Evidence map›Paper›PMID 18836471›Full record

ReviewOncogene2008

The tumor microenvironment and its role in promoting tumor growth.

T L Whiteside

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06056791 (An Open-label, Phase I/IIa Dose Escalation and Expansion Study to Determine the Safety and Clinical Activity of an Immune Priming Cell Therapy), which is not on this map. Cited by 1,232 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,232citing papers in PubMed, 2 pooled it
17.7field-weighted citation impact, top 1% 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.

NCT06056791 phase1 / phase2completednot on this mapstarted 2023, after this paper: background citation

An Open-label, Phase I/IIa Dose Escalation and Expansion Study to Determine the Safety and Clinical Activity of an Immune Priming Cell Therapy (INKmune) in Patients With Metastatic Castration Resistant Prostate Cancer (mCRPC)

TypeinterventionalSponsorInmune Bio, Inc.Ran2023 to 2025Enrolled12ConditionsCancer, Metastatic Castration-resistant Prostate Cancer, mCRPCArmsINKmune
3 · Its place in the literature

Who cites it

1,232 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2,354 citations in OpenAlex.

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1,172 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

1 author at 1 institution in 1 country.

T L WhitesideUniversity of Pittsburgh School of Medicine and The Hillman Cancer Center, Pittsburgh, PA 15213, USA. whitesidetl@upmc.edu
UPMC Hillman Cancer Center · US

Funding

Tissue Procurement / ImmunohistologyP01CA109688 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECICH, MICHAEL JOHN · 2006 to 2010
$5.9M
NCI NIH HHS P0-1 CA109688NCI NIH HHS P01 CA109688
6 · The paper itself

Abstract

The tumor microenvironment is created by the tumor and dominated by tumor-induced interactions. Although various immune effector cells are recruited to the tumor site, their anti-tumor functions are downregulated, largely in response to tumor-derived signals. Infiltrates of inflammatory cells present in human tumors are chronic in nature and are enriched in regulatory T cells (T(reg)) as well as myeloid suppressor cells (MSC). Immune cells in the tumor microenvironment not only fail to exercise antitumor effector functions, but they are co-opted to promote tumor growth. Sustained activation of the NF-kappaB pathway in the tumor milieu represents one mechanism that appears to favor tumor survival and drive abortive activation of immune cells. The result is tumor escape from the host immune system. Tumor escape is accomplished through the activation of one or several molecular mechanisms that lead to inhibition of immune cell functions or to apoptosis of anti-tumor effector cells. The ability to block tumor escape depends on a better understanding of cellular and molecular pathways operating in the tumor microenvironment. Novel therapeutic strategies that emerge are designed to change the pro-tumor microenvironment to one favoring acute responses and potent anti-tumor activity.

Indexed as

Cell ProliferationAnimalsCell CommunicationExtracellular FluidHumansImmunotherapyInflammationModels, BiologicalNeoplasmsTumor BurdenTumor Escape

Identifiers

PMID18836471
PMCPMC3689267
OpenAlexW2126882378

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.