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Record W2980188423 · doi:10.1182/blood.v120.21.291.291

ITIM-Containing Inhibitory Receptors Are Required to Balance Oncogenic Signaling Strength in Ph+ ALL

2012· article· en· W2980188423 on OpenAlexaff
Zhengshan Chen, Huimin Geng, Maike Buchner, Lars Klemm, Kaveh Hemati, Seyedmehdi Shojaee, Mak W Tak, John E. Coligan, William L. Carroll, Cheryl L. Willman, Markus Müschen

Bibliographic record

VenueBlood · 2012
Typearticle
Languageen
FieldMedicine
TopicMonoclonal and Polyclonal Antibodies Research
Canadian institutionsOntario Institute for Cancer Research
Fundersnot available
KeywordsLYNReceptorSignal transductionBiologyImmune systemImmunologyCell biologyCancer researchMolecular biologyTyrosine kinaseBiochemistry

Abstract

fetched live from OpenAlex

Abstract Abstract 291 Background: ITIM (immunoreceptor tyrosine-based inhibition motifs) motifs in the cytoplasmic tail of inhibitory receptors recruit inhibitory phosphatases. Upon ligation, these phosphatases inhibit signal transduction from tyrosine kinases including BCR-ABL1. ITIM-receptors are critical in the control of immune responses of B and T cells. Surprisingly, we found that a number of inhibitory ITIM-receptors are expressed at very high levels on the surface of patient-derived Ph+ acute lymphoblastic leukemia (ALL) cells compared to normal pre-B cells. In this study, three central ITIM-receptors were identified and analyzed for their function in Ph+ALL: PECAM1 (platelet/endothelial cell adhesion molecule 1/CD31), CD300A and LAIR1 (leukocyte-associated immunoglobulin-like receptor 1). Results: Microarray data showed mRNA levels of PECAM1, CD300A and LAIR1 were about 5-fold higher (p<0.005) in Ph+ ALL (n=15) than normal human pre-B cells (n=8). We confirmed this difference at the protein level by flow cytometry studying patient-derived Ph+ALL (n=11) and pre-B cells from normal bone marrow samples (n=2). These findings seem counterintuitive because signaling from these receptors would attenuate the signaling strength downstream of BCR-ABL1. Importantly, we found that high expression levels of ITIM-receptors are predictive of poor outcome in two clinical trials. In the COG trial (P9906; n=207) for children with high-risk ALL, we found that mRNA levels of PECAM1, CD300A and LAIR1 at diagnosis positively correlated with early minimal residual disease (MRD) findings on day 29 (p<0.0005), and negatively correlated with overall survival (OS) rate (p<0.02) or relapse free survival (RFS) rate (p<0.05). In ECOG trial E2993 for adults with ALL (n=215), we found that PECAM1 mRNA level in ALL patients negatively correlated with OS rate (p=0.0285). These results collectively indicate that inhibitory ITIM-receptors contribute to the course of human ALL disease. To study the role of PECAM1, CD300A and LAIR1 in Ph+ ALL in genetic experiments, we transformed pre-B cells from Pecam1−/−, Cd300a−/− and wildtype mice with BCR-ABL1. Compared to wildtype ALL cells, Pecam1−/− or Cd300a−/− ALL cells showed increased ROS levels. Consistent with higher levels of ROS, the Pecam1−/− and Cd300a−/− ALL cells accumulate p53, p21 and p27 protein, are prone to G0/G1cell cycle arrest and cellular senescence. Colony forming assays revealed that Pecam1- and cd300-deficient leukemia cells also formed 10-fold fewer colonies in methyl cellulose compared to wildtype ALL cells (p<0.0001). For Lair1, we performed genetic loss-of-function experiments by inducible activation of Cre in Lair1fl/fl leukemia cells. Inducible deletion of Lair1 resulted in drastic upregulation of ROS, accumulation of Arf, p53 and p21, cellular senescence and subsequent leukemia cell death. Transplanting Lair1fl/fl ALL cells into NOD-SCID mice, we found that Lair1 deletion resulted in rapid leukemia regression and prolonged survival of recipient mice. Leukemia cell death caused by Lair1 deletion could be rescued by overexpression of the inhibitory phosphatase Ptpn6 (SHP1) indicating that the protective effect of the Lair1 is indeed mediated by ITIM-based recruitment of inhibitory phosphatases. To test whether these findings are also relevant to other subtypes of ALL, we used a model for NRASG12D-driven ALL. BCR-ABL1 (∼25%) and NRAS lesions (∼30%) account for more than half of cases of ALL. Consistent with our findings with BCR-ABL1, NRASG12D Pecam1−/−, Cd300a−/−leukemia cells were prone to G0/G1 cell cycle arrest and cellular senescence (p<0.01). Conclusion: These results indicated that inhibitory ITIM-receptors are critical regulators of oncogenic signaling strength in BCR-ABL1 and NRAS-driven ALL. Deficiency of ITIM-receptor signaling can be rescued by overexpression of the PTPN6 phosphatase. These findings are of particular relevance, because they identify ITIM-receptors and inhibitory phosphatases as members of a fundamentally novel class of therapeutic targets. The concept of pharmacological perturbance of oncogenic signaling equilibrium in leukemia cells by inhibition (e.g. TKI-treatment) or exaggeration of signaling strength (e.g. blockade of ITIM-receptors) may lead to the discovery of multiple additional therapeutic targets and broaden our repertoire of currently available pathways for therapeutic intervention. Disclosures: No relevant conflicts of interest to declare.

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 score0.002
Threshold uncertainty score0.006

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)0.0020.000

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 head0.041
GPT teacher head0.317
Teacher spread0.276 · 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".

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Citations0
Published2012
Admission routes1
Has abstractyes

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