Evidence map›Paper›PMID 20850540›Full record

ReviewSeminars in cancer biology2011

Intracellular signaling and hepatocellular carcinoma.

Polina Iakova, Lubov Timchenko, Nikolai A Timchenko

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. p53 mApoptosis : an international journal on programmed cell death · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Oncotarget · 2018
    Article
  11. Article
  12. Article
  13. Gankyrin Promotes Tumor-Suppressor Protein Degradation to Drive Hepatocyte Proliferation.Cellular and molecular gastroenterology and hepatology · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Polina IakovaDepartment of Pathology and Immunology and Huffington Center on Aging, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, United States.
Lubov Timchenko
Nikolai A Timchenko
Baylor College of Medicine · US

Funding

STUDIES OF THE MRG15 GENE IN CELL CYCLE AND CELL SENESCENCEP01AG020752 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI SMITH, JAMES · 2001 to 2005
$8.5M
Molecular Mechanisms of C/EBP Alpha Mediated Growth ArrestR01GM055188 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI TIMCHENKO, NIKOLAI A. · 1997 to 2013
$3.3M
Myotonic Dystrophy Type 2R01AR052791 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI TIMCHENKO, LUBOV T · 2005 to 2015
$3.1M
Molecular mechanisms of Myotonic Dystrophy 1R01AR044387 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI TIMCHENKO, LUBOV T · 1997 to 2012
$2.8M
Regulation of Cell Growth by RNA Binding ProteinsR01CA100070 · NCI · BAYLOR COLLEGE OF MEDICINE · PI TIMCHENKO, NIKOLAI A. · 2003 to 2012
$2.6M
Role of Age in Liver CancerR01CA159942 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI TIMCHENKO, NIKOLAI A. · 2011 to 2015
$1.6M
Mechanisms of decay of toxic CUGn RNA in DM1 patientsR03NS063298 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI TIMCHENKO, LUBOV T · 2008 to 2009
$154k
NCI NIH HHS CA100070NCI NIH HHS R01 CA100070NCI NIH HHS R01 CA159942NIAMS NIH HHS AR044387NIAMS NIH HHS AR052791NIAMS NIH HHS R01 AR044387NIAMS NIH HHS R01 AR052791NIA NIH HHS AG20752NIA NIH HHS P01 AG020752NIGMS NIH HHS GM55188NIGMS NIH HHS R01 GM055188NINDS NIH HHS NS063298NINDS NIH HHS R03 NS063298
6 · The paper itself

Abstract

Liver cancer is the fifth most common cancer and the third most common cause of cancer related death in the world. The recent development of new techniques for the investigations of global change in the gene expression, signaling pathways and wide genome binding has provided novel information for the mechanisms underlying liver cancer progression. Although these studies identified gene expression signatures in hepatocellular carcinoma, the early steps of the development of hepatocellular carcinomas (HCC) are not well understood. The development of HCC is a multistep process which includes the progressive alterations of gene expression leading to the increased proliferation and to liver cancer. This review summarizes recent progress in the identification of the key steps of the development of HCC with the focus on early events of carcinogenesis and on the role of translational and epigenetic alterations in the development of HCC. Quiescent stage of the liver is supported by several tumor suppressor proteins including p53, Rb and C/EBPα. Studies with chemical models of liver carcinogenesis and with human HCC have shown that the elevation of gankyrin is responsible for the elimination of these three proteins at early steps of carcinogenesis. Later stages of progression of the liver cancer are associated with alterations in many signaling pathways including translation which leads to epigenetic silencing/activation of many genes. Particularly, recent reports suggest a critical role of histone deacetylase 1, HDAC1, in the development of HCC through the interactions with transcription factors such as C/EBP family proteins.

Indexed as

Signal TransductionAnimalsCarcinoma, HepatocellularCCAAT-Enhancer-Binding ProteinsDisease Models, AnimalHumansIntracellular SpaceLiver NeoplasmsMiceMice, KnockoutProteasome Endopeptidase ComplexRetinoblastoma ProteinRNA-Binding ProteinsTumor Suppressor Protein p53CCAAT-Enhancer-Binding ProteinsFxr1h protein, mouseProteasome Endopeptidase ComplexRetinoblastoma ProteinRNA-Binding ProteinsTumor Suppressor Protein p53

Identifiers

PMID20850540
PMCPMC3228644
OpenAlexW1965365608

What OpenQuestion holds

Textmetadata
LicenceTDM
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.