Cancer-immune interactions in ER-positive breast cancers: PI3K pathway alterations and tumor-infiltrating lymphocytes
Introduction The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that gen...
Uloženo v:
| Vydáno v: | Breast cancer research : BCR Ročník 21; číslo 1; s. 90 - 12 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
07.08.2019
BioMed Central Ltd BMC |
| Témata: | |
| ISSN: | 1465-542X, 1465-5411, 1465-542X |
| On-line přístup: | Získat plný text |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Introduction
The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations.
Methods
We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between
PIK3CA
hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment.
Results
CD8-positive lymphocytes were significantly more abundant in
PIK3CA
-mutated tumors (OR = 1.65; 95% CI 1.03–2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14–3.41; multivariable model including
PIK3CA
status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells.
Conclusion
These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. |
|---|---|
| AbstractList | Introduction
The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations.
Methods
We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between
PIK3CA
hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment.
Results
CD8-positive lymphocytes were significantly more abundant in
PIK3CA
-mutated tumors (OR = 1.65; 95% CI 1.03–2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14–3.41; multivariable model including
PIK3CA
status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells.
Conclusion
These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. Abstract Introduction The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations. Methods We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment. Results CD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03–2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14–3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells. Conclusion These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations.INTRODUCTIONThe presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations.We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment.METHODSWe included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment.CD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03-2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14-3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells.RESULTSCD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03-2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14-3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells.These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment.CONCLUSIONThese exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations. We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment. CD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03-2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14-3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells. These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. Introduction The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations. Methods We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment. Results CD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03-2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14-3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells. Conclusion These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. Keywords: Luminal breast cancer, Tumor-infiltrating lymphocytes, PIK3CA mutations, PI3K pathway The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive breast cancer. However, the role of TILs in luminal breast cancer is less clear. Emerging evidence has now demonstrated that genetic aberrations in malignant cells influence the immune landscape of tumors. Phosphatidylinositol 3-kinase (PI3K) is the most common altered pathway in ER-positive breast cancer. It is unknown whether changes in the PI3K pathway result in a different composition of the breast tumor microenvironment. Here we present the retrospective analysis of a prospective randomized trial in ER-positive breast cancer on the prognostic and predictive value of specific tumor-associated lymphocytes in the context of PI3K alterations. We included 563 ER-positive tumors from a multicenter trial for stage I to III postmenopausal breast cancer patients, who were randomized to tamoxifen or no adjuvant therapy. The amount of CD8-, CD4-, and FOXP3-positive cells was evaluated by immunohistochemistry and quantified by imaging-analysis software. We analyzed the associations between PIK3CA hotspot mutations, PTEN expression, phosphorylated proteins of the PI3K and MAPK pathway (p-AKT, p-ERK1/2, p-4EBP1, p-p70S6K), and recurrence-free interval after adjuvant tamoxifen or no adjuvant treatment. CD8-positive lymphocytes were significantly more abundant in PIK3CA-mutated tumors (OR = 1.65; 95% CI 1.03-2.68). While CD4 and FOXP3 were not significantly associated with prognosis, patients with tumors classified as CD8-high had increased risk of recurrence (HR = 1.98; 95% CI 1.14-3.41; multivariable model including PIK3CA status, treatment arm, and other standard clinicopathological variables). Lymphocytes were more often present in tumors with increased PI3K downstream phosphorylation. This was most pronounced for FOXP3-positive cells. These exploratory analyses of a prospective trial in luminal breast cancer suggest high CD8 infiltration is associated with unfavorable outcome and that PI3K pathway alterations might be associated with the composition of the tumor microenvironment. |
| ArticleNumber | 90 |
| Audience | Academic |
| Author | Kuppen, Peter J. K. Kruger, Dinja T. Sanders, Joyce Horlings, Hugo M. Linn, Sabine C. Kok, Marleen van der Noort, Vincent Giardiello, Daniele Sobral-Leite, Marcelo Van de Vijver, Koen Opdam, Mark Blok, Erik J. Schmidt, Marjanka K. Beelen, Karin J. van Vlierberghe, Ronald L. P. Salomon, Izhar |
| Author_xml | – sequence: 1 givenname: Marcelo surname: Sobral-Leite fullname: Sobral-Leite, Marcelo organization: Division of Molecular Pathology, Netherlands Cancer Institute, Coordenação de Pesquisa, Instituto Nacional do Câncer – sequence: 2 givenname: Izhar surname: Salomon fullname: Salomon, Izhar organization: Division of Molecular Pathology, Netherlands Cancer Institute – sequence: 3 givenname: Mark surname: Opdam fullname: Opdam, Mark organization: Division of Molecular Pathology, Netherlands Cancer Institute – sequence: 4 givenname: Dinja T. surname: Kruger fullname: Kruger, Dinja T. organization: Division of Molecular Pathology, Netherlands Cancer Institute, Department of Medical Oncology, VU University Medical Centre – sequence: 5 givenname: Karin J. surname: Beelen fullname: Beelen, Karin J. organization: Division of Molecular Pathology, Netherlands Cancer Institute, Division of Medical Oncology, Reinier de Graaf Hospital – sequence: 6 givenname: Vincent surname: van der Noort fullname: van der Noort, Vincent organization: Department of Biometrics, Netherlands Cancer Institute – sequence: 7 givenname: Ronald L. P. surname: van Vlierberghe fullname: van Vlierberghe, Ronald L. P. organization: Department of Surgery, Leiden University Medical Center – sequence: 8 givenname: Erik J. surname: Blok fullname: Blok, Erik J. organization: Department of Surgery, Leiden University Medical Center, Department of Medical Oncology, Leiden University Medical Centre – sequence: 9 givenname: Daniele surname: Giardiello fullname: Giardiello, Daniele organization: Division of Molecular Pathology, Netherlands Cancer Institute – sequence: 10 givenname: Joyce surname: Sanders fullname: Sanders, Joyce organization: Division of Pathology, Netherlands Cancer Institute – sequence: 11 givenname: Koen surname: Van de Vijver fullname: Van de Vijver, Koen organization: Department of Pathology, Netherlands Cancer Institute, Department of Pathology, Ghent University Hospital – sequence: 12 givenname: Hugo M. surname: Horlings fullname: Horlings, Hugo M. organization: Division of Pathology, Netherlands Cancer Institute – sequence: 13 givenname: Peter J. K. surname: Kuppen fullname: Kuppen, Peter J. K. organization: Department of Surgery, Leiden University Medical Center – sequence: 14 givenname: Sabine C. surname: Linn fullname: Linn, Sabine C. organization: Division of Molecular Pathology, Netherlands Cancer Institute, Division of Medical Oncology, Netherlands Cancer Institute, Department of Pathology, University Medical Center Utrecht – sequence: 15 givenname: Marjanka K. surname: Schmidt fullname: Schmidt, Marjanka K. organization: Division of Molecular Pathology, Netherlands Cancer Institute – sequence: 16 givenname: Marleen surname: Kok fullname: Kok, Marleen email: m.kok@nki.nl organization: Division of Medical Oncology, Netherlands Cancer Institute, Division of Molecular Oncology and Immunology, Netherlands Cancer Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31391067$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kluL1DAYhousuAf9Ad5IwRtvuuZLmkO9EJZh1cEFRRS8C2kmncnQJmOSrsy_N53uyo7Ikouc3vfJl-Q9L06cd6YoXgK6BBDsbQSCqKgQNBUAZxV-UpxBzWhFa_zz5MH4tDiPcYsQcEHFs-KUAGkAMX5WjAvltAmVHYbRmdK6ZILSyXoX86S8_lbtfLTJ3pqyDUbFVOqDIb4rvy7J53Kn0ua32peqn4yzT7lVmcbBZ6rrbJ-mdbcu-_2w23i9TyY-L552qo_mxV1_Ufz4cP198am6-fJxubi6qTSrIVWEdZrDCnWdUG2rATek1aYRGHEtOt0CwbSGmiuioFFIMYE5X2FWIyIEGEEuiuXMXXm1lbtgBxX20isrDws-rKUKyereSNrQpqOE1byhNdNY1Up1zNBaAwGNaGa9n1m7sR3MShuXL9YfQY93nN3Itb-VjIlcEcqAN3eA4H-NJiY52KhN3ytn_Bglxjz_UD6NZenrWbpWubT8ij4T9SSXV7RhtOGYT6rL_6hyW5nB6hyV_Pjm2PDq4RX-1n4fhyzgs0AHH2MwndQ2HX41k20vAckpeHIOnszBk1PwJM5O-Md5D3_Mg2dPzFq3NkFu_RhcDsQjpj_wEuqS |
| CitedBy_id | crossref_primary_10_3390_cancers14194844 crossref_primary_10_1016_j_compbiomed_2025_110343 crossref_primary_10_1158_0008_5472_CAN_22_1829 crossref_primary_10_3390_cancers13040765 crossref_primary_10_1002_cjp2_226 crossref_primary_10_1016_j_ebiom_2025_105823 crossref_primary_10_1038_s41416_023_02451_3 crossref_primary_10_3390_ijms22010173 crossref_primary_10_1158_1078_0432_CCR_22_2746 crossref_primary_10_1186_s13058_020_01364_w crossref_primary_10_1158_0008_5472_CAN_21_0253 crossref_primary_10_1158_1078_0432_CCR_20_1923 crossref_primary_10_1097_CM9_0000000000002411 crossref_primary_10_1080_2162402X_2024_2379062 crossref_primary_10_1186_s13058_025_01999_7 crossref_primary_10_1038_s41467_022_29498_9 crossref_primary_10_3389_fonc_2021_644612 crossref_primary_10_1017_erm_2023_16 crossref_primary_10_1371_journal_pone_0314364 crossref_primary_10_3389_fonc_2021_564296 crossref_primary_10_1016_j_apsb_2021_03_027 crossref_primary_10_1016_j_heliyon_2024_e34006 crossref_primary_10_1038_s41416_022_01705_w crossref_primary_10_3390_biomedicines12040763 crossref_primary_10_1186_s13058_023_01717_1 crossref_primary_10_1136_jitc_2022_006618 crossref_primary_10_3389_fonc_2020_598626 crossref_primary_10_12688_f1000research_108628_2 crossref_primary_10_3390_biology11060799 crossref_primary_10_1016_j_clbc_2023_03_007 crossref_primary_10_1038_s44276_025_00152_3 crossref_primary_10_3389_fimmu_2021_674192 crossref_primary_10_3389_fimmu_2021_610149 crossref_primary_10_1016_j_canlet_2022_215593 crossref_primary_10_1016_j_clbc_2022_06_004 crossref_primary_10_3389_fonc_2021_774088 crossref_primary_10_1155_2021_9921466 crossref_primary_10_1186_s12885_025_13992_6 crossref_primary_10_3390_cancers15102846 crossref_primary_10_3389_fonc_2020_00950 crossref_primary_10_1007_s10549_020_05771_7 crossref_primary_10_1016_j_annonc_2020_11_022 crossref_primary_10_1007_s12032_023_02037_2 crossref_primary_10_1016_j_canlet_2020_04_013 crossref_primary_10_1038_s41467_021_25769_z crossref_primary_10_3390_cancers15184479 crossref_primary_10_1186_s12885_023_11411_2 crossref_primary_10_1016_j_ajpath_2021_07_012 crossref_primary_10_3390_cancers13174287 crossref_primary_10_3390_cancers13143626 crossref_primary_10_1111_his_14328 crossref_primary_10_3390_ijms25126501 crossref_primary_10_1186_s13058_019_1239_4 crossref_primary_10_1038_s41598_023_48002_x crossref_primary_10_3389_fmolb_2024_1481912 crossref_primary_10_1186_s12935_020_01465_8 crossref_primary_10_3390_cells10020223 crossref_primary_10_1007_s10549_022_06637_w crossref_primary_10_1016_j_cbi_2024_111055 crossref_primary_10_3390_cancers15030767 crossref_primary_10_3390_cancers17111833 crossref_primary_10_1016_j_coemr_2020_10_004 crossref_primary_10_1038_s41698_025_01035_z crossref_primary_10_1007_s12672_025_03379_1 crossref_primary_10_1158_1078_0432_CCR_20_1731 crossref_primary_10_1158_2159_8290_CD_22_0475 crossref_primary_10_1038_s41523_022_00416_y crossref_primary_10_1177_17588359211064653 crossref_primary_10_1016_j_ctarc_2020_100207 crossref_primary_10_1016_j_anndiagpath_2024_152294 crossref_primary_10_1158_1078_0432_CCR_21_2718 crossref_primary_10_1038_s41523_021_00346_1 crossref_primary_10_1186_s13058_020_01384_6 crossref_primary_10_1002_jcp_29898 crossref_primary_10_1016_j_tranon_2024_102140 crossref_primary_10_3389_fgene_2024_1403587 |
| Cites_doi | 10.2466/pr0.1966.19.1.3 10.4049/jimmunol.174.5.2591 10.1111/j.1467-9469.2004.00404.x 10.1038/nrclinonc.2015.215 10.1186/bcr3606 10.1177/0962280206070650 10.1007/s10549-011-1647-3 10.1126/science.1203486 10.1186/1471-2407-8-57 10.1016/S1470-2045(17)30904-X 10.1007/s10549-015-3269-7 10.1056/NEJM197108052850606 10.1371/journal.pone.0140293 10.1158/0008-5472.CAN-17-2210 10.1016/j.cell.2017.11.013 10.1016/j.ctrv.2016.03.004 10.1038/onc.2008.384 10.1016/j.ejca.2013.11.003 10.1038/s41416-018-0221-8 10.1177/001316446002000104 10.5455/aim.2016.24.38-41 10.1016/S1470-2045(17)30376-5 10.1007/s10549-018-4785-z 10.1016/j.cell.2014.12.033 10.1158/1078-0432.CCR-17-3452 10.1158/1541-7786.MCR-14-0387 10.1007/s10549-010-0987-8 10.1200/JCO.2010.30.5037 10.1007/s10555-016-9637-x 10.1056/NEJMoa1813904 10.1016/S0140-6736(12)61963-1 10.1084/jem.20042276 10.1186/s12885-018-4516-1 10.1016/0169-2607(91)90072-2 10.1186/s13058-014-0432-8 10.1038/srep15179 10.1158/2159-8290.CD-17-0037 10.1093/annonc/mdu191 10.1016/S1470-2045(17)30688-5 10.1080/2162402X.2017.1320626 10.1001/jamaoncol.2016.1061 10.1016/j.tranon.2016.01.001 10.1186/bcr3598 10.1016/S0140-6736(11)60993-8 10.1200/JCO.2016.34.15_suppl.TPS618 10.1007/s10549-016-3883-z |
| ContentType | Journal Article |
| Copyright | The Author(s). 2019 COPYRIGHT 2019 BioMed Central Ltd. |
| Copyright_xml | – notice: The Author(s). 2019 – notice: COPYRIGHT 2019 BioMed Central Ltd. |
| DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1186/s13058-019-1176-2 |
| DatabaseName | Springer Nature OA Free Journals (WRLC) CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Anatomy & Physiology |
| EISSN | 1465-542X |
| EndPage | 12 |
| ExternalDocumentID | oai_doaj_org_article_5959f536479546c2a4aaf6e54c131c05 PMC6686400 A596597276 31391067 10_1186_s13058_019_1176_2 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Top Institute Pharma grantid: T3-502 funderid: http://dx.doi.org/10.13039/501100004522 – fundername: Conselho Nacional de Desenvolvimento Científico e Tecnológico grantid: 99999.001321/2013-07 funderid: http://dx.doi.org/10.13039/501100003593 – fundername: Stichting A Sister's Hope grantid: - funderid: http://dx.doi.org/10.13039/501100008382 – fundername: KWF Kankerbestrijding grantid: -; - funderid: http://dx.doi.org/10.13039/501100004622 – fundername: ; grantid: 99999.001321/2013-07 – fundername: ; grantid: -; - – fundername: ; grantid: - – fundername: ; grantid: T3-502 |
| GroupedDBID | --- 04C 0R~ 23N 2WC 4.4 53G 5GY 5VS 6J9 7X7 8FI 8FJ AAFWJ AAJSJ AASML AAWTL ABUWG ACGFO ACGFS ACJQM ACMJI ACPRK ADBBV ADFRT ADUKV AENEX AFKRA AFPKN AHBYD AHMBA AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIAM AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BMSDO BPHCQ BVXVI C6C CCPQU CS3 DIK DU5 E3Z EBD EBLON EBS EIHBH EJD F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO ICW IHR INH INR ITC KQ8 O5R O5S OK1 P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PUEGO RBZ ROL RPM RSV SBL SOJ TR2 U2A UKHRP WOQ AAYXX AFFHD CITATION ACRMQ ADINQ ALIPV C24 CGR CUY CVF ECM EIF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-c641t-36fc71d0ff8abbc1293bce98207c8fcb13254147a3a19a0a68277d26403881e83 |
| IEDL.DBID | RSV |
| ISICitedReferencesCount | 86 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000479194200002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1465-542X 1465-5411 |
| IngestDate | Fri Oct 03 12:52:00 EDT 2025 Tue Nov 04 01:58:54 EST 2025 Thu Sep 04 17:14:35 EDT 2025 Tue Nov 11 09:52:02 EST 2025 Tue Nov 04 17:42:56 EST 2025 Thu Jan 02 22:58:22 EST 2025 Sat Nov 29 03:59:38 EST 2025 Tue Nov 18 20:50:38 EST 2025 Sat Sep 06 07:25:04 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | PI3K pathway mutations Tumor-infiltrating lymphocytes Luminal breast cancer PIK3CA mutations |
| Language | English |
| License | Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c641t-36fc71d0ff8abbc1293bce98207c8fcb13254147a3a19a0a68277d26403881e83 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://link.springer.com/10.1186/s13058-019-1176-2 |
| PMID | 31391067 |
| PQID | 2270011316 |
| PQPubID | 23479 |
| PageCount | 12 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_5959f536479546c2a4aaf6e54c131c05 pubmedcentral_primary_oai_pubmedcentral_nih_gov_6686400 proquest_miscellaneous_2270011316 gale_infotracmisc_A596597276 gale_infotracacademiconefile_A596597276 pubmed_primary_31391067 crossref_citationtrail_10_1186_s13058_019_1176_2 crossref_primary_10_1186_s13058_019_1176_2 springer_journals_10_1186_s13058_019_1176_2 |
| PublicationCentury | 2000 |
| PublicationDate | 2019-08-07 |
| PublicationDateYYYYMMDD | 2019-08-07 |
| PublicationDate_xml | – month: 08 year: 2019 text: 2019-08-07 day: 07 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationTitle | Breast cancer research : BCR |
| PublicationTitleAbbrev | Breast Cancer Res |
| PublicationTitleAlternate | Breast Cancer Res |
| PublicationYear | 2019 |
| Publisher | BioMed Central BioMed Central Ltd BMC |
| Publisher_xml | – name: BioMed Central – name: BioMed Central Ltd – name: BMC |
| References | HR Ali (1176_CR5) 2014; 25 CC Engels (1176_CR8) 2015; 149 Q Shen (1176_CR18) 2017; 7 DT Kruger (1176_CR34) 2018; 119 J Vermont (1176_CR38) 1991; 35 K Baker (1176_CR6) 2011; 58 SM Mahmoud (1176_CR12) 2011; 127 V Kotoula (1176_CR44) 2016; 158 B Shang (1176_CR13) 2015; 5 Erik J. Blok (1176_CR45) 2018; 171 JJ Bartko (1176_CR36) 1966; 19 G Papaxoinis (1176_CR41) 2015; 10 JB Vermorken (1176_CR32) 1998; 50 K Beelen (1176_CR33) 2018; 18 A Guerrero-Zotano (1176_CR19) 2016; 35 C Davies (1176_CR2) 2013; 381 K Beelen (1176_CR22) 2014; 16 H Ghebeh (1176_CR31) 2008; 8 CA Crane (1176_CR43) 2009; 28 F Andre (1176_CR46) 2019; 380 PA Antony (1176_CR28) 2005; 174 R Forrest (1176_CR35) 2014; 50 A Di Leo (1176_CR47) 2018; 19 JZ Huang (1176_CR42) 2004; 31 S Liu (1176_CR10) 2014; 16 Hope S. Rugo (1176_CR26) 2018; 24 J Cohen (1176_CR40) 1960; 20 J Baselga (1176_CR24) 2017; 18 C Davies (1176_CR1) 2011; 378 ZL Teo (1176_CR48) 2017; 77 CG Craddock (1176_CR27) 1971; 285 C Denkert (1176_CR7) 2018; 19 SM Mahmoud (1176_CR11) 2011; 29 RD Schreiber (1176_CR29) 2011; 331 HC Kraemer (1176_CR39) 2006; 15 JP Layer (1176_CR15) 2017; 6 JC Marie (1176_CR30) 2005; 201 D Roshani (1176_CR37) 2016; 24 SX Yang (1176_CR21) 2016; 45 MS Rooney (1176_CR17) 2015; 160 P Savas (1176_CR4) 2016; 13 F Liu (1176_CR9) 2011; 130 K Beelen (1176_CR23) 2014; 16 F Andre (1176_CR25) 2016; 34 1176_CR16 SE Stanton (1176_CR3) 2016; 2 RM Kortlever (1176_CR14) 2017; 171 HA Azim (1176_CR20) 2016; 9 |
| References_xml | – volume: 58 start-page: 1107 issue: 7 year: 2011 ident: 1176_CR6 publication-title: Histopathology – volume: 19 start-page: 3 issue: 1 year: 1966 ident: 1176_CR36 publication-title: Psychol Rep doi: 10.2466/pr0.1966.19.1.3 – volume: 174 start-page: 2591 issue: 5 year: 2005 ident: 1176_CR28 publication-title: J Immunol doi: 10.4049/jimmunol.174.5.2591 – volume: 31 start-page: 515 issue: 4 year: 2004 ident: 1176_CR42 publication-title: Scand J Stat doi: 10.1111/j.1467-9469.2004.00404.x – volume: 13 start-page: 228 issue: 4 year: 2016 ident: 1176_CR4 publication-title: Nat Rev Clin Oncol doi: 10.1038/nrclinonc.2015.215 – volume: 16 start-page: R13 issue: 1 year: 2014 ident: 1176_CR23 publication-title: Breast Cancer Res doi: 10.1186/bcr3606 – volume: 15 start-page: 525 issue: 6 year: 2006 ident: 1176_CR39 publication-title: Stat Methods Med Res doi: 10.1177/0962280206070650 – volume: 130 start-page: 645 issue: 2 year: 2011 ident: 1176_CR9 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-011-1647-3 – volume: 331 start-page: 1565 issue: 6024 year: 2011 ident: 1176_CR29 publication-title: Science doi: 10.1126/science.1203486 – volume: 8 start-page: 57 year: 2008 ident: 1176_CR31 publication-title: BMC Cancer doi: 10.1186/1471-2407-8-57 – volume: 19 start-page: 40 issue: 1 year: 2018 ident: 1176_CR7 publication-title: Lancet Oncol doi: 10.1016/S1470-2045(17)30904-X – volume: 149 start-page: 587 issue: 3 year: 2015 ident: 1176_CR8 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-015-3269-7 – volume: 285 start-page: 324 issue: 6 year: 1971 ident: 1176_CR27 publication-title: N Engl J Med doi: 10.1056/NEJM197108052850606 – volume: 10 issue: 10 year: 2015 ident: 1176_CR41 publication-title: PLoS One doi: 10.1371/journal.pone.0140293 – volume: 77 start-page: 6340 issue: 22 year: 2017 ident: 1176_CR48 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-17-2210 – volume: 171 start-page: 1301 issue: 6 year: 2017 ident: 1176_CR14 publication-title: Cell doi: 10.1016/j.cell.2017.11.013 – volume: 45 start-page: 87 year: 2016 ident: 1176_CR21 publication-title: Cancer Treat Rev doi: 10.1016/j.ctrv.2016.03.004 – volume: 28 start-page: 306 issue: 2 year: 2009 ident: 1176_CR43 publication-title: Oncogene doi: 10.1038/onc.2008.384 – volume: 50 start-page: 544 issue: 3 year: 2014 ident: 1176_CR35 publication-title: Eur J Cancer doi: 10.1016/j.ejca.2013.11.003 – volume: 119 start-page: 832 issue: 7 year: 2018 ident: 1176_CR34 publication-title: Br J Cancer doi: 10.1038/s41416-018-0221-8 – volume: 20 start-page: 37 issue: 1 year: 1960 ident: 1176_CR40 publication-title: Educ Psychol Meas doi: 10.1177/001316446002000104 – volume: 24 start-page: 38 issue: 1 year: 2016 ident: 1176_CR37 publication-title: Acta Informatica Medica doi: 10.5455/aim.2016.24.38-41 – volume: 18 start-page: 904 issue: 7 year: 2017 ident: 1176_CR24 publication-title: Lancet Oncol doi: 10.1016/S1470-2045(17)30376-5 – volume: 171 start-page: 65 issue: 1 year: 2018 ident: 1176_CR45 publication-title: Breast Cancer Research and Treatment doi: 10.1007/s10549-018-4785-z – volume: 160 start-page: 48 issue: 1–2 year: 2015 ident: 1176_CR17 publication-title: Cell doi: 10.1016/j.cell.2014.12.033 – volume: 24 start-page: 2804 issue: 12 year: 2018 ident: 1176_CR26 publication-title: Clinical Cancer Research doi: 10.1158/1078-0432.CCR-17-3452 – ident: 1176_CR16 doi: 10.1158/1541-7786.MCR-14-0387 – volume: 127 start-page: 99 issue: 1 year: 2011 ident: 1176_CR12 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-010-0987-8 – volume: 29 start-page: 1949 issue: 15 year: 2011 ident: 1176_CR11 publication-title: J Clin Oncol doi: 10.1200/JCO.2010.30.5037 – volume: 35 start-page: 515 issue: 4 year: 2016 ident: 1176_CR19 publication-title: Cancer Metastasis Rev doi: 10.1007/s10555-016-9637-x – volume: 380 start-page: 1929 issue: 20 year: 2019 ident: 1176_CR46 publication-title: N Engl J Med doi: 10.1056/NEJMoa1813904 – volume: 381 start-page: 805 issue: 9869 year: 2013 ident: 1176_CR2 publication-title: Lancet doi: 10.1016/S0140-6736(12)61963-1 – volume: 201 start-page: 1061 issue: 7 year: 2005 ident: 1176_CR30 publication-title: J Exp Med doi: 10.1084/jem.20042276 – volume: 18 start-page: 761 issue: 1 year: 2018 ident: 1176_CR33 publication-title: BMC Cancer doi: 10.1186/s12885-018-4516-1 – volume: 35 start-page: 141 issue: 2 year: 1991 ident: 1176_CR38 publication-title: Comput Methods Prog Biomed doi: 10.1016/0169-2607(91)90072-2 – volume: 16 start-page: 432 issue: 5 year: 2014 ident: 1176_CR10 publication-title: Breast Cancer Res doi: 10.1186/s13058-014-0432-8 – volume: 50 start-page: 329 issue: abstracts poste year: 1998 ident: 1176_CR32 publication-title: Breast Cancer Res Treat – volume: 5 start-page: 15179 year: 2015 ident: 1176_CR13 publication-title: Sci Rep doi: 10.1038/srep15179 – volume: 7 start-page: 1320 issue: 11 year: 2017 ident: 1176_CR18 publication-title: Cancer Discovery doi: 10.1158/2159-8290.CD-17-0037 – volume: 25 start-page: 1536 issue: 8 year: 2014 ident: 1176_CR5 publication-title: Ann Oncol doi: 10.1093/annonc/mdu191 – volume: 19 start-page: 87 issue: 1 year: 2018 ident: 1176_CR47 publication-title: Lancet Oncol doi: 10.1016/S1470-2045(17)30688-5 – volume: 6 issue: 6 year: 2017 ident: 1176_CR15 publication-title: Oncoimmunology doi: 10.1080/2162402X.2017.1320626 – volume: 2 start-page: 1354 issue: 10 year: 2016 ident: 1176_CR3 publication-title: JAMA Oncol doi: 10.1001/jamaoncol.2016.1061 – volume: 9 start-page: 114 issue: 2 year: 2016 ident: 1176_CR20 publication-title: Transl Oncol doi: 10.1016/j.tranon.2016.01.001 – volume: 16 start-page: R6 issue: 1 year: 2014 ident: 1176_CR22 publication-title: Breast Cancer Res doi: 10.1186/bcr3598 – volume: 378 start-page: 771 issue: 9793 year: 2011 ident: 1176_CR1 publication-title: Lancet doi: 10.1016/S0140-6736(11)60993-8 – volume: 34 start-page: TPS618 issue: 15_suppl year: 2016 ident: 1176_CR25 publication-title: J Clin Oncol doi: 10.1200/JCO.2016.34.15_suppl.TPS618 – volume: 158 start-page: 307 issue: 2 year: 2016 ident: 1176_CR44 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-016-3883-z |
| SSID | ssj0017858 |
| Score | 2.5672064 |
| Snippet | Introduction
The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and... The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and HER2-positive... Introduction The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in triple-negative and... Abstract Introduction The presence of tumor-infiltrating lymphocytes (TILs) is correlated with good prognosis and outcome after (immuno)therapy in... |
| SourceID | doaj pubmedcentral proquest gale pubmed crossref springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 90 |
| SubjectTerms | Adjuvant chemotherapy Analysis Biomarkers, Tumor Biomedical and Life Sciences Biomedicine Breast cancer Cancer Research Care and treatment Cellular signal transduction Disease Susceptibility - immunology Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Profiling Genetic aspects Humans Immunohistochemistry Immunotherapy Luminal breast cancer Lymphocytes Lymphocytes, Tumor-Infiltrating - immunology Lymphocytes, Tumor-Infiltrating - metabolism Lymphocytes, Tumor-Infiltrating - pathology Mutation Neoplasm Staging Neoplasms - etiology Neoplasms - metabolism Neoplasms - mortality Neoplasms - pathology Oncology Outcome and process assessment (Medical care) Phosphatidylinositol 3-Kinase - genetics Phosphatidylinositol 3-Kinase - metabolism Phospholipids PI3K pathway PIK3CA mutations Postmenopausal women Prognosis Proteins Receptors, Estrogen - metabolism Research Article Surgical Oncology T-Lymphocyte Subsets - immunology T-Lymphocyte Subsets - metabolism T-Lymphocyte Subsets - pathology Tamoxifen Transcriptome Tumor-infiltrating lymphocytes Tumors |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fi9QwEA5yiPgi550_6p0SQRSUcE3bpIlv63GHIh6HKNxbSLOpLux1Zds92f_emSS7XE_UFx_bJG2amSTfdCbfEPKimILVA0YXcw5TmFWiZFbxigGYww1KQDMbkk3UZ2fq4kKfX0v1hTFhkR44DtyR0EK3AlnOtaikK2xlbSu9qBwvuYvspXmtN8ZU8h_USqjkw-RKHvWwUgsM2tKM81qyYrQLBbL-35fka3vSzXjJG07TsBed7pJ7CUTSSez8fXLLd3tkf9KBAX25pi9pCOsM_8v3yJ1PyXu-T1bHKOIlm-GZEE-RKWIZzzX0cEFPPrMYwnXlaYOx6gN1oUH_lp5_KD9SzF78065p8LDHP33UdlM6rC4X8NSunc0DCW_3jc7XoCULtwYg-4B8PT35cvyepbQLzMmKD6zE4z98mretsk3jEBA0zmsUnlOta8B-xdzhtS0t1za3UhV1PQVghcQy3KvyIdnpFp1_TChISWiwwVQrNCAHiXAPEFXhC68aq9uM5BsxGJc4yTE1xtwE20RJEyVnQHJISy5NkZHX2yY_IiHH3yq_Q9luKyKXdrgBGmaShpl_aVhGXqFmGJzx0Dln08EF-ETkzjITgaSMgANlRg5HNWGmulHx841uGSzC8LbOL1a9KYL7H14HdR5FXdv2uQSMjjx_GalHWjj6qHFJN_seiMJhwEEqeUbebPTVpBWq__OYPfkfY3ZA7hY42zC2pj4kO8Ny5Z-S2-5qmPXLZ2Gu_gKaYj6_ priority: 102 providerName: Directory of Open Access Journals |
| Title | Cancer-immune interactions in ER-positive breast cancers: PI3K pathway alterations and tumor-infiltrating lymphocytes |
| URI | https://link.springer.com/article/10.1186/s13058-019-1176-2 https://www.ncbi.nlm.nih.gov/pubmed/31391067 https://www.proquest.com/docview/2270011316 https://pubmed.ncbi.nlm.nih.gov/PMC6686400 https://doaj.org/article/5959f536479546c2a4aaf6e54c131c05 |
| Volume | 21 |
| WOSCitedRecordID | wos000479194200002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVADU databaseName: BioMed Central Open Access Free customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: RBZ dateStart: 19990101 isFulltext: true titleUrlDefault: https://www.biomedcentral.com/search/ providerName: BioMedCentral – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: DOA dateStart: 20000101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: 7X7 dateStart: 20150101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: BENPR dateStart: 20150101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: PIMPY dateStart: 20150101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVAVX databaseName: SpringerLink Contemporary customDbUrl: eissn: 1465-542X dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0017858 issn: 1465-542X databaseCode: RSV dateStart: 19991201 isFulltext: true titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22 providerName: Springer Nature |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3rb9MwED_BhhBfeGw8AqMyEgIJFJGXE4dv3dSJCa2KxkPlk-W4zqjUJShph_rfc-ckFRkPCb5USn1O_Dif73zn3wE8D-Zo9aDR5WpNKcwiHrpK-JGLyhxtUByrKZtsIplOxWyWZt097qaPdu9dklZS22Ut4jcNSltOgVep6_tJ7KLc3eUENkMm-ofPW9dBIrjo3Je_rTbYgCxO_6_S-Kft6Gqo5BV_qd2Gju_8Vwfuwu1O62Tjlk3uwTVT7sH-uESL-2LDXjAbB2oP2Pfg5mnnbt-H9RHxRO0u6BKJYQQtUbcXIRp8YJMzt435ujQsp-D2FdO2QvOWZSfhe0bpjr-rDbMu-fZokKlyzlbriwrfWhaLpUXtLc_ZcoNsVekNar734dPx5OPRO7fL0-DqOPJXbkj3hfy5VxRC5bkmDSLXJqXZ1qLQORq8lGw8UaHyU-WpWARJMkdNjJBofCPCB7BTVqV5BIxHmqdotImCp6hqxKQfogoWmMCIXKWFA14_eVJ3IOaUS2MprTEjYtmOssRRJhzzWAYOvNpW-dYiePyN-JA4YktI4Nv2j6o-l91aljzlacEJeD_lUawDFSlVxAbb7oe-9rgDL4mfJIkIbJxW3U0H7CKBbckxJxRHVBxjBw4GlLi09aD4Wc-RkoooHq401bqRgY0XwM8hzcOWQ7dtDlGpJ2BAB5IB7w46NSwpF18tsjgOOM6K58DrnoNlJ9KaP4_Z43-ifgK3AloCFHWTHMDOql6bp3BDX64WTT2C68kssb9iBLuHk2l2NrLHJPiUnZxmX0Z2sf8AYYlJWw |
| linkProvider | Springer Nature |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3rb9MwELfQQMAXHhuwwAAjIZCYLPKyY_OtTJs2basmGGjfLMd1tkpdgpJ0qP89d05akfGQ4GPjc-rH3fkud_4dIa_jCXg94HQxa7GEWcoTZmSUMjDm8IDi0M34YhPZeCzPztRJf4-7WWa7L0OSXlN7sZbifQPalmPilWJRlAkGevdmilV20EX__HUVOsgkl3348rfdBgeQx-n_VRv_dBxdT5W8Fi_1x9De_f-awANyr7c66ahjk4fkhivXycaoBI_7ckHfUJ8H6j-wr5Pbx324fYPMd5AnajbFSySOIrRE3V2EaOAH3f3EupyvK0dzTG5vqfUdmg_05CA5pFju-LtZUB-S7z4NUlNOaDu_rOCtZTGdedTe8pzOFsBWlV2A5fuIfNnbPd3ZZ32dBmZFGrUswftC0SQsCmny3KIFkVuncLetLGwODi8WG89MYiJlQiNknGUTsMQQiSZyMnlM1sqqdJuE8tRyBU6bLLgCU0OgfQgmWOxiJ3OjioCEy83Ttgcxx1oaM-2dGSl0t8oaVhlxzIWOA_Ju1eVbh-DxN-KPyBErQgTf9g-q-lz3sqy54qrgCLyveCpsbFJjCuFg7FES2ZAH5C3yk0YVAYOzpr_pAFNEsC094ojiCIajCMjWgBJE2w6aXy05UmMT5sOVrpo3Ovb5AvB3QPOk49DVmBMw6hEYMCDZgHcHkxq2lNMLjywOCw67EgZke8nBuldpzZ_X7Ok_Ub8kd_ZPj4_00cH48Bm5G6M4YAZOtkXW2nrunpNb9qqdNvULL9Y_AD1ORi8 |
| linkToPdf | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3db9MwELfQhiZeGGwwAgOMhEACRcuXHYe3MlYxDapqfGhvluM6o1LnTEk61P-eOyepyPiQEI-tz63t3J3vcne_I-R5NAOvB5wuX2tsYZaw2FciTHww5vCCYjBNuWYT6WQizs6yadfntO6z3fuQZFvTgChNtjm4nBWtiAt-UIPmZZiElflhmHIfdPBmAo4M5nSdfvq6DiOkgokulPnbaYPLyGH2_6qZf7qarqdNXouduitpvP3fm7lDbnfWKB217HOX3DB2h-yOLHjiFyv6grr8UPfifYdsfezC8LtkeYi8UvlzLC4xFCEnqrZAooYP9OjUb3PBrgzNMem9odpNqN_Q6XF8QrEN8ne1oi5U374ypMrOaLO8KOFXbTFfODRfe04XK2C3Uq_AIr5HvoyPPh--97v-Db7mSdj4MdYRhbOgKITKc42WRa5NhlygRaFzcISxCXmqYhVmKlBcRGk6AwsNEWpCI-L7ZMOW1jwglCWaZeDMiYJlYIJwtBvBNItMZESussIjQf8gpe7AzbHHxkI6J0dw2Z6yhFNGfHMuI4-8Wk-5bJE9_kb8FrljTYig3O6LsjqXnYxLlrGsYAjIn7GE60glShXcwNrDONQB88hL5C2JqgMWp1VXAQFbRBAuOWKI7ggGJffI_oASRF4Php_13ClxCPPkrCmXtYxcHgH8HdDstdy6XnMMxj4CBnokHfDxYFPDETv_5hDH4cDhqQQeed1zs-xUXf3nM3v4T9RPydb03Vh-OJ6cPCK3IpQGTMxJ98lGUy3NY3JTXzXzunriJPwHHlRPEw |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Cancer-immune+interactions+in+ER-positive+breast+cancers%3A+PI3K+pathway+alterations+and+tumor-infiltrating+lymphocytes&rft.jtitle=Breast+cancer+research+%3A+BCR&rft.au=Sobral-Leite%2C+Marcelo&rft.au=Salomon%2C+Izhar&rft.au=Opdam%2C+Mark&rft.au=Kruger%2C+Dinja+T&rft.date=2019-08-07&rft.issn=1465-542X&rft.eissn=1465-542X&rft.volume=21&rft.issue=1&rft.spage=90&rft_id=info:doi/10.1186%2Fs13058-019-1176-2&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1465-542X&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1465-542X&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1465-542X&client=summon |