Evidence map›Paper›PMID 15314693›Full record

ArticleThe Journal of clinical investigation2004

Prevalent expression of the immunostimulatory MHC class I chain-related molecule is counteracted by shedding in prostate cancer.

Jennifer D Wu, Lily M Higgins, Alexander Steinle, David Cosman, Kathy Haugk, Stephen R Plymate

Abstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

153 citing papers in PubMed, 301 citations in OpenAlex.

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  18. Reversal of Lactate and PD-1-mediated Macrophage Immunosuppression Controls Growth of PTEN/p53-deficient Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
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93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Jennifer D WuDepartment of Medicine, University of Washington, 325 9th Avenue, Seattle, WA 98104, USA. wuj@u.washington.edu
Lily M Higgins
Alexander Steinle
David Cosman
Kathy Haugk
Stephen R Plymate
University of Washington · USAmgen (United States) · USGeriatric Research Education and Clinical Center · USUniversity of Tübingen · DE

Funding

Transmembrane Proteases and Prostate CarcinogenesisP01CA085859 · NCI · UNIVERSITY OF WASHINGTON · PI VESSELLA, ROBERT LOUIS · 2002 to 2013
$21.2M
REGULATION OF PROSTATE EPITHELIAL CELL GROWTHR01DK052683 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI WARE, JOY LAURIN · 1998 to 2005
$1.3M
NCI NIH HHS P01 CA085859NCI NIH HHS P01 CA 85859NIDDK NIH HHS R01 DK052683NIDDK NIH HHS R01 DK 52683
6 · The paper itself

Abstract

The MHC class I chain-related molecules (MICs) have previously been shown to be induced on most epithelial tumor cells. Engagement of MIC by the activating immune receptor NKG2D triggers NK cells and augments antigen-specific CTL anti-tumor immunity. The MIC-NKG2D system was proposed to participate in epithelial tumor immune surveillance. Paradoxically, studies suggest that tumors may evade MIC-NKG2D-mediated immunity by MIC shedding-induced impairment of effector cell function. Here we demonstrate the first evidence to our knowledge of a significant correlation of MIC shedding and deficiency in NK cell function with the grade of disease in prostate cancer. MIC is widely expressed in prostate carcinoma. The presence of surface target MIC, however, is counteracted by shedding. A significant increase in serum levels of soluble MIC (sMIC) and deficiency in NK cell function was shown in patients with advanced cancer. Finally, the deficiency in NK cell function can be overcome by treatment with IL-2 or IL-15 in vitro. Our results suggest that (a) deficiency in MIC-NKG2D immune surveillance may contribute to prostate cancer progression, (b) sMIC may be a novel biomarker for prostate cancer, and (c) using cytokines to restore MIC-NKG2D-mediated immunity may have clinical significance for prostate cancer in cell-based adaptive immunotherapy.

Indexed as

AgedAged, 80 and overCarcinomaCD56 AntigenCell Line, TumorCytotoxicity, ImmunologicHistocompatibility Antigens Class IHLA-A AntigensHumansImmunologic SurveillanceInterleukin-15Interleukin-2Killer Cells, NaturalLymphocyte ActivationMaleMiddle AgedCD56 AntigenHistocompatibility Antigens Class IHLA-A AntigensInterleukin-15Interleukin-2KLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KProstate-Specific AntigenReceptors, ImmunologicReceptors, Natural Killer Cell

Identifiers

PMID15314693
PMCPMC503776
OpenAlexW1972814015

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.