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Record W2929422481

Pre-clinical studies of CHIR258, a small molecule inhibitor that targets FGFR3, for the treatment of t(4;14) multiple myeloma

2004· article· en· W2929422481 on OpenAlexaff
Suzanne Trudel, Zhihua Li, Ellen Wei, Marion Wiesmann, Gena Lapointe, Isabelle Lee, Carla Heise, Alex L. Harris, Keith Stewart

Bibliographic record

VenueCancer Research · 2004
Typearticle
Languageen
FieldMedicine
TopicMultiple Myeloma Research and Treatments
Canadian institutionsPrincess Margaret Cancer Centre
Fundersnot available
KeywordsCancer researchChromosomal translocationFibroblast growth factor receptor 3Tyrosine kinaseReceptor tyrosine kinaseIn vitroMolecular biologyBiologyCell cultureTyrosine-kinase inhibitorMultiple myelomaApoptosisKinaseFibroblast growth factorReceptorSignal transductionCancerCell biologyImmunologyBiochemistryGeneticsGene
DOInot available

Abstract

fetched live from OpenAlex

5626 The t(4;14) translocation that occurs uniquely in a subset (15%) of multiple myeloma (MM) patients results in the ectopic expression of the receptor tyrosine kinase (RTK), FGFR3. Wild-type (WT) FGFR3 induces proliferative signals in MM cells and appears to be weakly transforming in a hematopoeitic mouse model. The subsequent acquisition of FGFR3 activating mutations in some MM is associated with disease progression and is strongly transforming in experimental models. The clinical impact of t(4;14) translocation has been demonstrated in 3 large studies each reporting a marked reduction in overall survival. We have previously shown that inhibition of activated FGFR3 causes morphologic differentiation followed by apoptosis of FGFR3 expressing MM cell lines, validating activated FGFR3 as a therapeutic target in t(4;14) MM and encouraging the clinical development of FGFR3 inhibitors for the treatment of these poor-prognosis patients. CHIR258 is a small molecule kinase inhibitor that targets Class III-V RTKs and inhibits FGFR3 with an IC 50 of 5 nM in vitro kinase assays. Potent anti-tumor and anti-angiogenic activity has been demonstrated in vitro and in vivo . We have employed the IL-6 dependent murine myeloma cell line, B9 that has been engineered to stably express either WT FGFR3 (B9-WT) or the K650E mutant FGFR3 (B9-TD) to screen CHIR258 for FGFR3 activity. CHIR258 inhibited FGF-mediated growth of B9-WT and B9-TD with an IC50 of 25nM and 80 nM respectively as determined by MTT assay. Growth of these cells could be rescued by IL-6 demonstrating selectivity of CHIR258 for FGFR3. At concentrations that prevented cell growth, CHIR258 inhibited in vitro FGFR3 autophosphorylation. We then confirmed the activity of CHIR258 against FGFR3 expressing MM cells. CHIR258 inhibited the growth of FGFR3 expressing KMS11 (Y373C), OPM2 (K650E), KMS18 (G384D) and H929 (WT FGFR3) cells with an IC 50 of 100 nM (KMS11 and OPM2 cells), 250 nM and 630 nM respectively. U266 cells, which lack FGFR3 expression, displayed minimal growth inhibition demonstrating that at effective concentrations, CHIR258 exhibits minimal nonspecific cytotoxicity on MM cells. Further characterization of this finding demonstrates that inhibition of cell growth is related to G1 cell cycle arrest and dose-dependent inhibition of ERK phosphorylation. CHIR258 also induced delayed, dose-responsive apoptosis of these cells . Apoptotic cells, assessed by annexin V staining, were detectable 2 (KMS11) and 5 (KMS18, OPM2) days after exposure to CHIR258 and increased with dose and days of treatment. Studies assessing in vivo activity of CHIR258 against FGFR3 expressing tumors in xenograft mice are ongoing and will be reported. These data indicate that the small molecule inhibitor, CHIR258 potently inhibits FGFR3 and has activity against human MM cells setting the stage for a Phase I/II clinical trial of this compound in t(4;14) MM.

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)0.001
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: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.004
Threshold uncertainty score0.015

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0010.000
Open science0.0000.000
Research integrity0.0010.002
Insufficient payload (model declined to judge)0.0040.001

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 head0.288
GPT teacher head0.503
Teacher spread0.214 · 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 designBench or experimental
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

Citations0
Published2004
Admission routes1
Has abstractyes

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