MétaCan
Menu
Back to cohort
Record W1992224115 · doi:10.1002/ajmg.a.33206

Overlapping spectra of <i>SMAD4</i> mutations in juvenile polyposis (JP) and JP–HHT syndrome

2010· article· en· W1992224115 on OpenAlexaff
Carol J. Gallione, Arthur S. Aylsworth, Jill Beis, Terri Berk, Barbara A. Bernhardt, Robin D. Clark, Carol L. Clericuzio, Cesare Danesino, Joanne M. Drautz, Jeffrey Fahl, Zheng Fan, Marie E. Faughnan, Arupa Ganguly, John Garvie, Katharine Henderson, Usha Kini, Tracey P. Leedom, Mark D. Ludman, Andreas Lux, Melissa Maisenbacher, Sara Mazzucco, Carla Olivieri, Johannes Kristian Ploos van Amstel, Nadia L. Prigoda-Lee, Reed E. Pyeritz, William Reardon, Kirk Vandezande, J. Deane Waldman, Robert I. White, Charles A. Williams, Douglas A. Marchuk

Bibliographic record

VenueAmerican Journal of Medical Genetics Part A · 2010
Typearticle
Languageen
FieldMedicine
TopicTracheal and airway disorders
Canadian institutionsSt. Michael's HospitalDalhousie UniversityUniversity of TorontoMount Sinai HospitalToronto Western HospitalIzaak Walton Killam Health Centre
Fundersnot available
KeywordsACVRL1MutationTelangiectasiaPhenotypeGenotypeMedicineGeneticsEndoglinGenetic testingGeneInternal medicineBiologyPathology

Abstract

fetched live from OpenAlex

Juvenile polyposis (JP) and hereditary hemorrhagic telangiectasia (HHT) are clinically distinct diseases caused by mutations in SMAD4 and BMPR1A (for JP) and endoglin and ALK1 (for HHT). Recently, a combined syndrome of JP-HHT was described that is also caused by mutations in SMAD4. Although both JP and JP-HHT are caused by SMAD4 mutations, a possible genotype:phenotype correlation was noted as all of the SMAD4 mutations in the JP-HHT patients were clustered in the COOH-terminal MH2 domain of the protein. If valid, this correlation would provide a molecular explanation for the phenotypic differences, as well as a pre-symptomatic diagnostic test to distinguish patients at risk for the overlapping but different clinical features of the disorders. In this study, we collected 19 new JP-HHT patients from which we identified 15 additional SMAD4 mutations. We also reviewed the literature for other reports of JP patients with HHT symptoms with confirmed SMAD4 mutations. Our combined results show that although the SMAD4 mutations in JP-HHT patients do show a tendency to cluster in the MH2 domain, mutations in other parts of the gene also cause the combined syndrome. Thus, any mutation in SMAD4 can cause JP-HHT. Any JP patient with a SMAD4 mutation is, therefore, at risk for the visceral manifestations of HHT and any HHT patient with SMAD4 mutation is at risk for early onset gastrointestinal cancer. In conclusion, a patient who tests positive for any SMAD4 mutation must be considered at risk for the combined syndrome of JP-HHT and monitored accordingly.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.002
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.007

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.002
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0020.001
Science and technology studies0.0000.001
Scholarly communication0.0000.000
Open science0.0000.001
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.008
GPT teacher head0.271
Teacher spread0.263 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations147
Published2010
Admission routes1
Has abstractyes

Explore more

Same venueAmerican Journal of Medical Genetics Part ASame topicTracheal and airway disordersFrench-language works237,207