ReviewVirchows Archiv : an international journal of pathology2004
Carcinoma of the prostate: inherited susceptibility, somatic gene defects and androgen receptors.
Review in Virchows Archiv : an international journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 20 citations in OpenAlex.
- Quantitative analysis of a panel of gene expression in prostate cancer--with emphasis on NPY expression analysis.Journal of Zhejiang University. Science. B · 2007Article
- Current practice of Gleason grading of prostate carcinoma.Virchows Archiv : an international journal of pathology · 2006Review
- Tissue print micropeel: a new technique for mapping tumor invasion in prostate cancer.Current urology reports · 2006Review
- Class reunion: PTEN joins the nuclear crew.Oncogene · 2005Review
- Dynamic structure of the SPANX gene cluster mapped to the prostate cancer susceptibility locus HPCX at Xq27.Genome research · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple factors contribute to the development of prostate carcinoma (PCa) and to its progression to an androgen-independent state. In addition to the expected role of androgens and their receptors in facilitating the development of PCa, mutations in a growing number of candidate hereditary prostate cancer loci and genes, such as RNASEL and MSR1, have been detected, suggesting that defects in critical pathways involving DNA damage response, apoptosis and innate immunity may have a particularly important role in the initiation of PCa. Many somatic mutations, gene deletions, gene amplifications, chromosomal rearrangements, and changes in DNA methylation are detectable in PCa cells at the time of diagnosis. The identification of key molecular alteration cells implicates carcinogen defenses, including GSTP1, growth factor signaling pathways (such as PTEN and p27) and androgens as critical determinants of the phenotype of PCa.
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.