Evidence map›Paper›PMID 17102633›Full record

ReviewCell cycle (Georgetown, Tex.)2006

Effects of histone deacetylase inhibitors on HIF-1.

Dongming Liang, Xianguo Kong, Nianli Sang

Open access · hybridAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

50 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Clinical progress and functional modalities of HDAC inhibitor-based combination therapies in cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. ACY-241, a histone deacetylase 6 inhibitor, suppresses the epithelial-mesenchymal transition in lung cancer cells by downregulating hypoxia-inducible factor-1 alpha.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. HIF‑1α in cerebral ischemia (Review).Molecular medicine reports · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Exposomes to Exosomes: Exosomes as Tools to Study Epigenetic Adaptive Mechanisms in High-Altitude Humans.International journal of environmental research and public health · 2021
    Review
  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

3 authors at 2 institutions in 1 country.

Dongming LiangCardeza Foundation, Department of Medicine and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Xianguo Kong
Nianli Sang
Sidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

Transactivating of Activity of HIF-1 in tumorigenesisK01CA098809 · NCI · THOMAS JEFFERSON UNIVERSITY · PI SANG, NIANLI · 2003 to 2007
$714k
NCI NIH HHS CA098809NCI NIH HHS K01 CA098809
6 · The paper itself

Abstract

Hypoxia inducible factors (HIF) are the master transcriptional regulators of angiogenesis and energy metabolism in mammals. Histone deacetylase inhibitors (HDAIs) are among the promising anti -cancer compounds currently in clinical trials. In addition to inducing hyperacetylation of histones, HDAIs have been found to repress HIF function, which has been construed as an important pharmacological mechanism underlying the HDAI -mediated repression of tumor growth and angiogenesis. While HDAIs are potent inhibitors of HIF function and thus may be useful in the prevention and treatment of cancers, a major dilemma is that they may induce hyperacetylation of nonspecific targets thus causing side effects. A better understanding is now required of the molecular and biochemical mechanisms underlying the anti -HIF effects of these compounds. Here we summarize the recent advances towards a better understanding of these molecular and biochemical mechanisms.

Indexed as

Histone Deacetylase InhibitorsNeovascularization, PathologicEnzyme InhibitorsGene Expression RegulationHistonesHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitModels, BiologicalNeoplasmsOxygenTranscriptional ActivationTranscription FactorsEnzyme InhibitorsHistone Deacetylase InhibitorsHistonesHypoxia-Inducible Factor 1, alpha SubunitOxygenTranscription Factors

Identifiers

PMID17102633
PMCPMC4505804
OpenAlexW1968068668

What OpenQuestion holds

Textmetadata
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.