ReviewOncogene2006
Mitochondriotoxic compounds for cancer therapy.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed.
- mLumiOpto Is a Mitochondrial-Targeted Gene Therapy for Treating Cancer.Cancer research · 2024Article
- An Innovative Mitochondrial-targeted Gene Therapy for Cancer Treatment.bioRxiv : the preprint server for biology · 2024Article
- A viral interferon regulatory factor degrades RNA-binding protein hnRNP Q1 to enhance aerobic glycolysis via recruiting E3 ubiquitin ligase KLHL3 and decaying GDPD1 mRNA.Cell death and differentiation · 2022Article
- Mitochondrial Inhibition: a Treatment Strategy in Cancer?Current oncology reports · 2021Review
- Targeting Dormant Ovarian Cancer CellsMolecular cancer therapeutics · 2021Article
- Epigenetic Regulation and Dietary Control of Triple Negative Breast Cancer.Frontiers in nutrition · 2020Review
- Detection of 8-oxoguanine and apurinic/apyrimidinic sites using a fluorophore-labeled probe with cell-penetrating ability.BMC molecular and cell biology · 2019Article
- Antiproliferative Effects ofIranian journal of medical sciences · 2018Article
- Article
- Dual subcellular compartment delivery of doxorubicin to overcome drug resistant and enhance antitumor activity.Scientific reports · 2015Article
- Article
- Transcriptomic analysis of pancreatic cancer cells in response to metformin and aspirin: an implication of synergy.Scientific reports · 2015Article
- Mitochondria as therapeutic targets for cancer stem cells.World journal of stem cells · 2015Review
- Anticancer/antiviral agent Akt inhibitor-IV massively accumulates in mitochondria and potently disrupts cellular bioenergetics.ACS chemical biology · 2015Article
- p53-mediated activation of the mitochondrial protease HtrA2/Omi prevents cell invasion.The Journal of cell biology · 2014Article
- Article
- Metformin directly acts on mitochondria to alter cellular bioenergetics.Cancer & metabolism · 2014Article
- Article
- Visualizing chemical structure-subcellular localization relationships using fluorescent small molecules as probes of cellular transport.Journal of cheminformatics · 2013Article
- Oxyphenisatin acetate (NSC 59687) triggers a cell starvation response leading to autophagy, mitochondrial dysfunction, and autocrine TNFα-mediated apoptosis.Cancer medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the hallmarks of cancer cells is their increased resistance to apoptosis induction. Alterations in many apoptosis regulators belonging to the intrinsic pathway confer emerging neoplastic cells with a selective growth advantage in the hostile tumor microenvironment. The realization that those same defects contribute to resistance to radiation and chemotherapeutic agents have prompted the unrelenting search for mitochondria-targeted compounds for the treatment of cancer. Mitochondria play a central role in the process of cell death. They serve as integrators of upstream effector mechanisms. Most importantly, mitochondrial outer membrane permeabilization becomes a commitment point during cell death. Thus, strategies aimed at directly triggering this event by either blocking the activity of antiapoptotic factors or by interfering with vital mitochondrial functions may help to overcome resistance to standard cancer therapy.
Indexed as
Identifiers
16892091What OpenQuestion holds
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.