ReviewOncogene2003
Alterations in the apoptotic machinery and their potential role in anticancer drug resistance.
Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed.
- Effects of lapatinib monotherapy: results of a randomised phase II study in therapy-naive patients with locally advanced squamous cell carcinoma of the head and neck.British journal of cancer · 2011Trial
- Evaluation of theFrontiers in chemistry · 2023Article
- Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer.Frontiers in pharmacology · 2023Review
- Halogenated boroxine increases propensity to apoptosis in leukemia (UT-7) but not non-tumor cells in vitro.FEBS open bio · 2023Article
- Conjugation of the 9-kDa Isoform of Granulysin with Liposomes Potentiates Its Cytotoxicity.International journal of molecular sciences · 2022Article
- Cancer and Apoptosis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Analysis of PANoptosis-Related LncRNA-miRNA-mRNA Network Reveals LncRNA SNHG7 Involved in Chemo-Resistance in Colon Adenocarcinoma.Frontiers in oncology · 2022Article
- Article
- Chemical Characteristics and Anticancer Activity of Essential Oil fromMolecules (Basel, Switzerland) · 2020Article
- Evaluation of the Cardiac Protection Conferred by Proanthocyanidins in Grape Seeds against Development of Ehrlich Solid Tumors in Mice.BioMed research international · 2020Article
- Enhancement of Ionization Efficiency Using Zeolite in Matrix-Assisted Laser Desorption/Ionization Mass Spectrometry of Multiple Drugs in Cancer Cells (Mass Spectrometry of Multiple Drugs in Cells Using Zeolite).Mass spectrometry (Tokyo, Japan) · 2020Article
- Erianin inhibits human cervical cancer cell through regulation of tumor protein p53 via the extracellular signal-regulated kinase signaling pathway.Oncology letters · 2018Article
- P53/PUMA are potential targets that mediate the protection of brain-derived neurotrophic factor (BDNF)/TrkB from etoposide-induced cell death in neuroblastoma (NB).Apoptosis : an international journal on programmed cell death · 2018Article
- Selective induction of cancer cell death by VDAC1-based peptides and their potential use in cancer therapy.Molecular oncology · 2018Article
- VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress.Cell stress · 2017Article
- Pazopanib, a novel multi-kinase inhibitor, shows potent antitumor activity in colon cancer through PUMA-mediated apoptosis.Oncotarget · 2017Article
- In vitro and in vivo anticancer studies of 2'-hydroxy chalcone derivatives exhibit apoptosis in colon cancer cells by HDAC inhibition and cell cycle arrest.EXCLI journal · 2017Article
- Cyanidin-3-o-glucoside directly binds to ERα36 and inhibits EGFR-positive triple-negative breast cancer.Oncotarget · 2016Article
- Smac mimetic LCL161 overcomes protective ER stress induced by obatoclax, synergistically causing cell death in multiple myeloma.Oncotarget · 2016Article
- Apoptotic Pathways Linked to Endocrine System as Potential Therapeutic Targets for Benign Prostatic Hyperplasia.International journal of molecular sciences · 2016Review
16 more citing papers are in PubMed but not listed here.
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
Abstract
Anticancer drugs can potentially kill cells in two fundamentally different ways, by interfering with cellular processes that are essential for maintenance of viability or by triggering an endogenous physiological cell death mechanism. Apoptosis is a form of physiological cell death mediated by caspases, a unique family of intracellular cysteine proteases. Zymogen forms of these proteases are found in virtually all somatic cells, but remain latent until their activation is induced by ligation of specific cell surface receptors (the so-called "death receptors"), by mitochondrial alterations that allow release of cytochrome c and other intermembrane components, or possibly by other mechanisms. Most anticancer drugs activate the mitochondrial pathway. This apoptotic pathway is regulated by pro- and antiapoptotic members of the Bcl-2 family of proteins. Once activated, certain caspases might also be controlled by the inhibitor of apoptosis (IAP) proteins. Alterations in apoptotic pathway components or their regulators have been detected in a variety of cancers, suggesting that loss of the ability of cells to undergo apoptosis might contribute to carcinogenesis. Because cancer therapies such as radiation, glucocorticoids, and chemotherapeutic drugs exert their beneficial effects, at least in part, by inducing apoptosis of cancer cells, the same alterations in apoptotic pathways would be predicted to contribute to resistance. A key issue is whether the direct toxic activity of these treatments is of benefit when neoplastic cells contain changes that diminish their ability to undergo apoptosis.
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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.