Evidence map›Paper›PMID 27225803›Full record

ArticleThe Prostate2016

Generation of a C57BL/6 MYC-Driven Mouse Model and Cell Line of Prostate Cancer.

Leigh Ellis, ShengYu Ku, Qiuhui Li, Gissou Azabdaftari, Joseph Seliski, Brian Olson, Colleen S Netherby, Dean G Tang, Scott I Abrams, David W Goodrich and 1 more

Abstract read
In one paragraph

Article in The Prostate, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

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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.

Leigh EllisGenitourinary Program, Roswell Park Cancer Institute, Buffalo, New York.
ShengYu KuGenitourinary Program, Roswell Park Cancer Institute, Buffalo, New York.
Qiuhui LiDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York.
Gissou AzabdaftariGenitourinary Program, Roswell Park Cancer Institute, Buffalo, New York.
Joseph SeliskiUniversity of Wisconsin Carbone Cancer Center, Madison, Wisconsin.
Brian OlsonUniversity of Wisconsin Carbone Cancer Center, Madison, Wisconsin.
Colleen S NetherbyDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
Dean G TangDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York.
Scott I AbramsDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
David W GoodrichDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York.
Roberto PiliDepartment of Medicine, Indiana University-Simon Cancer Center, Indianapolis, Indiana.

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
MULTIDISCIPLINARY APPROACHES TUMOR IMMUNOLOGYT32CA085183 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Scott I. Abrams · 2001 to 2026
$3.1M
IRF-8 as a Negative Regulator of CD11b+Gr-1+ Myeloid Cell Production and FunctionR01CA140622 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ABRAMS, SCOTT I. · 2011 to 2015
$2.0M
NCI NIH HHS P30 CA016056NCI NIH HHS P50 CA058236NCI NIH HHS R01 CA140622NCI NIH HHS T32 CA085183
6 · The paper itself

Abstract

introductionTransgenic mouse modeling is a favorable tool to reflect human prostate tumorigenesis and interactions between prostate cancer and the microenvironment. The use of GEMMs and derived cell lines represent powerful tools to study prostate cancer initiation and progression with an associated tumor microenvironment. Notably, such models provide the capacity for rapid preclinical therapy studies including immune therapies for prostate cancer treatment.

methodsBackcrossing FVB Hi-MYC mice with C57BL/6N mice, we established a Hi-MYC transgenic mouse model on a C57BL/6 background (B6MYC). In addition, using a conditional reprogramming method, a novel C57BL/6 MYC driven prostate adenocarcinoma cell line was generated.

resultsOur results demonstrate that disease progression is significantly delayed in B6MYC when compared to their FVB counterparts. Current data also indicates infiltrating immune cells are present in pre-cancer lesions, prostate intraepithelial neoplasia (PIN). Further, immunophenotyping of this immune infiltrate demonstrates the predominant population as myeloid-derived suppressor cells (MDSC). Also, we successfully generated a B6MYC-CaP cell line, and determined that this new PCa cell line express markers of luminal epithelial lineage. DISCUSSION: This novel model of PCa provides a new platform to understand the cross talk between MYC driven prostate cancer and the microenvironment. Importantly, these models will be an ideal tool to support the clinical development of immunotherapy as well as other novel therapeutic strategies for prostate cancer treatment. Prostate 76:1192-1202, 2016. © 2016 Wiley Periodicals, Inc.

Indexed as

Disease Models, AnimalDisease ProgressionAnimalsCell Line, TumorMaleMiceMice, Inbred C57BLMice, TransgenicProstatic NeoplasmsTumor Microenvironmentcell linemouse modelMYCprostate cancer

Identifiers

PMID27225803
PMCPMC6123824

What OpenQuestion holds

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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.