Das neue ISUP 2014/WHO 2016 Prostatakarzinom-Grading – Status quo 5 Jahre nach seiner Einführung

Hupe, Marie C.; Offermann, Anne; Sailer, Verena; Merseburger, Axel S.

doi:10.1055/a-0918-9473

Cited by 3 publications

(1 citation statement)

References 23 publications

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“…Prior to treatment, individual PCa stages are defined, with prostatic adenocarcinomas being the predominant variant [3]. To precisely assess cancer aggressiveness and thus determine appropriate therapy options, the Gleason score or the resulting WHO grading systems are recommended [11,12]. Both systems are based on the evaluation of histological tumor structures, differentiation stages, and gland cell morphologies.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Several Pathways for Efficient Killing of Prostate Cancer Stem Cells: A Central Role of NF-κB RELA

Witte

Pfitzenmaier

Storm

et al. 2021

IJMS

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Prostate cancer is a common cause of death worldwide. Here, we isolated cancer stem cells (CSCs) from four adenocarcinomas of the prostate (Gleason scores from 3 + 3 up to 4 + 5). CSCs were characterized by the expression of the stem cell markers TWIST, the epithelial cell adhesion molecule (EPCAM), the transcription factors SNAI1 (SNAIL) and SNAI2 (SLUG) and cancer markers such as CD44 and prominin-1 (CD133). All investigated CSC populations contained a fraction highly positive for aldehyde dehydrogenase (ALDH) function and displayed robust expressions of programmed cell death 1 (PD-1) ligands. Furthermore, we investigated immunotherapeutic approaches but had no success even with the clinically used PD-1 inhibitor pembrolizumab. In addition, we studied another death-inducing pathway via interferon gamma signaling and detected high-level upregulations of human leukocyte antigen A (HLA-A) and beta 2-microglobulin (B2M) with only moderate killing efficacy. To examine further killing mechanisms in prostate cancer stem cells (PCSCs), we analyzed NF-κB signaling. Surprisingly, two patient-specific populations of PCSCs were found: one with canonical NF-κB signaling and another one with blunted NF-κB activation, which can be efficiently killed by tumor necrosis factor (TNF). Thus, culturing of PCSCs and analysis of respective NF-κB induction potency after surgery might be a powerful tool for optimizing patient-specific treatment options, such as the use of TNF-inducing chemotherapeutics and/or NF-κB inhibitors.

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Section: Introductionmentioning

confidence: 99%