Ipatasertib plus paclitaxel for PIK3CA/AKT1/PTEN-altered hormone receptor-positive HER2-negative advanced breast cancer: primary results from cohort B of the IPATunity130 randomized phase 3 trial
Purpose PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC). Methods Cohort B of the randomized, double-blind, pl...
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| Vydané v: | Breast Cancer Research and Treatment Ročník 191; číslo 3; s. 565 - 576 |
|---|---|
| Hlavní autori: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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New York
Springer Science and Business Media LLC
01.02.2022
Springer US Springer Springer Nature B.V |
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| ISSN: | 0167-6806, 1573-7217, 1573-7217 |
| On-line prístup: | Získať plný text |
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| Abstract | Purpose
PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC).
Methods
Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative
PIK3CA
/
AKT1/PTEN
-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1–21) or placebo, plus paclitaxel (80 mg/m
2
, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS).
Results
Overall, 146 patients were randomized to ipatasertib–paclitaxel and 76 to placebo–paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71–1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib–paclitaxel versus placebo–paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib–paclitaxel vs 1% with placebo–paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%).
Conclusion
Adding ipatasertib to paclitaxel did not improve efficacy in
PIK3CA/AKT1/PTEN
-altered HR+ HER2-negative aBC. The ipatasertib–paclitaxel safety profile was consistent with each agent’s known adverse effects.
Trial registration
NCT03337724. |
|---|---|
| AbstractList | PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC).
Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1-21) or placebo, plus paclitaxel (80 mg/m
, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS).
Overall, 146 patients were randomized to ipatasertib-paclitaxel and 76 to placebo-paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71-1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib-paclitaxel versus placebo-paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib-paclitaxel vs 1% with placebo-paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%).
Adding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib-paclitaxel safety profile was consistent with each agent's known adverse effects. Trial registration NCT03337724. Purpose PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC). Methods Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA / AKT1/PTEN -altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1–21) or placebo, plus paclitaxel (80 mg/m 2 , days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS). Results Overall, 146 patients were randomized to ipatasertib–paclitaxel and 76 to placebo–paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71–1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib–paclitaxel versus placebo–paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib–paclitaxel vs 1% with placebo–paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%). Conclusion Adding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN -altered HR+ HER2-negative aBC. The ipatasertib–paclitaxel safety profile was consistent with each agent’s known adverse effects. Trial registration NCT03337724. PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC). Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1-21) or placebo, plus paclitaxel (80 mg/m.sup.2, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS). Overall, 146 patients were randomized to ipatasertib-paclitaxel and 76 to placebo-paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71-1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib-paclitaxel versus placebo-paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade [greater than or equal to] 3 adverse events were diarrhea (12% with ipatasertib-paclitaxel vs 1% with placebo-paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%). Adding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib-paclitaxel safety profile was consistent with each agent's known adverse effects. Purpose PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC). Methods Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1-21) or placebo, plus paclitaxel (80 mg/m.sup.2, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS). Results Overall, 146 patients were randomized to ipatasertib-paclitaxel and 76 to placebo-paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71-1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib-paclitaxel versus placebo-paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade [greater than or equal to] 3 adverse events were diarrhea (12% with ipatasertib-paclitaxel vs 1% with placebo-paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%). Conclusion Adding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib-paclitaxel safety profile was consistent with each agent's known adverse effects. Trial registration NCT03337724. PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC).PURPOSEPI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC).Cohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1-21) or placebo, plus paclitaxel (80 mg/m2, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS).METHODSCohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1-21) or placebo, plus paclitaxel (80 mg/m2, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS).Overall, 146 patients were randomized to ipatasertib-paclitaxel and 76 to placebo-paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71-1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib-paclitaxel versus placebo-paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib-paclitaxel vs 1% with placebo-paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%).RESULTSOverall, 146 patients were randomized to ipatasertib-paclitaxel and 76 to placebo-paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71-1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib-paclitaxel versus placebo-paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib-paclitaxel vs 1% with placebo-paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%).Adding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib-paclitaxel safety profile was consistent with each agent's known adverse effects. Trial registration NCT03337724.CONCLUSIONAdding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib-paclitaxel safety profile was consistent with each agent's known adverse effects. Trial registration NCT03337724. PurposePI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel in PI3K pathway-mutant HR+ unresectable locally advanced/metastatic breast cancer (aBC).MethodsCohort B of the randomized, double-blind, placebo-controlled, phase 3 IPATunity130 trial enrolled patients with HR+ HER2-negative PIK3CA/AKT1/PTEN-altered measurable aBC who were considered inappropriate for endocrine-based therapy (demonstrated insensitivity to endocrine therapy or visceral crisis) and were candidates for taxane monotherapy. Patients with prior chemotherapy for aBC or relapse < 1 year since (neo)adjuvant chemotherapy were ineligible. Patients were randomized 2:1 to ipatasertib (400 mg, days 1–21) or placebo, plus paclitaxel (80 mg/m2, days 1, 8, 15), every 28 days until disease progression or unacceptable toxicity. The primary endpoint was investigator-assessed progression-free survival (PFS).ResultsOverall, 146 patients were randomized to ipatasertib–paclitaxel and 76 to placebo–paclitaxel. In both arms, median investigator-assessed PFS was 9.3 months (hazard ratio, 1.00, 95% CI 0.71–1.40) and the objective response rate was 47%. Median paclitaxel duration was 6.9 versus 8.8 months in the ipatasertib–paclitaxel versus placebo–paclitaxel arms, respectively; median ipatasertib/placebo duration was 8.0 versus 9.1 months, respectively. The most common grade ≥ 3 adverse events were diarrhea (12% with ipatasertib–paclitaxel vs 1% with placebo–paclitaxel), neutrophil count decreased (9% vs 7%), neutropenia (8% vs 9%), peripheral neuropathy (7% vs 3%), peripheral sensory neuropathy (3% vs 5%) and hypertension (1% vs 5%).ConclusionAdding ipatasertib to paclitaxel did not improve efficacy in PIK3CA/AKT1/PTEN-altered HR+ HER2-negative aBC. The ipatasertib–paclitaxel safety profile was consistent with each agent’s known adverse effects.Trial registration NCT03337724. |
| Audience | Academic |
| Author | Qinshu Lian Sarah-Jayne Reilly Bruno Kovic Sung-Bae Kim Steven J. Isakoff Mafalda Oliveira Carlos Barrios Matthew J. Wongchenko Rebecca A. Dent Zbigniew Nowecki Shigehira Saji Igor Bondarenko Joyce O’Shaughnessy Aruna Mani Nicholas Turner Heather Hinton |
| Author_xml | – sequence: 1 givenname: Nicholas orcidid: 0000-0001-8937-0873 surname: Turner fullname: Turner, Nicholas email: Nick.Turner@icr.ac.uk organization: Breast Unit, The Royal Marsden NHS Foundation Trust, Breast Cancer Now Research Centre, The Institute of Cancer Research – sequence: 2 givenname: Rebecca A. surname: Dent fullname: Dent, Rebecca A. organization: Division of Medical Oncology, National Cancer Centre Singapore – sequence: 3 givenname: Joyce surname: O’Shaughnessy fullname: O’Shaughnessy, Joyce organization: Department of Medical Oncology, Texas Oncology, Baylor University Medical Center, US Oncology – sequence: 4 givenname: Sung-Bae surname: Kim fullname: Kim, Sung-Bae organization: Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine – sequence: 5 givenname: Steven J. surname: Isakoff fullname: Isakoff, Steven J. organization: Division of Hematology and Oncology, Massachusetts General Hospital – sequence: 6 givenname: Carlos surname: Barrios fullname: Barrios, Carlos organization: Latin American Cooperative Oncology Group, Oncology Research Service, Hospital São Lucas, PUCRS – sequence: 7 givenname: Shigehira surname: Saji fullname: Saji, Shigehira organization: Department of Medical Oncology, Fukushima Medical University Hospital – sequence: 8 givenname: Igor surname: Bondarenko fullname: Bondarenko, Igor organization: Oncology and Medical Radiology Department – sequence: 9 givenname: Zbigniew surname: Nowecki fullname: Nowecki, Zbigniew organization: Oncology Centre, Instytut im. Marii-Sklodowskiej – sequence: 10 givenname: Qinshu surname: Lian fullname: Lian, Qinshu organization: Biostatistics, Genentech, Inc – sequence: 11 givenname: Sarah-Jayne surname: Reilly fullname: Reilly, Sarah-Jayne organization: Pharma Development, Roche Products Ltd – sequence: 12 givenname: Heather surname: Hinton fullname: Hinton, Heather organization: Product Development Safety, F. Hoffmann-La Roche Ltd – sequence: 13 givenname: Matthew J. surname: Wongchenko fullname: Wongchenko, Matthew J. organization: Oncology Biomarker Development, Genentech, Inc – sequence: 14 givenname: Bruno surname: Kovic fullname: Kovic, Bruno organization: Patient-Centered Outcomes Research, Product Development, Hoffmann-La Roche Limited – sequence: 15 givenname: Aruna surname: Mani fullname: Mani, Aruna organization: Product Development Oncology, Genentech, Inc – sequence: 16 givenname: Mafalda surname: Oliveira fullname: Oliveira, Mafalda organization: Medical Oncology Department, Vall d’Hebron University Hospital, Vall d’Hebron Institute of Oncology (VHIO) |
| BackLink | https://cir.nii.ac.jp/crid/1872272492604510976$$DView record in CiNii https://www.ncbi.nlm.nih.gov/pubmed/34860318$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Contributor | Vall d'Hebron Barcelona Hospital Campus [Turner N] Breast Unit, The Royal Marsden NHS Foundation Trust, London SW3 6JJ, UK. Breast Cancer Now Research Centre, The Institute of Cancer Research, London, UK. [Dent RA] Division of Medical Oncology, National Cancer Centre Singapore, Singapore, Singapore. [O'Shaughnessy J] Department of Medical Oncology, Texas Oncology, Baylor University Medical Center, US Oncology, Dallas, TX, USA. [Kim SB] Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. [Isakoff SJ] Division of Hematology and Oncology, Massachusetts General Hospital, Boston, MA, USA. [Barrios C] Latin American Cooperative Oncology Group, Oncology Research Service, Hospital São Lucas, PUCRS, Porto Alegre, RS, Brazil. [Oliveira M] Servei d’Oncologia Mèdica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain Turner, Nicholas Institut Català de la Salut |
| Contributor_xml | – sequence: 1 fullname: Institut Català de la Salut – sequence: 2 fullname: [Turner N] Breast Unit, The Royal Marsden NHS Foundation Trust, London SW3 6JJ, UK. Breast Cancer Now Research Centre, The Institute of Cancer Research, London, UK. [Dent RA] Division of Medical Oncology, National Cancer Centre Singapore, Singapore, Singapore. [O'Shaughnessy J] Department of Medical Oncology, Texas Oncology, Baylor University Medical Center, US Oncology, Dallas, TX, USA. [Kim SB] Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. [Isakoff SJ] Division of Hematology and Oncology, Massachusetts General Hospital, Boston, MA, USA. [Barrios C] Latin American Cooperative Oncology Group, Oncology Research Service, Hospital São Lucas, PUCRS, Porto Alegre, RS, Brazil. [Oliveira M] Servei d’Oncologia Mèdica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain – sequence: 3 fullname: Vall d'Hebron Barcelona Hospital Campus – sequence: 4 fullname: Turner, Nicholas |
| Copyright | The Author(s) 2021 2021. The Author(s). COPYRIGHT 2022 Springer The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: The Author(s) 2021 – notice: 2021. The Author(s). – notice: COPYRIGHT 2022 Springer – notice: The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1007/s10549-021-06450-x |
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| Keywords | HER2 negative Ipatasertib First-line Hormone receptor positive PI3K/AKT |
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| License | 2021. The Author(s). 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/. |
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| PublicationTitle | Breast Cancer Research and Treatment |
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PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel... PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel in PI3K... Purpose PI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib-paclitaxel... PurposePI3K/AKT pathway alterations are frequent in hormone receptor-positive (HR+) breast cancers. IPATunity130 Cohort B investigated ipatasertib–paclitaxel... |
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| SubjectTerms | 1-Phosphatidylinositol 3-kinase AKT protein AKT1 protein Analysis Antineoplastic Combined Chemotherapy Protocols Antineoplastic Combined Chemotherapy Protocols - adverse effects Breast cancer Breast Neoplasms Breast Neoplasms - drug therapy Breast Neoplasms - genetics Cancer research Care and treatment Chemotherapy Class I Phosphatidylinositol 3-Kinases Class I Phosphatidylinositol 3-Kinases - genetics Clinical Trial Clinical trials Diarrhea Double-Blind Method Endocrine therapy ErbB-2 protein Female First-line HER2 negative Hormone receptor positive Hormones Humans Ipatasertib Leukocytes (neutrophilic) Mama - Càncer - Tractament Medicaments antineoplàstics - Efectes secundaris Medicine Medicine & Public Health Metastases NCT NCT03337724 neoplasias::neoplasias por localización::neoplasias de la mama [ENFERMEDADES] Neoplasm Recurrence, Local Neoplasms::Neoplasms by Site::Breast Neoplasms [DISEASES] Neutropenia Oncology Other subheadings::Other subheadings::/adverse effects [Other subheadings] Other subheadings::Other subheadings::/drug therapy [Other subheadings] Otros calificadores::Otros calificadores::/efectos adversos [Otros calificadores] Otros calificadores::Otros calificadores::/farmacoterapia [Otros calificadores] Paclitaxel Paclitaxel - adverse effects Peripheral neuropathy Phosphatidylinositol 3-Kinases PI3K/AKT Piperazines Placebos Proto-Oncogene Proteins c-akt PTEN Phosphohydrolase PTEN Phosphohydrolase - genetics PTEN protein Pyrimidines Receptor, ErbB-2 Receptor, ErbB-2 - genetics terapéutica::terapéutica::farmacoterapia::protocolos antineoplásicos::terapéutica::farmacoterapia::protocolos de quimioterapia antineoplásica combinada [TÉCNICAS Y EQUIPOS ANALÍTICOS, DIAGNÓSTICOS Y TERAPÉUTICOS] Therapeutics::Therapeutics::Drug Therapy::Antineoplastic Protocols::Therapeutics::Drug Therapy::Antineoplastic Combined Chemotherapy Protocols [ANALYTICAL, DIAGNOSTIC AND THERAPEUTIC TECHNIQUES, AND EQUIPMENT] Toxicity |
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| Title | Ipatasertib plus paclitaxel for PIK3CA/AKT1/PTEN-altered hormone receptor-positive HER2-negative advanced breast cancer: primary results from cohort B of the IPATunity130 randomized phase 3 trial |
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