Evidence map›Paper›PMID 30429453›Full record

ArticleExperimental & molecular medicine2018

Clinical significance of APOB inactivation in hepatocellular carcinoma.

Gena Lee, Yun Seong Jeong, Do Won Kim, Min Jun Kwak, Jiwon Koh, Eun Wook Joo, Ju-Seog Lee, Susie Kah, Yeong-Eun Sim, Sun Young Yim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

41 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 4 institutions in 2 countries.

Gena LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yun Seong JeongDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Do Won KimDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Min Jun KwakDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jiwon KohDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Eun Wook JooDepartment of Gynecology, School of Medicine, Kyung Hee University, Seoul, Korea.
Ju-Seog LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Susie KahDepartment of Internal Medicine, School of Medicine, Kyung Hee University, Seoul, Korea.
Yeong-Eun SimDepartment of Internal Medicine, School of Medicine, Kyung Hee University, Seoul, Korea.
Sun Young YimDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. eug203@naver.com.
The University of Texas MD Anderson Cancer Center · USKyung Hee University · KRKorea University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings from The Cancer Genome Atlas project have provided a comprehensive map of genomic alterations that occur in hepatocellular carcinoma (HCC), including unexpected mutations in apolipoprotein B (APOB). We aimed to determine the clinical significance of this non-oncogenetic mutation in HCC. An Apob gene signature was derived from genes that differed between control mice and mice treated with siRNA specific for Apob (1.5-fold difference; P < 0.005). Human gene expression data were collected from four independent HCC cohorts (n = 941). A prediction model was constructed using Bayesian compound covariate prediction, and the robustness of the APOB gene signature was validated in HCC cohorts. The correlation of the APOB signature with previously validated gene signatures was performed, and network analysis was conducted using ingenuity pathway analysis. APOB inactivation was associated with poor prognosis when the APOB gene signature was applied in all human HCC cohorts. Poor prognosis with APOB inactivation was consistently observed through cross-validation with previously reported gene signatures (NCIP A, HS, high-recurrence SNUR, and high RS subtypes). Knowledge-based gene network analysis using genes that differed between low-APOB and high-APOB groups in all four cohorts revealed that low-APOB activity was associated with upregulation of oncogenic and metastatic regulators, such as HGF, MTIF, ERBB2, FOXM1, and CD44, and inhibition of tumor suppressors, such as TP53 and PTEN. In conclusion, APOB inactivation is associated with poor outcome in patients with HCC, and APOB may play a role in regulating multiple genes involved in HCC development.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsApolipoproteins BBiomarkers, TumorCarcinoma, HepatocellularFemaleGene Regulatory NetworksHep G2 CellsHumansLiver NeoplasmsMaleMiceMiddle AgedTranscriptomeApolipoproteins BBiomarkers, Tumor

Identifiers

PMID30429453
PMCPMC6235894
OpenAlexW2901438563

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.