Evidence map›Paper›PMID 20960198›Full record

ArticleDer Pathologe2010

[Hereditary bone tumors].

G Jundt, D Baumhoer

Abstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Der Pathologe, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. [Hereditary bone tumors].Der Pathologe · 2017
    Article
  2. Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

G JundtKnochentumor-Referenzzentrum am Institut für Pathologie, Universitätsspital Basel, Schönbeinstr. 40, 4031, Basel, Schweiz. gernot.jundt@unibas.ch
D Baumhoer
University Hospital of Basel · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Familial diseases leading to bone tumor formation are rare. They are mainly caused by genetic alterations of cell cycle constituent genes, such as retinoblastoma syndrome (RB1) and Li-Fraumeni syndrome (p53), of genes involved in growth-regulating transcriptional cascades, such as enchondromatosis (PTHR1) and multiple hereditary exostoses (EXT1, EXT2) or of genes maintaining chromosomal stability, such as Rothmund-Thomson (RECQL4), Werner (WRN) and Bloom syndromes (BLM). This leads to multiple benign bone tumors, which may undergo secondary malignant transformation (enchondromatosis: enchondromas, multiple hereditary exostoses: osteochondromas) or bone sarcomas, mainly osteosarcomas, such as primary (Li-Fraumeni, Rothmund-Thomson, Werner and Bloom syndromes) or secondary manifestations (retinoblastoma syndrome) of the underlying disease. Some of these lesions also carry an increased risk for developing additional malignant diseases. In contrast to sporadically occurring similar tumors, differences in manifestation in time, topography or histology may be present which can aid in the correct recognition of the underlying syndrome.

Indexed as

Bone NeoplasmsChromosome MappingHumansLi-Fraumeni SyndromeOsteochondromaOsteosarcomaRetinal NeoplasmsRetinoblastomaRothmund-Thomson SyndromeTranscription, Genetic

Identifiers

PMID20960198
OpenAlexW1983201712

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.