Evidence map›Paper›PMID 20395201›Full record

ArticleCancer research2010

Ectopic expression of X-linked lymphocyte-regulated protein pM1 renders tumor cells resistant to antitumor immunity.

Tae Heung Kang, Kyung Hee Noh, Jin Hee Kim, Hyun Cheol Bae, Ken Y Lin, Archana Monie, Sara I Pai, Chien-Fu Hung, T-C Wu, Tae Woo Kim

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  6. NBCe1 NaWorld journal of cardiology · 2018
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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

10 authors at 2 institutions in 1 country.

Tae Heung KangDivison of Infection and Immunology, Graduate School of Medicine, Korea University, Seoul, South Korea.
Kyung Hee Noh
Jin Hee Kim
Hyun Cheol Bae
Ken Y Lin
Archana Monie
Sara I Pai
Chien-Fu Hung
T-C Wu
Tae Woo Kim
Johns Hopkins University · USYale University · US

Funding

Treatment of HIV- and HIV+ Patients with HPV16+ CIN2/3 Using pNGLV4a-hCRTE6E7L2 DNA vaccine administered intramuscularly via electroporationP50CA098252 · NCI · JOHNS HOPKINS UNIVERSITY · PI Richard Bruce Roden · 2003 to 2026
$53.5M
Tumor Suppressor Gene Promoter Hypermethylation for Detection of Head/Neck CancerP50CA096784 · NCI · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 2002 to 2006
$11.3M
ENHANCING HPV-16 E6-SPECIFIC ANTITUMOR IMMUNITYR01CA114425 · NCI · JOHNS HOPKINS UNIVERSITY · PI WU, TZYY-CHOOU · 2005 to 2016
$3.0M
NCI NIH HHS 1R01 CA114425-01NCI NIH HHS P50 CA096784NCI NIH HHS P50 CA098252NCI NIH HHS P50 CA96784-06NCI NIH HHS R01 CA114425
6 · The paper itself

Abstract

Tumor immune escape is a major obstacle in cancer immunotherapy, but the mechanisms involved remain poorly understood. We have previously developed an immune evasion tumor model using an in vivo immune selection strategy and revealed Akt-mediated immune resistance to antitumor immunity induced by various cancer immunotherapeutic agents. In the current study, we used microarray gene analysis to identify an Akt-activating candidate molecule overexpressed in immune-resistant tumors compared with parental tumors. X-linked lymphocyte-regulated protein pM1 (XLR) gene was the most upregulated in immune-resistant tumors compared with parental tumor cells. Furthermore, the retroviral transduction of XLR in parental tumor cells led to activation of Akt, resulting in upregulation of antiapoptotic proteins and the induction of immune resistance phenotype in parental tumor cells. In addition, we found that transduction of parental tumor cells with other homologous genes from the mouse XLR family, such as synaptonemal complex protein 3 (SCP3) and XLR-related, meiosis-regulated protein (XMR) and its human counterpart of SCP3 (hSCP3), also led to activation of Akt, resulting in the upregulation of antiapoptotic proteins and induction of immune resistance phenotype. Importantly, characterization of a panel of human cervical cancers revealed relatively higher expression levels of hSCP3 in human cervical cancer tissue compared with normal cervical tissue. Thus, our data indicate that ectopic expression of XLR and its homologues in tumor cells represents a potentially important mechanism for tumor immune evasion and serves as a promising molecular target for cancer immunotherapy.

Indexed as

Genes, X-LinkedAnimalsApoptosisCell Cycle ProteinsDNA-Binding ProteinsFemaleHumansImmune SystemImmunotherapyLymphocytesMiceMice, Inbred C57BLNeoplasmsNuclear ProteinsCell Cycle ProteinsDNA-Binding ProteinsNuclear ProteinsSYCP3 protein, humanSycp3 protein, mouseXLRL protein, humanXlr nuclear protein, mouse

Identifiers

PMID20395201
PMCPMC2861497
OpenAlexW2169532106

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.