ArticleAnatomical record (Hoboken, N.J. : 2007)2025
Embryonic cranial cartilage defects in the Fgfr3
Article in Anatomical record (Hoboken, N.J. : 2007), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 3 citations in OpenAlex.
- Signalling Pathways and Mechanical Forces Interact in Craniofacial Development and Homeostasis.International dental journal · 2026Review
- Demystifying machine learning approaches in digital bone imaging using microCT and HRpQCT.Bone reports · 2026Review
- Embryonic cranial cartilage defects in the Fgfr3Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- Universal conditional networks (UniCoN) for multi-age embryonic cartilage segmentation with Sparsely annotated data.Scientific reports · 2025Article
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- CONUNETR: A CONDITIONAL TRANSFORMER NETWORK FOR 3D MICRO-CT EMBRYONIC CARTILAGE SEGMENTATION.Proceedings. IEEE International Symposium on Biomedical Imaging · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Achondroplasia, the most common chondrodysplasia in humans, is caused by one of two gain of function mutations localized in the transmembrane domain of fibroblast growth factor receptor 3 (FGFR3) leading to constitutive activation of FGFR3 and subsequent growth plate cartilage and bone defects. Phenotypic features of achondroplasia include macrocephaly with frontal bossing, midface hypoplasia, disproportionate shortening of the extremities, brachydactyly with trident configuration of the hand, and bowed legs. The condition is defined primarily on postnatal effects on bone and cartilage, and embryonic development of tissues in affected individuals is not well studied. Using the Fgfr3
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.