ArticleJournal of Cancer2012
Telomerase-independent paths to immortality in predictable cancer subtypes.
Article in Journal of Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 48 citations in OpenAlex.
- miRNAs and related genetic biomarkers according to the WHO glioma classification: From diagnosis to future therapeutic targets.Non-coding RNA research · 2024Review
- Telomere length analysis in amyotrophic lateral sclerosis using large-scale whole genome sequence data.Frontiers in cellular neuroscience · 2022Article
- Common pathways and functional profiles reveal underlying patterns in Breast, Kidney and Lung cancers.Biology direct · 2021Article
- Novel therapeutic strategies targeting telomere maintenance mechanisms in high-risk neuroblastoma.Journal of experimental & clinical cancer research : CR · 2020Review
- The molecular oncology of bilateral high-grade thalamic astrocytomas in children.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019Review
- Role of the cGAS-STING pathway in cancer development and oncotherapeutic approaches.EMBO reports · 2018Review
- Detection of the alternative lengthening of telomeres pathway in malignant gliomas for improved molecular diagnosis.Journal of neuro-oncology · 2017Article
- Measurement of Telomere Length in Colorectal Cancers for Improved Molecular Diagnosis.International journal of molecular sciences · 2017Article
- Withaferin-A kills cancer cells with and without telomerase: chemical, computational and experimental evidences.Cell death & disease · 2017Article
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- Cellularly active N-hydroxyurea FEN1 inhibitors block substrate entry to the active site.Nature chemical biology · 2016Article
- Review
- Genetic Inactivation of ATRX Leads to a Decrease in the Amount of Telomeric Cohesin and Level of Telomere Transcription in Human Glioma Cells.Molecular and cellular biology · 2015Article
- Circulating specific biomarkers in diagnosis of hepatocellular carcinoma and its metastasis monitoring.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Tumors that mimic asbestos-related mesothelioma: time to consider a genetics-based tumor registry?Frontiers in genetics · 2014Article
- The alternative lengthening of telomere phenotype is significantly associated with loss of ATRX expression in high-grade pediatric and adult astrocytomas: a multi-institutional study of 214 astrocytomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013Article
- Nuclear condensation and cell cycle arrest induced by telomerase siRNA in neuroblastoma cells.Journal of neuro-oncology · 2013Article
- Break-induced replication and genome stability.Biomolecules · 2012Article
- PML body meets telomere: the beginning of an ALTernate ending?Nucleus (Austin, Tex.)Review
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
The vast majority of cancers commandeer the activity of telomerase - the remarkable enzyme responsible for prolonging cellular lifespan by maintaining the length of telomeres at the ends of chromosomes. Telomerase is only normally active in embryonic and highly proliferative somatic cells. Thus, targeting telomerase is an attractive anti-cancer therapeutic rationale currently under investigation in various phases of clinical development. However, previous reports suggest that an average of 10-15% of all cancers lose the functional activity of telomerase and most of these turn to an Alternative Lengthening of Telomeres pathway (ALT). ALT-positive tumours will therefore not respond to anti-telomerase therapies and there is a real possibility that such drugs would be toxic to normal telomerase-utilising cells and ultimately select for resistant cells that activate an ALT mechanism. ALT exploits certain DNA damage response (DDR) components to counteract telomere shortening and rapid trimming. ALT has been reported in many cancer subtypes including sarcoma, gastric carcinoma, central nervous system malignancies, subtypes of kidney (Wilm's Tumour) and bladder carcinoma, mesothelioma, malignant melanoma and germ cell testicular cancers to name but a few. A recent heroic study that analysed ALT in over six thousand tumour samples supports this historical spread, although only reporting an approximate 4% prevalence. This review highlights the various methods of ALT detection, unravels several molecular ALT models thought to promote telomere maintenance and elongation, spotlights the DDR components known to facilitate these and explores why certain tissues are more likely to subvert DDR away from its usually protective functions, resulting in a predictive pattern of prevalence in specific cancer subsets.
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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.