Evidence map›Paper›PMID 21512508›Full record

ArticleGene therapy2011

Tumor growth and metastasis suppression by Glipr1 gene-modified macrophages in a metastatic prostate cancer model.

K Tabata, S Kurosaka, M Watanabe, K Edamura, T Satoh, G Yang, E Abdelfattah, J Wang, A Goltsov, D Floryk and 1 more

Abstract read
In one paragraph

Article in Gene therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
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

11 authors at 3 institutions in 2 countries.

K TabataScott Department of Urology, Baylor College of Medicine, Houston, TX, USA.
S Kurosaka
M Watanabe
K Edamura
T Satoh
G Yang
E Abdelfattah
J Wang
A Goltsov
D Floryk
T C Thompson
Baylor College of Medicine · USSpanish Oncology Genitourinary Group · ESThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
Progression/Oncogene Induced Prostate CancerR01CA050588 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMPSON, TIMOTHY CHARLES · 1989 to 2011
$3.5M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388NCI NIH HHS R01 CA050588NCI NIH HHS R01 CA50588
6 · The paper itself

Abstract

We previously identified the mouse and human Glipr1 and GLIPR1/RTVP-1 genes, respectively, as direct p53 targets with proapoptotic activities in various cancer cell lines, including prostate cancer (PCa). Intratumoral injection of an adenoviral vector capable of efficient transduction and expression of Glipr1 (AdGlipr1) yielded promising therapeutic results in an orthotopic, metastatic mouse model of PCa. AdGlipr1-transduced macrophages (Mφ/Glipr1) generated greater surface expression of CD40, CD80 and major histocompatibility complex class II molecules and greater production of interleukin 12 (IL-12) and IL-6 in vitro than control macrophages did. Mechanistic analysis indicated that increased production of IL-12 in Mφ/Glipr1 depends on activation of the p38 signaling cascade. Mφ/Glipr1 injected into orthotopic 178-2BMA tumors in vivo resulted in significantly suppressed prostate tumor growth and spontaneous lung metastases and longer survival relative to those observed in control-treated mice. Furthermore, these preclinical data indicate the generation of systemic natural killer cell activity and tumor-specific cytotoxic T lymphocyte responses. Trafficking studies confirmed that intratumorally injected Mφ/Glipr1 could migrate to draining lymph nodes. Overall, our data suggest that this novel gene-modified cell approach is an effective treatment avenue that induces antitumor immune responses in preclinical studies.

Indexed as

AdenoviridaeAnimalsB7-1 AntigenCD40 AntigensGenetic TherapyGenetic VectorsInterleukin-12Interleukin-6Killer Cells, NaturalKineticsMacrophagesMaleMiceNeoplasm MetastasisProstatic NeoplasmsProteinsB7-1 AntigenCD40 AntigensGLIPR-2 protein, mouseInterleukin-12Interleukin-6Proteins

Identifiers

PMID21512508
PMCPMC3881531
OpenAlexW2113938742

What OpenQuestion holds

Textmetadata
LicenceTDM
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.