Evidence map›Paper›PMID 18381452›Full record

ArticleCancer research2008

Signatures associated with rejection or recurrence in HER-2/neu-positive mammary tumors.

Andrea Worschech, Maciej Kmieciak, Keith L Knutson, Harry D Bear, Aladar A Szalay, Ena Wang, Francesco M Marincola, Masoud H Manjili

Abstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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  7. Synthesis and characterization of intrinsically radiolabeled quantum dots for bimodal detection.American journal of nuclear medicine and molecular imaging · 2012
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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

8 authors at 4 institutions in 1 country.

Andrea WorschechDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Massey Cancer Center, Richmond, VA 23298, USA.
Maciej Kmieciak
Keith L Knutson
Harry D Bear
Aladar A Szalay
Ena Wang
Francesco M Marincola
Masoud H Manjili
Fleet Science Center · USGenelux (United States) · USMayo Clinic · USVirginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
Enhancement of HER-2/neu-based therapy using HSP110R01CA104757 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MANJILI, MASOUD H. · 2005 to 2008
$912k
Immunogenetics of Vaccine TherapyZIACL002115 · CLC · CLINICAL CENTER · PI MARINCOLA, FRANCESCO M · 2009 to 2010
$0k
Immunogenetic Study of Infectious Diseases and CancerZIACL002118 · CLC · CLINICAL CENTER · PI MARINCOLA, FRANCESCO M · 2009 to 2012
$0k
NCI NIH HHS P30 CA016059NCI NIH HHS P30CA16059NCI NIH HHS R01 CA104757
6 · The paper itself

Abstract

We have previously shown T-cell-mediated rejection of the neu-overexpressing mammary carcinoma cells (MMC) in wild-type FVB mice. However, following rejection of primary tumors, a fraction of animals experienced a recurrence of a neu antigen-negative variant (ANV) of MMC (tumor evasion model) after a long latency period. In the present study, we determined that T cells derived from wild-type FVB mice can specifically recognize MMC by secreting IFN-gamma and can induce apoptosis of MMC in vitro. Neu transgenic (FVBN202) mice develop spontaneous tumors and cannot reject it (tumor tolerance model). To dissect the mechanisms associated with rejection or tolerance of MMC tumors, we compared transcriptional patterns within the tumor microenvironment of MMC undergoing rejection with those that resisted it either because of tumor evasion/antigen loss recurrence (ANV tumors) or because of intrinsic tolerance mechanisms displayed by the transgenic mice. Gene profiling confirmed that immune rejection is primarily mediated through activation of IFN-stimulated genes and T-cell effector mechanisms. The tumor evasion model showed combined activation of Th1 and Th2 with a deviation toward Th2 and humoral immune responses that failed to achieve rejection likely because of lack of target antigen. Interestingly, the tumor tolerance model instead displayed immune suppression pathways through activation of regulatory mechanisms that included in particular the overexpression of interleukin-10 (IL-10), IL-10 receptor, and suppressor of cytokine signaling (SOCS)-1 and SOCS-3. These data provide a road map for the identification of novel biomarkers of immune responsiveness in clinical trials.

Indexed as

AnimalsApoptosisBiomarkers, TumorCell Line, TumorErb-b2 Receptor Tyrosine KinasesFemaleImmune ToleranceImmunotherapy, AdoptiveInterleukin-10Mammary Neoplasms, ExperimentalMiceNeoplasm Recurrence, LocalRatsReceptors, Interleukin-10Suppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsBiomarkers, TumorErb-b2 Receptor Tyrosine KinasesInterleukin-10Receptors, Interleukin-10Socs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID18381452
PMCPMC2478745
OpenAlexW2117267351

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.