Myeloid-Derived Suppressor Cells in Nonmetastatic Urothelial Carcinoma of Bladder Is Associated With Pathologic Complete Response and Overall Survival.


Journal

Clinical genitourinary cancer
ISSN: 1938-0682
Titre abrégé: Clin Genitourin Cancer
Pays: United States
ID NLM: 101260955

Informations de publication

Date de publication:
12 2020
Historique:
received: 22 12 2019
revised: 02 03 2020
accepted: 03 03 2020
pubmed: 29 4 2020
medline: 19 8 2021
entrez: 29 4 2020
Statut: ppublish

Résumé

Myeloid-derived suppressor cells (MDSC) have immunosuppressive activity and enhance tumor progression. We hypothesized that lower blood MDSC would correlate with pathologic complete response and better outcomes in nonmetastatic urothelial carcinoma (UC). Before cystectomy, blood MDSC were measured in whole blood (WB) and peripheral blood mononuclear cells using flow cytometry. MDSC were defined as CD33 Overall, 109 patients were included: 86% men with median (range) age of 67 (30-88) years, 76% with pure UC, 29% intravesical therapy, and 41% neoadjuvant chemotherapy. Twenty-one patients (19%) had pT0N0 and 23 (24%) < pT2N0. Median (range) follow-up time was 17.4 (0.4-42.4) months. Total MDSC and polymorphonuclear MDSC percentage in peripheral blood mononuclear cells was significantly lower in patients with pT0N0 disease (P = .03). One- and 2-year OS rates were 94% (95% confidence interval [CI], 90-99) and 83% (95% CI, 75-93), respectively. In the multivariate Cox model after adjusting for age and gender, patients with higher WB M-MDSC and UnC-MDSC had shorter OS (optimal cutoff points by recursive partitioning analysis, hazard ratio = 7.5 [95% CI, 2.5-22.8], P = .0004; hazard ratio = 3.4 [95% CI, 1.0-11.0], P = .046, respectively). In patients with nonmetastatic UC of bladder, higher WB M-MDSC and UnC-MDSC before cystectomy had negative prognostic value. Prospective validation is warranted.

Sections du résumé

BACKGROUND
Myeloid-derived suppressor cells (MDSC) have immunosuppressive activity and enhance tumor progression. We hypothesized that lower blood MDSC would correlate with pathologic complete response and better outcomes in nonmetastatic urothelial carcinoma (UC).
PATIENTS AND METHODS
Before cystectomy, blood MDSC were measured in whole blood (WB) and peripheral blood mononuclear cells using flow cytometry. MDSC were defined as CD33
RESULTS
Overall, 109 patients were included: 86% men with median (range) age of 67 (30-88) years, 76% with pure UC, 29% intravesical therapy, and 41% neoadjuvant chemotherapy. Twenty-one patients (19%) had pT0N0 and 23 (24%) < pT2N0. Median (range) follow-up time was 17.4 (0.4-42.4) months. Total MDSC and polymorphonuclear MDSC percentage in peripheral blood mononuclear cells was significantly lower in patients with pT0N0 disease (P = .03). One- and 2-year OS rates were 94% (95% confidence interval [CI], 90-99) and 83% (95% CI, 75-93), respectively. In the multivariate Cox model after adjusting for age and gender, patients with higher WB M-MDSC and UnC-MDSC had shorter OS (optimal cutoff points by recursive partitioning analysis, hazard ratio = 7.5 [95% CI, 2.5-22.8], P = .0004; hazard ratio = 3.4 [95% CI, 1.0-11.0], P = .046, respectively).
CONCLUSION
In patients with nonmetastatic UC of bladder, higher WB M-MDSC and UnC-MDSC before cystectomy had negative prognostic value. Prospective validation is warranted.

Identifiants

pubmed: 32340875
pii: S1558-7673(20)30053-7
doi: 10.1016/j.clgc.2020.03.004
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

500-508

Subventions

Organisme : NCI NIH HHS
ID : L30 CA220908
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Jaleh Fallah (J)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

Claudia Marcela Diaz-Montero (CM)

Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Patricia Rayman (P)

Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Wei Wei (W)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

James H Finke (JH)

Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Jin S Kim (JS)

Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Paul G Pavicic (PG)

Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Marcelo Lamenza (M)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

Priscilla Dann (P)

Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland, OH.

Donna Company (D)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

Andrew Stephenson (A)

Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland, OH.

Steven Campbell (S)

Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland, OH.

George Haber (G)

Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland, OH.

Byron Lee (B)

Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland, OH.

Omar Mian (O)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH; Lerner Research Institute, Cleveland Clinic, Cleveland, OH.

Timothy Gilligan (T)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

Jorge A Garcia (JA)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.

Brian Rini (B)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH; Division of Hematology & Oncology, Vanderbilt-Ingram Cancer Center, Nashville, TN.

Moshe C Ornstein (MC)

Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH. Electronic address: ornstem@ccf.org.

Petros Grivas (P)

Department of Medicine, Division of Oncology, University of Washington and Fred Hutchinson Cancer Research Center, Seattle, WA. Electronic address: pgrivas@uw.edu.

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