surname: Hortobagyi fullname: Hortobagyi, Gabriel N. organization: Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center – sequence: 16 givenname: Filip orcidid: 0000-0002-8123-4065 surname: Janku fullname: Janku, Filip organization: Department of Investigational Cancer Therapeutics (Phase I Trials Program), The University of Texas MD Anderson Cancer Center – sequence: 17 givenname: Stacy L. surname: Moulder fullname: Moulder, Stacy L. email: smoulder@mdanderson.org organization: Department of Investigational Cancer Therapeutics (Phase I Trials Program), The University of Texas MD Anderson Cancer Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30139837$$D View this record in MEDLINE/PubMed |
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| Issue | 11 |
| Keywords | Triple‐negative breast cancer mTOR inhibitor Metaplastic breast cancer Mesenchymal |
| Language | English |
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| Notes | . Disclosures of potential conflicts of interest may be found at the end of this article Contributed equally ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Disclosures of potential conflicts of interest may be found at the end of this article. |
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| PublicationDate | November 2018 |
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Triple‐negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different “targetable” molecular aberrations. Metaplastic... Triple-negative breast cancer (TNBC) is a heterogeneous disease with subtypes having different "targetable" molecular aberrations. Metaplastic breast cancers... This article reports the results of a post hoc analysis of a clinical trial, comparing outcomes of 14 patients with advanced nonmetaplastic triple‐negative... |
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| SubjectTerms | Breast Cancer Mesenchymal Metaplastic breast cancer mTOR inhibitor Triple‐negative breast cancer |
| Title | Comparative Effectiveness of an mTOR‐Based Systemic Therapy Regimen in Advanced, Metaplastic and Nonmetaplastic Triple‐Negative Breast Cancer |
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