Evidence map›Paper›PMID 28856167›Full record

ArticleJournal of clinical & experimental oncology2017

Expressions of Orphan Nuclear Receptor TR3/Nur77 in Chronic Hepatopathy and Its Clinical Significance.

Yingling Zeng, Xiaoguang Ye, Degui Liao, Shizhang Huang, Huinan Mao, Dezheng Zhao, Huiyan Zeng

Abstract read
In one paragraph

Article in Journal of clinical & experimental oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 57% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

7 authors at 4 institutions in 2 countries.

Yingling ZengDepartments of Preventative Medicine, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.
Xiaoguang YeDepartments of Infectious Diseases, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.
Degui LiaoDepartments of Pathology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.
Shizhang HuangDepartments of Pathology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.
Huinan MaoDepartments of Preventative Medicine, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.
Dezheng ZhaoCenter for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
Huiyan ZengCenter for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNBeth Israel Deaconess Medical Center · USCenter for Vascular Biology Research · US

Funding

Orphan Nuclear Receptor TR3 in tumor angiogenesis and associated microvessel permR01CA133235 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2009 to 2013
$1.7M
Targeting orphan nuclear receptor TR3/Nur77 for tumor angiogenesisR03CA191463 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2015 to 2016
$174k
Down Syndrome Candidate Region 1 isoform 1L in tumor growth and metastasisR03CA194795 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2015 to 2016
$174k
NCI NIH HHS R01 CA133235NCI NIH HHS R03 CA191463NCI NIH HHS R03 CA194795
6 · The paper itself

Abstract

objectiveAlthough great success has been achieved in cancer treatment, current cancer therapies, including anti-tumorigenesis and anti-angiogenesis, still face the problems of insufficient efficacy, resistance and intrinsic refractoriness, in addition to their toxic side effects. There is a demand to identify additional targets that can be blocked to turn off the downstream effects of most, if not all, pathways. Our studies suggest that orphan nuclear receptor TR3 (human)/Nur77 (mouse) is such a target. Most recently, we reported that TR3/Nur77 expression in human hepatic cancer tissues correlates well with tumor progress, suggesting that TR3 is a specific therapeutic target for hepatic cancers. However, the correlation of TR3/Nur77 expression in hepatocellular carcinoma (HCC) with chronic hepatitis has not been studied.

methodsThe expression of TR3/Nur77 was analyzed in human primary hepatic cancer specimens from patients that have complete medical records with Immunohistochemically staining. The statistical analysis was used to access the significance of TR3 expression in tumor tissues, cirrhosis tissues and chronic hepatitis tissues with and without hepatitis B virus infection (HBV(+) and HBV(-)), which were obtained from para-tumor tissues.

resultsThe positive rates of TR3/Nur77 expression in hepatocellular carcinoma, cancerous liver cirrhosis and chronic hepatitis are 66.67%, 30%, and 20%, respectively, which are statistic significant (p<0.05). The positive rates of TR3/Nur77 expression in hepatocellular carcinoma are statistic significant (p<0.05) with 81.25% and 20% in HBV (+) or HBV (-), respectively.

conclusionThe positive expression rate of TR3/Nur77 in hepatocellular carcinoma is higher than that in chronic hepatitis and cirrhosis. The positive rate of TR3/Nur77 expression in hepatocellular carcinoma is higher with HBV infection than that without infection. Our results suggest that TR3/Nur77 plays an important role in the progression of chronic hepatitis, and the occurrence and development of HCC.

Indexed as

Chronic hepatitisCirrhosisHepatitis B virus (HBV)Hepatocellular carcinomaNuclear orphan receptor TR3Nur77

Identifiers

PMID28856167
PMCPMC5573240
OpenAlexW2626740745

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Registered trials

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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.