Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer

Adrianna A. Mendes; Jiayun Lu; Harsimar B. Kaur; Siqun L. Zheng; Jianfeng Xu; Jessica Hicks; Adam B. Weiner; Edward M. Schaeffer; Ashley E. Ross; Steven P. Balk; Mary Ellen Taplin; Nathan A. Lack; Emirhan Tekoglu; Janielle P. Maynard; Angelo M. De Marzo; Emmanuel S. Antonarakis; Karen S. Sfanos; Corinne E. Joshu; Eugene Shenderov; Tamara L. Lotan

doi:10.1002/cncr.34190

Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer

Adrianna A. Mendes, Jiayun Lu, Harsimar B. Kaur, Siqun L. Zheng, Jianfeng Xu, Jessica Hicks, Adam B. Weiner, Edward M. Schaeffer, Ashley E. Ross, Steven P. Balk, Mary Ellen Taplin, Nathan A. Lack, Emirhan Tekoglu, Janielle P. Maynard, Angelo M. De Marzo, Emmanuel S. Antonarakis, Karen S. Sfanos, Corinne E. Joshu, Eugene Shenderov, Tamara L. Lotan

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

Background: B7 homolog 3 (B7-H3) is an immunomodulatory molecule that is highly expressed in prostate cancer (PCa) and belongs to the B7 superfamily, which includes PD-L1. Immunotherapies (antibodies, antibody-drug conjugates, and chimeric antigen receptor T cells) targeting B7-H3 are currently in clinical trials; therefore, elucidating the molecular and immune microenvironment correlates of B7-H3 expression may help to guide trial design and interpretation. The authors tested the interconnected hypotheses that B7-H3 expression is associated with genetic racial ancestry, immune cell composition, and androgen receptor signaling in PCa. Methods: An automated, clinical-grade immunohistochemistry assay was developed by to digitally quantify B7-H3 protein expression across 2 racially diverse cohorts of primary PCa (1 with previously reported transcriptomic data) and pretreatment and posttreatment PCa tissues from a trial of intensive neoadjuvant hormonal therapy. Results: B7-H3 protein expression was significantly lower in self-identified Black patients and was inversely correlated with the percentage African ancestry. This association with race was independent of the significant association of B7-H3 protein expression with ERG/ETS and PTEN status. B7-H3 messenger RNA expression, but not B7-H3 protein expression, was significantly correlated with regulatory (FOXP3-positive) T-cell density. Finally, androgen receptor activity scores were significantly correlated with B7-H3 messenger RNA expression, and neoadjuvant intensive hormonal therapy was associated with a significant decrease in B7-H3 protein expression. Conclusions: The current data underscore the importance of studying racially and molecularly diverse PCa cohorts in the immunotherapy era. This study is among the first to use genetic ancestry markers to add to the emerging evidence that PCa in men of African ancestry may have a distinct biology associated with B7-H3 expression. Lay Summary: B7-H3 is an immunomodulatory molecule that is highly expressed in prostate cancer and is under investigation in clinical trials. The authors determined that B7-H3 protein expression is inversely correlated with an individual's proportion of African ancestry. The results demonstrate that B7-H3 messenger RNA expression is correlated with the density of tumor T-regulatory cells. Finally, in the first paired analysis of B7-H3 protein expression before and after neoadjuvant intensive hormone therapy, the authors determined that hormone therapy is associated with a decrease in B7-H3 protein levels, suggesting that androgen signaling may positively regulate B7-H3 expression. These results may help to guide the design of future clinical trials and to develop biomarkers of response in such trials.

Original language	English (US)
Pages (from-to)	2269-2280
Number of pages	12
Journal	Cancer
Volume	128
Issue number	12
DOIs	https://doi.org/10.1002/cncr.34190
State	Published - Jun 15 2022
Externally published	Yes

Bibliographical note

Funding Information:
Ashley E. Ross reports personal fees and honoraria from Veracyte, Astellas, Bayer, Pfizer, Blue Earth, Myovant, and Janssen outside the submitted work. Mary‐Ellen Taplin reports honoraria from AstraZeneca, AbbVie, Astellas, Bauer, Blue Earth, Constellation, Celegene, Epizyme, GlaxoSmithKline, Incyte, Janssen, Myovant, Roviant, UpToDate, the University of Pittsburgh, and the American Society for Clinical Oncology; and participation on a data safety monitoring board or advisory board for Clovis, Pfizer, and Myovant outside the submitted work. Nathan A. Lack reports personal fees from Nido Bioscience outside the submitted work. Angelo M. De Marzo reports research support from Janssen and Myriad during the conduct of the study and personal fees from Cepheid and Merck outside the submitted work. Emmanuel S. Antonarakis reports research funding to his institution from Janssen, Johnson & Johnson, Sanofi, Dendreon, Genentech, Novartis, Merck, Bristol Myers Squibb, AstraZeneca, and Constellation; grants or contracts from AstraZeneca, Celgene, Clovis, and Sanofi; personal fees from Aikido Pharma, Blue Earth Diagnostics, Dendreon, EcoR1, KeyQuest Health, Janssen, Pfizer, and Projects in Knowledge; is a co‐inventor of an AR‐V7 biomarker technology that has been licensed to Qiagen; and reports participation on a data safety monitoring board or advisory board for Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Clovis, Constellation, Curium, Eli Lilly and Company, Exact Sciences, Foundation Medicine, Invitae, Ismar, Merck, Orion, Sanofi, and Tempus outside the submitted work. Corinne E. Joshu reports institutional grants or contracts from the American Cancer Society and the National Institutes of Health outside the submitted work. Eugene Shenderov reports institutional research funding from Macrogenics and personal fees from Biopharma, Inc, Firstthough.IO, and Guidepoint Global outside the submitted work. Tamara L. Lotan reports research support from Roche/Ventana, DeepBio, and Myriad Genetics and support for attending meetings and/or travel from the Prostate Cancer Foundation outside the submitted work. The remaining authors made no disclosures.

Funding Information:
This research was supported in part by 2 Health Disparity Research Awards from the Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program (CDMRP‐PCRP) (W81XWH‐15‐1‐0661 to Edward M. Schaeffer and Tamara L. Lotan; W81XWH‐17‐1‐0286 to Karen S. Sfanos and Tamara L. Lotan). Additional funding and resources were provided by the National Institutes of Health/National Cancer Institute Prostate Specialized Centers Research Excellence (grant P50CA58236) and a National Cancer Institute Cancer Center Support grant (5P30CA006973‐52). Eugene Shenderov was supported by a Prostate Cancer Foundation Young Investigator Award and Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program grant (W81XWH‐19‐1‐0511). Adriana A. Mendes was supported by a grant from the National Cancer Institute (T32CA193145).

Publisher Copyright:
© 2022 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.

Keywords

African American
B7 homolog 3 (B7-H3)
ERG
PTEN
T cells
androgen receptor (AR)
prostatic adenocarcinoma
tumor-infiltrating lymphocytes

PubMed: MeSH publication types

Journal Article

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1002/cncr.34190

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Mendes, A. A., Lu, J., Kaur, H. B., Zheng, S. L., Xu, J., Hicks, J., Weiner, A. B., Schaeffer, E. M., Ross, A. E., Balk, S. P., Taplin, M. E., Lack, N. A., Tekoglu, E., Maynard, J. P., De Marzo, A. M., Antonarakis, E. S., Sfanos, K. S., Joshu, C. E., Shenderov, E., & Lotan, T. L. (2022). Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer. Cancer, 128(12), 2269-2280. https://doi.org/10.1002/cncr.34190

Mendes, AA, Lu, J, Kaur, HB, Zheng, SL, Xu, J, Hicks, J, Weiner, AB, Schaeffer, EM, Ross, AE, Balk, SP, Taplin, ME, Lack, NA, Tekoglu, E, Maynard, JP, De Marzo, AM, Antonarakis, ES, Sfanos, KS, Joshu, CE, Shenderov, E & Lotan, TL 2022, 'Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer', Cancer, vol. 128, no. 12, pp. 2269-2280. https://doi.org/10.1002/cncr.34190

@article{b416d8ed40f44847a14d34d39a27b1ec,

title = "Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer",

abstract = "Background: B7 homolog 3 (B7-H3) is an immunomodulatory molecule that is highly expressed in prostate cancer (PCa) and belongs to the B7 superfamily, which includes PD-L1. Immunotherapies (antibodies, antibody-drug conjugates, and chimeric antigen receptor T cells) targeting B7-H3 are currently in clinical trials; therefore, elucidating the molecular and immune microenvironment correlates of B7-H3 expression may help to guide trial design and interpretation. The authors tested the interconnected hypotheses that B7-H3 expression is associated with genetic racial ancestry, immune cell composition, and androgen receptor signaling in PCa. Methods: An automated, clinical-grade immunohistochemistry assay was developed by to digitally quantify B7-H3 protein expression across 2 racially diverse cohorts of primary PCa (1 with previously reported transcriptomic data) and pretreatment and posttreatment PCa tissues from a trial of intensive neoadjuvant hormonal therapy. Results: B7-H3 protein expression was significantly lower in self-identified Black patients and was inversely correlated with the percentage African ancestry. This association with race was independent of the significant association of B7-H3 protein expression with ERG/ETS and PTEN status. B7-H3 messenger RNA expression, but not B7-H3 protein expression, was significantly correlated with regulatory (FOXP3-positive) T-cell density. Finally, androgen receptor activity scores were significantly correlated with B7-H3 messenger RNA expression, and neoadjuvant intensive hormonal therapy was associated with a significant decrease in B7-H3 protein expression. Conclusions: The current data underscore the importance of studying racially and molecularly diverse PCa cohorts in the immunotherapy era. This study is among the first to use genetic ancestry markers to add to the emerging evidence that PCa in men of African ancestry may have a distinct biology associated with B7-H3 expression. Lay Summary: B7-H3 is an immunomodulatory molecule that is highly expressed in prostate cancer and is under investigation in clinical trials. The authors determined that B7-H3 protein expression is inversely correlated with an individual's proportion of African ancestry. The results demonstrate that B7-H3 messenger RNA expression is correlated with the density of tumor T-regulatory cells. Finally, in the first paired analysis of B7-H3 protein expression before and after neoadjuvant intensive hormone therapy, the authors determined that hormone therapy is associated with a decrease in B7-H3 protein levels, suggesting that androgen signaling may positively regulate B7-H3 expression. These results may help to guide the design of future clinical trials and to develop biomarkers of response in such trials.",

keywords = "African American, B7 homolog 3 (B7-H3), ERG, PTEN, T cells, androgen receptor (AR), prostatic adenocarcinoma, tumor-infiltrating lymphocytes",

author = "Mendes, {Adrianna A.} and Jiayun Lu and Kaur, {Harsimar B.} and Zheng, {Siqun L.} and Jianfeng Xu and Jessica Hicks and Weiner, {Adam B.} and Schaeffer, {Edward M.} and Ross, {Ashley E.} and Balk, {Steven P.} and Taplin, {Mary Ellen} and Lack, {Nathan A.} and Emirhan Tekoglu and Maynard, {Janielle P.} and {De Marzo}, {Angelo M.} and Antonarakis, {Emmanuel S.} and Sfanos, {Karen S.} and Joshu, {Corinne E.} and Eugene Shenderov and Lotan, {Tamara L.}",

note = "Funding Information: Ashley E. Ross reports personal fees and honoraria from Veracyte, Astellas, Bayer, Pfizer, Blue Earth, Myovant, and Janssen outside the submitted work. Mary‐Ellen Taplin reports honoraria from AstraZeneca, AbbVie, Astellas, Bauer, Blue Earth, Constellation, Celegene, Epizyme, GlaxoSmithKline, Incyte, Janssen, Myovant, Roviant, UpToDate, the University of Pittsburgh, and the American Society for Clinical Oncology; and participation on a data safety monitoring board or advisory board for Clovis, Pfizer, and Myovant outside the submitted work. Nathan A. Lack reports personal fees from Nido Bioscience outside the submitted work. Angelo M. De Marzo reports research support from Janssen and Myriad during the conduct of the study and personal fees from Cepheid and Merck outside the submitted work. Emmanuel S. Antonarakis reports research funding to his institution from Janssen, Johnson & Johnson, Sanofi, Dendreon, Genentech, Novartis, Merck, Bristol Myers Squibb, AstraZeneca, and Constellation; grants or contracts from AstraZeneca, Celgene, Clovis, and Sanofi; personal fees from Aikido Pharma, Blue Earth Diagnostics, Dendreon, EcoR1, KeyQuest Health, Janssen, Pfizer, and Projects in Knowledge; is a co‐inventor of an AR‐V7 biomarker technology that has been licensed to Qiagen; and reports participation on a data safety monitoring board or advisory board for Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Clovis, Constellation, Curium, Eli Lilly and Company, Exact Sciences, Foundation Medicine, Invitae, Ismar, Merck, Orion, Sanofi, and Tempus outside the submitted work. Corinne E. Joshu reports institutional grants or contracts from the American Cancer Society and the National Institutes of Health outside the submitted work. Eugene Shenderov reports institutional research funding from Macrogenics and personal fees from Biopharma, Inc, Firstthough.IO, and Guidepoint Global outside the submitted work. Tamara L. Lotan reports research support from Roche/Ventana, DeepBio, and Myriad Genetics and support for attending meetings and/or travel from the Prostate Cancer Foundation outside the submitted work. The remaining authors made no disclosures. Funding Information: This research was supported in part by 2 Health Disparity Research Awards from the Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program (CDMRP‐PCRP) (W81XWH‐15‐1‐0661 to Edward M. Schaeffer and Tamara L. Lotan; W81XWH‐17‐1‐0286 to Karen S. Sfanos and Tamara L. Lotan). Additional funding and resources were provided by the National Institutes of Health/National Cancer Institute Prostate Specialized Centers Research Excellence (grant P50CA58236) and a National Cancer Institute Cancer Center Support grant (5P30CA006973‐52). Eugene Shenderov was supported by a Prostate Cancer Foundation Young Investigator Award and Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program grant (W81XWH‐19‐1‐0511). Adriana A. Mendes was supported by a grant from the National Cancer Institute (T32CA193145). Publisher Copyright: {\textcopyright} 2022 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.",

year = "2022",

month = jun,

day = "15",

doi = "10.1002/cncr.34190",

language = "English (US)",

volume = "128",

pages = "2269--2280",

journal = "Cancer",

issn = "0008-543X",

publisher = "John Wiley and Sons Inc.",

number = "12",

}

TY - JOUR

T1 - Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer

AU - Mendes, Adrianna A.

AU - Lu, Jiayun

AU - Kaur, Harsimar B.

AU - Zheng, Siqun L.

AU - Xu, Jianfeng

AU - Hicks, Jessica

AU - Weiner, Adam B.

AU - Schaeffer, Edward M.

AU - Ross, Ashley E.

AU - Balk, Steven P.

AU - Taplin, Mary Ellen

AU - Lack, Nathan A.

AU - Tekoglu, Emirhan

AU - Maynard, Janielle P.

AU - De Marzo, Angelo M.

AU - Antonarakis, Emmanuel S.

AU - Sfanos, Karen S.

AU - Joshu, Corinne E.

AU - Shenderov, Eugene

AU - Lotan, Tamara L.

N1 - Funding Information: Ashley E. Ross reports personal fees and honoraria from Veracyte, Astellas, Bayer, Pfizer, Blue Earth, Myovant, and Janssen outside the submitted work. Mary‐Ellen Taplin reports honoraria from AstraZeneca, AbbVie, Astellas, Bauer, Blue Earth, Constellation, Celegene, Epizyme, GlaxoSmithKline, Incyte, Janssen, Myovant, Roviant, UpToDate, the University of Pittsburgh, and the American Society for Clinical Oncology; and participation on a data safety monitoring board or advisory board for Clovis, Pfizer, and Myovant outside the submitted work. Nathan A. Lack reports personal fees from Nido Bioscience outside the submitted work. Angelo M. De Marzo reports research support from Janssen and Myriad during the conduct of the study and personal fees from Cepheid and Merck outside the submitted work. Emmanuel S. Antonarakis reports research funding to his institution from Janssen, Johnson & Johnson, Sanofi, Dendreon, Genentech, Novartis, Merck, Bristol Myers Squibb, AstraZeneca, and Constellation; grants or contracts from AstraZeneca, Celgene, Clovis, and Sanofi; personal fees from Aikido Pharma, Blue Earth Diagnostics, Dendreon, EcoR1, KeyQuest Health, Janssen, Pfizer, and Projects in Knowledge; is a co‐inventor of an AR‐V7 biomarker technology that has been licensed to Qiagen; and reports participation on a data safety monitoring board or advisory board for Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Clovis, Constellation, Curium, Eli Lilly and Company, Exact Sciences, Foundation Medicine, Invitae, Ismar, Merck, Orion, Sanofi, and Tempus outside the submitted work. Corinne E. Joshu reports institutional grants or contracts from the American Cancer Society and the National Institutes of Health outside the submitted work. Eugene Shenderov reports institutional research funding from Macrogenics and personal fees from Biopharma, Inc, Firstthough.IO, and Guidepoint Global outside the submitted work. Tamara L. Lotan reports research support from Roche/Ventana, DeepBio, and Myriad Genetics and support for attending meetings and/or travel from the Prostate Cancer Foundation outside the submitted work. The remaining authors made no disclosures. Funding Information: This research was supported in part by 2 Health Disparity Research Awards from the Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program (CDMRP‐PCRP) (W81XWH‐15‐1‐0661 to Edward M. Schaeffer and Tamara L. Lotan; W81XWH‐17‐1‐0286 to Karen S. Sfanos and Tamara L. Lotan). Additional funding and resources were provided by the National Institutes of Health/National Cancer Institute Prostate Specialized Centers Research Excellence (grant P50CA58236) and a National Cancer Institute Cancer Center Support grant (5P30CA006973‐52). Eugene Shenderov was supported by a Prostate Cancer Foundation Young Investigator Award and Congressionally Directed Medical Research Programs‐Prostate Cancer Research Program grant (W81XWH‐19‐1‐0511). Adriana A. Mendes was supported by a grant from the National Cancer Institute (T32CA193145). Publisher Copyright: © 2022 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.

PY - 2022/6/15

Y1 - 2022/6/15

N2 - Background: B7 homolog 3 (B7-H3) is an immunomodulatory molecule that is highly expressed in prostate cancer (PCa) and belongs to the B7 superfamily, which includes PD-L1. Immunotherapies (antibodies, antibody-drug conjugates, and chimeric antigen receptor T cells) targeting B7-H3 are currently in clinical trials; therefore, elucidating the molecular and immune microenvironment correlates of B7-H3 expression may help to guide trial design and interpretation. The authors tested the interconnected hypotheses that B7-H3 expression is associated with genetic racial ancestry, immune cell composition, and androgen receptor signaling in PCa. Methods: An automated, clinical-grade immunohistochemistry assay was developed by to digitally quantify B7-H3 protein expression across 2 racially diverse cohorts of primary PCa (1 with previously reported transcriptomic data) and pretreatment and posttreatment PCa tissues from a trial of intensive neoadjuvant hormonal therapy. Results: B7-H3 protein expression was significantly lower in self-identified Black patients and was inversely correlated with the percentage African ancestry. This association with race was independent of the significant association of B7-H3 protein expression with ERG/ETS and PTEN status. B7-H3 messenger RNA expression, but not B7-H3 protein expression, was significantly correlated with regulatory (FOXP3-positive) T-cell density. Finally, androgen receptor activity scores were significantly correlated with B7-H3 messenger RNA expression, and neoadjuvant intensive hormonal therapy was associated with a significant decrease in B7-H3 protein expression. Conclusions: The current data underscore the importance of studying racially and molecularly diverse PCa cohorts in the immunotherapy era. This study is among the first to use genetic ancestry markers to add to the emerging evidence that PCa in men of African ancestry may have a distinct biology associated with B7-H3 expression. Lay Summary: B7-H3 is an immunomodulatory molecule that is highly expressed in prostate cancer and is under investigation in clinical trials. The authors determined that B7-H3 protein expression is inversely correlated with an individual's proportion of African ancestry. The results demonstrate that B7-H3 messenger RNA expression is correlated with the density of tumor T-regulatory cells. Finally, in the first paired analysis of B7-H3 protein expression before and after neoadjuvant intensive hormone therapy, the authors determined that hormone therapy is associated with a decrease in B7-H3 protein levels, suggesting that androgen signaling may positively regulate B7-H3 expression. These results may help to guide the design of future clinical trials and to develop biomarkers of response in such trials.

AB - Background: B7 homolog 3 (B7-H3) is an immunomodulatory molecule that is highly expressed in prostate cancer (PCa) and belongs to the B7 superfamily, which includes PD-L1. Immunotherapies (antibodies, antibody-drug conjugates, and chimeric antigen receptor T cells) targeting B7-H3 are currently in clinical trials; therefore, elucidating the molecular and immune microenvironment correlates of B7-H3 expression may help to guide trial design and interpretation. The authors tested the interconnected hypotheses that B7-H3 expression is associated with genetic racial ancestry, immune cell composition, and androgen receptor signaling in PCa. Methods: An automated, clinical-grade immunohistochemistry assay was developed by to digitally quantify B7-H3 protein expression across 2 racially diverse cohorts of primary PCa (1 with previously reported transcriptomic data) and pretreatment and posttreatment PCa tissues from a trial of intensive neoadjuvant hormonal therapy. Results: B7-H3 protein expression was significantly lower in self-identified Black patients and was inversely correlated with the percentage African ancestry. This association with race was independent of the significant association of B7-H3 protein expression with ERG/ETS and PTEN status. B7-H3 messenger RNA expression, but not B7-H3 protein expression, was significantly correlated with regulatory (FOXP3-positive) T-cell density. Finally, androgen receptor activity scores were significantly correlated with B7-H3 messenger RNA expression, and neoadjuvant intensive hormonal therapy was associated with a significant decrease in B7-H3 protein expression. Conclusions: The current data underscore the importance of studying racially and molecularly diverse PCa cohorts in the immunotherapy era. This study is among the first to use genetic ancestry markers to add to the emerging evidence that PCa in men of African ancestry may have a distinct biology associated with B7-H3 expression. Lay Summary: B7-H3 is an immunomodulatory molecule that is highly expressed in prostate cancer and is under investigation in clinical trials. The authors determined that B7-H3 protein expression is inversely correlated with an individual's proportion of African ancestry. The results demonstrate that B7-H3 messenger RNA expression is correlated with the density of tumor T-regulatory cells. Finally, in the first paired analysis of B7-H3 protein expression before and after neoadjuvant intensive hormone therapy, the authors determined that hormone therapy is associated with a decrease in B7-H3 protein levels, suggesting that androgen signaling may positively regulate B7-H3 expression. These results may help to guide the design of future clinical trials and to develop biomarkers of response in such trials.

KW - African American

KW - B7 homolog 3 (B7-H3)

KW - ERG

KW - PTEN

KW - T cells

KW - androgen receptor (AR)

KW - prostatic adenocarcinoma

KW - tumor-infiltrating lymphocytes

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UR - http://www.scopus.com/inward/citedby.url?scp=85127283178&partnerID=8YFLogxK

U2 - 10.1002/cncr.34190

DO - 10.1002/cncr.34190

M3 - Article

C2 - 35333400

AN - SCOPUS:85127283178

SN - 0008-543X

VL - 128

SP - 2269

EP - 2280

JO - Cancer

JF - Cancer

IS - 12

ER -

Association of B7-H3 expression with racial ancestry, immune cell density, and androgen receptor activation in prostate cancer

Abstract

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