Evidence map›Paper›PMID 25833323›Full record

ArticleHepatology (Baltimore, Md.)2015

Hepatic stellate cell and monocyte interaction contributes to poor prognosis in hepatocellular carcinoma.

Juling Ji, Tobias Eggert, Anuradha Budhu, Marshonna Forgues, Atsushi Takai, Hien Dang, Qinghai Ye, Ju-Seog Lee, Ji Hoon Kim, Tim F Greten and 1 more

Registry-linked trialAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04862949 (Organ-specific Responses to Atezolizumab Plus Bevacizumab in Patients With Advanced Hepatocellular Carcinoma), which is not on this map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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.

NCT04862949 completednot on this mapstarted 2021, after this paper: background citation

Organ-specific Responses to Atezolizumab Plus Bevacizumab in Patients With Advanced Hepatocellular Carcinoma

TypeobservationalSponsorCHA UniversityRan2021 to 2023Enrolled131ConditionsAdvanced Hepatocellular CarcinomaArmsAtezolizumab plus bevacizumab
3 · Its place in the literature

Who cites it

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
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  17. Fibroblasts in liver cancer: functions and therapeutic translation.The lancet. Gastroenterology & hepatology · 2023
    Review
  18. Article
  19. Article
  20. Article

33 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

11 authors at 6 institutions in 3 countries.

Juling JiLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Tobias EggertGastrointestinal Malignancy Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Anuradha BudhuLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Marshonna ForguesLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Atsushi TakaiLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Hien DangLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Qinghai YeLiver Cancer Institute, Fudan University, Shanghai, China.
Ju-Seog LeeDepartment of Systems Biology, University of Texas, M.D. Anderson Cancer Center, Houston, TX.
Ji Hoon KimDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Tim F GretenGastrointestinal Malignancy Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Xin Wei WangLiver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
National Cancer Institute · USCenter for Cancer Research · USFudan University Shanghai Cancer Center · CNGenesis Foundation · USKorea University · KRThe University of Texas MD Anderson Cancer Center · US

Funding

Analysis of myeloid derived suppressor cells in miceZIABC011345 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GRETEN, TIM · 2010 to 2025
$19.5M
Strategies for improving early detection, diagnosis and treatment of liver cancerZIABC010313 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN WEI · 2009 to 2025
$18.1M
Molecular signatures for liver cancer diagnosis and treatment stratificationZ01BC010313 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN WEI · 1999 to 2008
$1.8M
The role of cancer stem cells in liver cancer heterogeneity and subtypesZ01BC010876 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN · 2008 to 2008
$490k
The identification of human hepatocellular carcinoma metastasis genesZ01BC010877 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN · 2008 to 2008
$327k
Intramural NIH HHS Z01 BC010313Intramural NIH HHS Z01 BC010876Intramural NIH HHS Z01 BC010877NCI NIH HHS Z01-BC 010313NCI NIH HHS Z01-BC010877
6 · The paper itself

Abstract

unlabelledHepatocellular carcinoma (HCC) patients suffer from a poor survival rate and a high incidence of postoperative recurrence. The hepatic microenvironment plays a significant role in the initiation, progression, and recurrence of HCC; however, the causal mechanisms of these phenomena are unclear. Given the predominant underlying fibrotic and cirrhotic conditions of the liver prone to HCC and its recurrence, alterations of components of the inflammatory milieu have been suggested as factors that promote HCC development. In particular, activated hepatic stellate cells (A-HSCs), which play a key role in liver fibrosis and cirrhosis, have been suggested as contributors to the HCC-prone microenvironment. Here, we have identified and validated an A-HSC-specific gene expression signature among nontumor tissues of 319 HCC patients that is significantly and independently associated with HCC recurrence and survival. Peritumoral, rather than tumor tissue-related, A-HSC-specific gene expression is associated with recurrence and poor survival. Analyses of A-HSC-specific gene signatures and further immunohistochemical validation in an additional 143 HCC patients have revealed that A-HSCs preferentially affect monocyte populations, shifting their gene expression from an inflammatory to an immunosuppressive signature. In addition, the interaction between A-HSCs and monocytes induces protumorigenic and progressive features of HCC cells by enhancing cell migration and tumor sphere formation.

conclusionA-HSCs play a significant role in promoting HCC progression through interaction with and alteration of monocyte activities within the liver microenvironment; thus, disrupting the interactions and signaling events between the inflammatory milieu and components of the microenvironment may be useful therapeutic strategies for preventing HCC tumor relapse.

Indexed as

Cell CommunicationAgedAnalysis of VarianceBiomarkers, TumorCarcinoma, HepatocellularCell MovementFemaleHepatic Stellate CellsHumansLiver NeoplasmsMaleMiddle AgedMonocytesMultivariate AnalysisNeoplasm Recurrence, LocalPredictive Value of TestsBiomarkers, Tumor

Identifiers

PMID25833323
PMCPMC4515211
OpenAlexW1493921738

What OpenQuestion holds

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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.