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Record W2243992364

Functional synergism between IGF-IR tyrosine kinase and NPM-ALK oncogene identifies a novel role of IGF-IR in malignant lymphoma.

2007· article· en· W2243992364 on OpenAlexaff
Ping Shi, Quan Lin, Abid S. Iqbal, Larry W. Kwak, Raymond Lai, Hesham M. Amin

Bibliographic record

VenueMolecular Cancer Therapeutics · 2007
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer, Hypoxia, and Metabolism
Canadian institutionsUniversity of Alberta
Fundersnot available
KeywordsAnaplastic lymphoma kinaseCancer researchAnaplastic large-cell lymphomaLymphomaAutocrine signallingBiologyTyrosine kinaseBCL10OncogeneReceptor tyrosine kinaseCancerSignal transductionCell cultureInternal medicineImmunologyMedicineCell cycleLung cancerCell biologyGenetics
DOInot available

Abstract

fetched live from OpenAlex

C89 Deregulated IGF-IR signaling induces significant pathogenetic effects in a variety of human epithelial carcinomas including those of the breast, prostate, ovary, and lung. Despite that it promotes the growth of stimulated hematopoietic cells; a specific role of IGF-IR in lymphoid malignancies has not been identified. The full-length anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase of the insulin receptor superfamily. In humans, physiologic expression of ALK is restricted to embryonic cells of neural origin. A subset of T-cell lymphoma, identified according to the WHO classification scheme as ALK+ anaplastic large-cell lymphoma, harbors the t(2;5)(p23;q35), which involves ALK and NPM genes. This translocation generates the chimeric protein NPM-ALK that possesses constitutively active ALK. NPM-ALK-expressing T-cell lymphoma is an aggressive type of malignant lymphoma with a tendency to affect children and young adults. Despite initial response to current therapeutic modalities, 30% - 40% of the patients relapse and some eventually succumb. In the present study, we explored a role of IGF-IR in NPM-ALK-expressing T-cell lymphoma. Our results demonstrate that IGF-IR and its ligand IGF-I are widely expressed in NPM-ALK-expressing lymphoma cell lines and primary tumors. In addition, several of these cell lines release IGF-I in an autocrine fashion. We also identified novel functional collaborations between IGF-IR and NPM-ALK by which the 2 molecules reciprocally interact to maintain their phosphorylation status. In further support of the role of IGF-IR, IGF-I enhanced the viability of serum-deprived NPM-ALK-expressing T-cell lymphoma cell lines and salvaged these cells from apoptotic death. Selective targeting of IGF-IR induced concentration- and time-dependent apoptotic cell death and cell cycle arrest, and decreased proliferation and colony formation of NPM-ALK-expressing T-cell lymphoma cells. These effects were due to downregulation of pAKT, pSTAT3, Bcl-2, Bcl-XL, Mcl-1, and upregulation of p21. The negative effects of IGF-IR blockade on NPM-ALK-expressing T-cell lymphoma cells could also be attributed to the decrease or increase in the binding of the transcription modulators STAT3 or FKHR to DNA, respectively. Our results identify for the first time a novel and direct role of IGF-IR in any type of malignant lymphoma. In addition, these findings increase current knowledge of the biology of IGF-IR and NPM-ALK. Importantly, these findings carry significant therapeutic implications as they identify IGF-IR as a legitimate molecular target in NPM-ALK-expressing T-cell lymphoma, and probably in other types of malignant lymphoma in the future.

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: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.009

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0030.001

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 head0.017
GPT teacher head0.262
Teacher spread0.245 · 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
Published2007
Admission routes1
Has abstractyes

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