Natural Killer Cell Infiltration in Prostate Cancers Predict Improved Patient Outcomes.


Journal

Prostate cancer and prostatic diseases
ISSN: 1476-5608
Titre abrégé: Prostate Cancer Prostatic Dis
Pays: England
ID NLM: 9815755

Informations de publication

Date de publication:
28 Feb 2024
Historique:
received: 08 10 2023
accepted: 22 01 2024
revised: 17 01 2024
medline: 29 2 2024
pubmed: 29 2 2024
entrez: 28 2 2024
Statut: aheadofprint

Résumé

Natural killer (NK) cells are non-antigen specific innate immune cells that can be redirected to targets of interest using multiple strategies, although none are currently FDA-approved. We sought to evaluate NK cell infiltration into tumors to develop an improved understanding of which histologies may be most amenable to NK cell-based therapies currently in the developmental pipeline. DNA (targeted/whole-exome) and RNA (whole-transcriptome) sequencing was performed from tumors from 45 cancer types (N = 90,916 for all cancers and N = 3365 for prostate cancer) submitted to Caris Life Sciences. NK cell fractions and immune deconvolution were inferred from RNA-seq data using quanTIseq. Real-world overall survival (OS) and treatment status was determined and Kaplan-Meier estimates were calculated. Statistical significance was determined using X In both a pan-tumor and prostate cancer (PCa) -specific setting, we demonstrated that NK cells represent a substantial proportion of the total cellular infiltrate (median range 2-9% for all tumors). Higher NK cell infiltration was associated with improved OS in 28 of 45 cancer types, including (PCa). NK cell infiltration was negatively correlated with common driver mutations and androgen receptor variants (AR-V7) in primary prostate biopsies, while positively correlated with negative immune regulators. Higher levels of NK cell infiltration were associated with patterns consistent with a compensatory anti-inflammatory response. Using the largest available dataset to date, we demonstrated that NK cells infiltrate a broad range of tumors, including both primary and metastatic PCa. NK cell infiltration is associated with improved PCa patient outcomes. This study demonstrates that NK cells are capable of trafficking to both primary and metastatic PCa and are a viable option for immunotherapy approaches moving forward. Future development of strategies to enhance tumor-infiltrating NK cell-mediated cytolytic activity and activation while limiting inhibitory pathways will be key.

Sections du résumé

BACKGROUND BACKGROUND
Natural killer (NK) cells are non-antigen specific innate immune cells that can be redirected to targets of interest using multiple strategies, although none are currently FDA-approved. We sought to evaluate NK cell infiltration into tumors to develop an improved understanding of which histologies may be most amenable to NK cell-based therapies currently in the developmental pipeline.
METHODS METHODS
DNA (targeted/whole-exome) and RNA (whole-transcriptome) sequencing was performed from tumors from 45 cancer types (N = 90,916 for all cancers and N = 3365 for prostate cancer) submitted to Caris Life Sciences. NK cell fractions and immune deconvolution were inferred from RNA-seq data using quanTIseq. Real-world overall survival (OS) and treatment status was determined and Kaplan-Meier estimates were calculated. Statistical significance was determined using X
RESULTS RESULTS
In both a pan-tumor and prostate cancer (PCa) -specific setting, we demonstrated that NK cells represent a substantial proportion of the total cellular infiltrate (median range 2-9% for all tumors). Higher NK cell infiltration was associated with improved OS in 28 of 45 cancer types, including (PCa). NK cell infiltration was negatively correlated with common driver mutations and androgen receptor variants (AR-V7) in primary prostate biopsies, while positively correlated with negative immune regulators. Higher levels of NK cell infiltration were associated with patterns consistent with a compensatory anti-inflammatory response.
CONCLUSIONS CONCLUSIONS
Using the largest available dataset to date, we demonstrated that NK cells infiltrate a broad range of tumors, including both primary and metastatic PCa. NK cell infiltration is associated with improved PCa patient outcomes. This study demonstrates that NK cells are capable of trafficking to both primary and metastatic PCa and are a viable option for immunotherapy approaches moving forward. Future development of strategies to enhance tumor-infiltrating NK cell-mediated cytolytic activity and activation while limiting inhibitory pathways will be key.

Identifiants

pubmed: 38418892
doi: 10.1038/s41391-024-00797-0
pii: 10.1038/s41391-024-00797-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIGMS NIH HHS
ID : T32 GM008244
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM008244
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA283892
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA111412
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA077598
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA111412
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA065493
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA283892
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA065493
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA111412
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA077598
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA077598
Pays : United States

Informations de copyright

© 2024. The Author(s).

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Auteurs

Nicholas A Zorko (NA)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA. zorko004@umn.edu.

Allison Makovec (A)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Andrew Elliott (A)

Caris Life Sciences, Phoenix, AZ, USA.

Samuel Kellen (S)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

John R Lozada (JR)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Ali T Arafa (AT)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Martin Felices (M)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Madison Shackelford (M)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Pedro Barata (P)

University Hospital Seidman Cancer Center, Cleveland, OH, USA.

Yousef Zakharia (Y)

Holden Comprehensive Cancer Center, Iowa City, IA, USA.

Vivek Narayan (V)

Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.

Mark N Stein (MN)

Herbert Irving Comprehensive Cancer Center, Columbia University New York, New York, NY, USA.

Kevin K Zarrabi (KK)

Sidney Kimmel Cancer Center, Jefferson Medical College, Philadelphia, PA, USA.

Akash Patniak (A)

University of Chicago Medicine Comprehensive Cancer Center, Chicago, IL, USA.

Mehmet A Bilen (MA)

Winship Cancer Institute of Emory University, Atlanta, GA, USA.

Milan Radovich (M)

Caris Life Sciences, Phoenix, AZ, USA.

George Sledge (G)

Caris Life Sciences, Phoenix, AZ, USA.

Wafik S El-Deiry (WS)

Legorreta Cancer Center, Brown University, Providence, RI, USA.

Elisabeth I Heath (EI)

Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.

Dave S B Hoon (DSB)

Saint John's Cancer Institute, Saint John's Health Center PHS, Santa Monica, CA, USA.

Chadi Nabhan (C)

Caris Life Sciences, Phoenix, AZ, USA.

Jeffrey S Miller (JS)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Justin H Hwang (JH)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Emmanuel S Antonarakis (ES)

Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, MN, USA.

Classifications MeSH