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Irradiated NK-92 Targets AML Leukemic Stem Cells in Vivo and Gene-Modified CD16+NK-92 Mediates Antibody Dependent Cell Mediated Cytotoxicity (ADCC) Against CD123+ Cells

2012· article· en· W2594993143 on OpenAlexaff
Brent A. Williams, Xinghua Wang, Sonam Maghera, Jeffrey V. Leyton, Raymond M. Reilly, Armand Keating

Bibliographic record

VenueBlood · 2012
Typearticle
Languageen
FieldMedicine
TopicCAR-T cell therapy research
Canadian institutionsUniversity of TorontoPrincess Margaret Cancer Centre
Fundersnot available
KeywordsAntibody-dependent cell-mediated cytotoxicityCancer researchLeukemiaStem cellCD38CD34Cytotoxic T cellBiologyImmunologyAntibodyMonoclonal antibodyIn vitroCell biology

Abstract

fetched live from OpenAlex

Abstract Abstract 1909 Introduction: Patients with acute myeloid leukemia (AML) in remission relapse frequently from residual leukemic stem cells (LSCs) that are CD34+CD38-CD123+. NK-92 is an infusible CD16- malignant NK cell line cytotoxic against AML and after irradiation for prevention of NK cell malignancy has minimal adverse events in Phase I trials. Here, we tested irradiated NK-92 (iNK-92) against primary AML in a NOD/SCID gamma null (NSG) xenograft model. To optimize killing of LSCs in vitro we utilized a gene modified CD16+NK-92 against the CD123+ leukemia cell line OCI/AML5 treated with and without an anti-CD123 monoclonal antibody (7G3) to facilitate antibody dependent cell mediated cytotoxicity (ADCC). Methods: NSG mice were irradiated with 225 or 325 cGy before infusion with primary AML blasts (1 or 3×10e6 cells). iNK-92 was started 1 or 10 days post AML infusion and given 1–3 times weekly (15 or 20×10e6 cells/dose) to a total dose of 60–75 ×10e6 cells/mouse. In vitro cytotoxicity was measured by the chromium release assay. OCI/AML5 or primary AML was pretreated with 7G3 or anti-Class I antibody respectively at 10 ug/ml 2 hours before ADCC assays. Results: We developed an NSG AML xenograft model using a CD34+CD38+ primary AML sample containing a small fraction of CD34+CD38- cells that were predominantly CD123+. 3×10e6 primary cells induced leukemia in NSG mice by 6 weeks and maintained comparable potency up to quaternary transplantations with a stable immunophenotype. In vitro cytotoxicity against LSCs was assessed by treating 1×10e6 first passage BM derived primary AML +/− 5×10e6 iNK-92 ×4 hours and injecting into 2 cohorts of 5 mice. At 6 weeks mice were sacrificed and bone marrow harvested. Average leukemic engraftment in the iNK-92 group (79.8, 3.48, 92.1, 81.3, 86.1, Av= 68.6%) was less than untreated AML inoculated group (95.0, 93.4, 19.4, 95, 97.3, Av=80.0%), but not statistically significant (p=0.62). Removing one poorly engrafted outlier mouse from each group yielded a higher engraftment in the control (Av=95.1%) versus the treatment group (Av=84.8%) and was significant (p=0.011). To test iNK-92 to treat engrafted leukemia, NSG mice were infused with 3×10e6 AML cells starting day 10 with 20×10e6 iNK-92 weekly ×6 doses. Survival was improved in the treatment group to near statistical significance (p=0.055), but all mice ultimately succumbed to disease. Addition of IL-2 to iNK-92 did not improve outcomes (p=0.13). 3×10e6 primary AML cells were also infused into 2 cohorts of 4 mice and treated +/− iNK-92 from day 2 and given 15×10e6 cells twice weekly to 75×10e6 total dose. BM (1×10e6 cells) from each of 4 primary recipients in control and treatment was serially transplanted 1:1 into four new NSG mice. BM engraftment occurred in all AML only cohort secondary mice (80.8, 93.3, 80.4, 96.4 Av=87.7%) while one mouse from iNK-92 group was leukemia free with engraftment at background levels of non-injected mice (96.4, 94.7, 1.8, 95.7 Av=72.2%). Proportion of LSCs in secondary transplanted mice was: AML (8.01, 9.48, 8.66, 5.25, Av=7.85%) and AML + iNK-92 (7.13, 3.46, 0.03, 4.0 Av=3.66%) which was statistically significant (p=0.05). CD16+NK-92 killed CD123+ OCI/AML5 cells at effector:target (E:T) ratios of 25:1, 10:1, 5:1 and 1:1 (% lysis +/−SD: 35.0 +/−4.0, 9.0+/−6.6, -2.0 +/−0.1, 1.7 +/−3.3) and was significantly enhanced (2–6x) when targets were coated with anti-CD123 mAb (% lysis +/−SD: 64.3 +/−3.1, 48.5 +/−4.1, 20.9 +/−0.1, 10.1+/−3.3). Further, CD16+NK-92 also killed primary AML at E:T ratios of 25:1, 10:1, 5:1 and 1:1 (% lysis +/−SD: 34.7 +/−4.6, 15.6 +/− 4.7, 11.5 +/− 2.0, 7.7 +/−1.6) which was significantly enhanced (2–3x) by coating with anti-Class I monoclonal antibodies (% lysis +/−SD: 64.8 +/−10.4, 31.1 +/− 8.9, 30.2 +/− 9.4, 23.9+/−2.8). Conclusion: iNK-92 reduces engraftment of AML and improves survival in a primary AML xenograft model. CD16+NK-92 cytotoxicity against primary AML is enhanced with anti-class I antibodies via ADCC, demonstrating that CD16+NK-92 can be redirected against bulk primary leukemia using a highly expressed cell surface marker. Finally, CD16+NK-92 cytotoxicity can be improved against OCI/AML5 with anti-CD123 antibodies via ADCC, providing the first proof-of-principle for the targeting of leukemic stem cells by combining humoral and cellular approaches. 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 integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.001

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 head0.020
GPT teacher head0.273
Teacher spread0.253 · 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
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