ArticleNeuro-oncology2012
Arlm1 is a male-specific modifier of astrocytoma resistance on mouse Chr 12.
Article in Neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- An Overview of Optic Pathway Glioma With Neurofibromatosis Type 1: Pathogenesis, Risk Factors, and Therapeutic Strategies.Investigative ophthalmology & visual science · 2024Review
- Sex differences in GBM revealed by analysis of patient imaging, transcriptome, and survival data.Science translational medicine · 2019Article
- Genome-wide expression profiling of glioblastoma using a large combined cohort.Scientific reports · 2018Article
- Exploring the genetic basis for clinical variation in neurofibromatosis type 1.Expert review of neurotherapeutics · 2016Article
- Review
- Intersections at the crossroads: Neurofibromatosis type 1, cAMP, sex, and glioma risk.Molecular & cellular oncology · 2016Article
- The Effects of Genetic Background of Mouse Models of Cancer: Friend or Foe?Cold Spring Harbor protocols · 2016Article
- The Use of Magnetic Resonance Imaging Screening for Optic Pathway Gliomas in Children with Neurofibromatosis Type 1.The Journal of pediatrics · 2015Article
- An integrative view on sex differences in brain tumors.Cellular and molecular life sciences : CMLS · 2015Review
- A RASopathy gene commonly mutated in cancer: the neurofibromatosis type 1 tumour suppressor.Nature reviews. Cancer · 2015Review
- The cyclic AMP pathway is a sex-specific modifier of glioma risk in type I neurofibromatosis patients.Cancer research · 2015Article
- Genetic modifiers of neurofibromatosis type 1-associated café-au-lait macule count identified using multi-platform analysis.PLoS genetics · 2014Article
- Sexually dimorphic RB inactivation underlies mesenchymal glioblastoma prevalence in males.The Journal of clinical investigation · 2014Article
- Eliminating barriers to personalized medicine: learning from neurofibromatosis type 1.Neurology · 2014Review
- Review
- Brain tumors in Neurofibromatosis type 1.Neuro-oncology advancesReview
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 2 institutions in 1 country.
Funding
Abstract
While many cancers show a sex bias, the genetic basis and molecular mechanisms underlying sex bias are not always clear. Astrocytoma and glioblastoma show male predominance in humans. We have shown previously that glial tumors forming in the Nf1-/+; Trp53-/+cis (NPcis) mouse model also show a sex bias in some genetic contexts. Using cross-species comparisons we have identified candidate male-specific modifiers of astrocytoma/glioblastoma. Linkage analysis of B6X(B6X129)-NPcis mice identifies a modifier of astrocytoma resistance specific to males, named Arlm1, on distal mouse Chr 12. Arlm1 is syntenic to human Chr 7p15, 7p21, 7q36, and 14q32 regions that are altered in human glioblastoma. A subset of these genes shows male-specific correlations to glioblastoma patient survival time and represents strong candidates for the Arlm1 modifier gene. Identification of male-specific modifier genes will lead to a better understanding of the molecular basis of male predominance in astrocytoma and glioblastoma.
Indexed as
Identifiers
What 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.