ReviewOncogene2001
Transcription therapy for cancer.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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.
Who cites it
44 citing papers in PubMed, 148 citations in OpenAlex.
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- Betanin-encapsulated starch nanoparticles: synthesis and cytotoxic effect on colon cancer.3 Biotech · 2024Article
- Review
- β-Cyclodextrin-poly (β-Amino Ester) Nanoparticles Are a Generalizable Strategy for High Loading and Sustained Release of HDAC Inhibitors.ACS applied materials & interfaces · 2021Article
- Etiologic Role of Kinases in the Progression of Human Cancers and Its Targeting Strategies.Indian journal of surgical oncology · 2021Article
- Biophysical Techniques for Target Validation and Drug Discovery in Transcription-Targeted Therapy.International journal of molecular sciences · 2020Review
- Starch nanoparticles for delivery of the histone deacetylase inhibitor CG-1521 in breast cancer treatment.International journal of nanomedicine · 2019Article
- Characterization of CADD522, a small molecule that inhibits RUNX2-DNA binding and exhibits antitumor activity.Oncotarget · 2017Article
- Anticancer Natural Compounds as Epigenetic Modulators of Gene Expression.Current genomics · 2017Review
- A designed DNA binding motif that recognizes extended sites and spans two adjacent major grooves.Chemical science · 2016Article
- Bisindole-PBD regulates breast cancer cell proliferation via SIRT-p53 axis.Cancer biology & therapy · 2015Article
- Anti-Epileptic Drug Targets Ewing Sarcoma.Journal of pharmaceutical sciences and pharmacology · 2014Article
- Iron complexation to histone deacetylase inhibitors SAHA and LAQ824 in PEGylated liposomes can considerably improve pharmacokinetics in rats.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2014Article
- Article
- Effects of endostatin and a new drug terpestacin against human neuroblastoma xenograft and cell lines.Pediatric surgery international · 2013Article
- Drugging the undruggable: transcription therapy for cancer.Biochimica et biophysica acta · 2013Review
- Enhanced Cytotoxic Effects of Combined Valproic Acid and the Aurora Kinase Inhibitor VE465 on Gynecologic Cancer Cells.Frontiers in oncology · 2013Article
- Lycorine induces cell-cycle arrest in the G0/G1 phase in K562 cells via HDAC inhibition.Cancer cell international · 2012Article
- The APL paradigm and the "co-clinical trial" project.Cancer discovery · 2011Review
- Transcriptional tools: Small molecules for modulating CBP KIX-dependent transcriptional activators.Biopolymers · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the post genome era it will soon be possible to associate a specific tumor type with a specific gene expression profile and to define each molecular lesion characteristic of any given cancer. It is intuitive that a successful therapeutic strategy for cancer should aim at blocking the aberrant biochemical activity triggered by the oncogene or the lack of tumor suppressor gene activity that ultimately leads to full-blown neoplastic transformation. However, an attractive alternative approach entails the blockade of the transcriptional consequences of such oncogenic activities irrespective of their original biochemical nature, thus antagonizing the key transcriptional events underlying cancer pathogenesis in any specific neoplastic cellular population. This approach is now rendered possible by major advances along several lines of investigation: (i) the possibility of analysing gene expression through high throughput methods; (ii) a more detailed knowledge of the regulatory regions and of the transcription factors that control gene expression also facilitated in the future by a comprehensive whole genome comparative analysis of these regulatory sequences; (iii) the ability of modulating gene expression at the single gene level through various approaches both pharmacological and biochemical; (iv) the opportunity of directly antagonizing the aberrant activities of oncogenic transcription factors through a detailed knowledge of their abnormal transcriptional function; (v) the possibility of validating, in vivo, in animal models the relevance for neoplastic transformation of specific transcriptional events as well as of testing the efficacy of 'transcription therapy' in faithful animal models of human cancer. Here, we will review the facts, the existing applications and the hypothesis underlying such therapeutic modality for cancer therapy.
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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.