ArticleNeuro-oncology2008
Evaluation of 1p36 markers and clinical outcome in a skull base chordoma study.
Article in Neuro-oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Prognostic molecular biomarkers in chordomas: A systematic review and identification of clinically usable biomarker panels.Frontiers in oncology · 2022Pooled it
- Immune microenvironment and immunotherapy for chordoma.Frontiers in oncology · 2024Review
- Molecular features and vulnerabilities of recurrent chordomas.Journal of experimental & clinical cancer research : CR · 2021Article
- LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis.International journal of biological sciences · 2021Article
- Chordoma: A Case Report and Review of Literature.The American journal of case reports · 2020Review
- Genomic and transcriptomic characterization of skull base chordoma.Oncotarget · 2017Article
- Low expression of miRNA-1290 associated with local invasion and recurrence in sacral chordoma.International journal of clinical and experimental pathology · 2017Article
- Immunophenotypic features of dedifferentiated skull base chordoma: An insight into the intratumoural heterogeneity.Contemporary oncology (Poznan, Poland) · 2017Review
- Chordoma: an update on the pathophysiology and molecular mechanisms.Current reviews in musculoskeletal medicine · 2015Article
- Epigenetic deregulations in chordoma.Cell proliferation · 2015Review
- Molecular genetic study of novel biomarkers for early diagnosis of oral squamous cell carcinoma.Medicina oral, patologia oral y cirugia bucal · 2015Article
- FAS/FASL are dysregulated in chordoma and their loss-of-function impairs zebrafish notochord formation.Oncotarget · 2014Article
- High-resolution whole-genome analysis of skull base chordomas implicates FHIT loss in chordoma pathogenesis.Neoplasia (New York, N.Y.) · 2012Article
- The biological basis for modern treatment of chordoma.Journal of neuro-oncology · 2011Review
- Systemic therapy options for unresectable and metastatic chordomas.Current oncology reports · 2011Review
- The prognostic value of Ki-67, p53, epidermal growth factor receptor, 1p36, 9p21, 10q23, and 17p13 in skull base chordomas.Archives of pathology & laboratory medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chordomas are rare embryogenetic tumors, arising from remnants of the notochord, characterized by local invasiveness and variable tendency for recurrence. No molecular markers are currently used in a clinical setting to distinguish chordomas with an indolent or an aggressive pattern. Among the genetic lesions observed in this tumor, one of the most commonly detected is 1p loss. In a previous study we observed 1p36 loss of heterozygosity (LOH) in 85% of the analyzed chordomas. We studied a group of 16 homogeneously treated skull base chordomas (SBCs), reporting 1p36 LOH in 75% of them and determining the expression pattern of eight apoptotic genes mapped at 1p36. No tumors shared a common expression profile with nucleus pulposus, which is considered the only adult normal tissue deriving from notochord. In particular, tumor necrosis factor receptor superfamily genes TNFRSF8, TNFRSF9, and TNFRSF14 were differently expressed compared with control in a higher percentage of tumors (40%-53%) than were the remaining analyzed genes, suggesting that the deregulation of these three genes might have a role in chordoma tumorigenesis. The presence/absence of LOH and the expression/nonexpression of each apoptotic gene were studied in a survival analysis. Our results suggest that the lack of 1p36 LOH or the presence of TNFRSF8 expression might be associated with a better prognosis in patients with SBCs.
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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.