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Record W1572312535

The RET signaling pathway: Linking developmental and neoplastic roles

2005· article· en· W1572312535 on OpenAlexaff
Lois M. Mulligan

Bibliographic record

VenueCancer Research · 2005
Typearticle
Languageen
FieldMedicine
TopicNeuroendocrine Tumor Research Advances
Canadian institutionsQueen's University
Fundersnot available
KeywordsBiologyCarcinogenesisNeural crestNeoplastic transformationCancer researchReceptor tyrosine kinaseMultiple endocrine neoplasia type 2MutationEndocrinologyCancerInternal medicineGeneticsGermline mutationSignal transductionGeneMedicine
DOInot available

Abstract

fetched live from OpenAlex

Proc Amer Assoc Cancer Res, Volume 46, 2005 SY27-1 Although many of the genes now recognized as contributing to neoplastic transformation have similar and predictable roles in cell growth, migration and proliferation in most cell types, a number of genes have now been recognized as having normal primary roles specifically in organismal development. Mutations of these genes contribute to tumorigenesis in specific characteristic cell types, however, in some cases the type of mutation, and the developmental window in which it occurs, can determine whether the genetic variant contributes to neoplastic changes or to an abnormality of normal development. One gene with two such diverse effects is the RET proto-oncogene. RET encodes a transmembrane receptor tyrosine kinase that is required for development of neural crest derivatives, the central and peripheral nervous systems and the kidney. Activating missense mutations of RET give rise to the inherited cancer syndrome multiple endocrine neoplasia type 2 (MEN 2) which is characterized by medullary thyroid carcinoma, the adrenal tumour pheochromocytoma and by parathyroid hyperplasia. In each case, these mutations result in constitutive activation of the receptor. Intriguingly however, mutations that result in inactivation of the RET receptor, or significant reduction in cell surface associated RET protein, lead to a common congenital abnormality Hirschsprung disease (HSCR), characterized by absence of the parasympathetic ganglia of varying extents of the distal colon. Comparisons of the diametrically opposite effects of MEN 2 and HSCR RET-mutations have suggested that many tissues are highly sensitive to relatively small changes in the levels of RET, but that different tissues have unique sensitivity to increased or decreased RET activity. Recent studies that have provided some insight into normal RET signal transduction and the mechanisms by which RET mutations contribute to disease phenotype will be discussed.

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)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Theoretical or conceptual · Consensus signal: none
GenreCandidate signal: Review · Consensus signal: Review
Teacher disagreement score0.007
Threshold uncertainty score0.024

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.001
Science and technology studies0.0000.001
Scholarly communication0.0010.001
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0070.002

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 head0.064
GPT teacher head0.399
Teacher spread0.335 · 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 designTheoretical or conceptual
Domainnot available
GenreReview

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

Citations0
Published2005
Admission routes1
Has abstractyes

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