Evidence map›Paper›PMID 25134458›Full record

ArticleLeukemia2015

Cytotoxicity of CD56-positive lymphocytes against autologous B-cell precursor acute lymphoblastic leukemia cells.

F Fei, M Lim, A A George, J Kirzner, D Lee, R Seeger, J Groffen, H Abdel-Azim, N Heisterkamp

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Proceedings From the Fourth Haploidentical Stem Cell Transplantation Symposium (HAPLO2016), San Diego, California, December 1, 2016.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

F Fei1] Section of Molecular Carcinogenesis, Los Angeles, CA, USA [2] Division of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
M Lim1] Section of Molecular Carcinogenesis, Los Angeles, CA, USA [2] Division of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
A A GeorgeDivision of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
J KirznerDivision of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
D LeeDivision of Pediatrics, Cell Therapy Section, MD Anderson Cancer Center, University of Texas, Houston, TX, USA.
R SeegerDivision of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
J Groffen1] Section of Molecular Carcinogenesis, Los Angeles, CA, USA [2] Division of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA [3] Leukemia and Lymphoma Program, Norris Comprehensive Cancer Center, University of Southern California, California, CA, USA.
H Abdel-AzimDivision of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
N Heisterkamp1] Section of Molecular Carcinogenesis, Los Angeles, CA, USA [2] Division of Hematology/Oncology and Bone Marrow Transplantation, Department of Pediatrics, The Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA [3] Leukemia and Lymphoma Program, Norris Comprehensive Cancer Center, University of Southern California, California, CA, USA.
Children's Hospital of Los Angeles · USGenesis Foundation · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
TREATMENT OF BCR/ABL CAUSED LEUKEMIAS WITH FTIsR01CA090321 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI HEISTERKAMP, NORA C · 2001 to 2017
$4.4M
Microenvironment-Leukemia Communication Through LectinsR01CA172040 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI GROFFEN, JOHN H, HEISTERKAMP, NORA C · 2013 to 2017
$1.7M
NCI NIH HHS CA090321NCI NIH HHS CA174020NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA090321NCI NIH HHS R01 CA172040
6 · The paper itself

Abstract

Precursor B-lineage acute lymphoblastic leukemia (pre-B ALL) affects hematopoietic development and therefore is associated with immune deficiencies that can be further exacerbated by chemotherapy. It is unclear if and when monoclonal antibodies (mAbs) that stimulate antibody-mediated cellular cytotoxicity (ADCC) can be used for treatment because this depends on the presence of functional effector cells. Here, we used flow cytometry to determine that patient samples at diagnosis, post-induction and relapse contain detectable numbers of CD56+ cells. We were able to selectively expand CD56+ immune effector cells from bone marrow and peripheral blood samples at diagnosis and at various stages of treatment by co-culture with artificial antigen-presenting K562 clone 9.mbIL-21 cells. Amplified CD56+CD3- cells had spontaneous and anti-B cell-activating factor receptor mAb-stimulated ADCC activity against allogeneic ALL cells, which could be further enhanced by IL-15. Importantly, matched CD56+ effector cells also killed autologous ALL cells grown out from leukemia samples of the same patient, through both spontaneous as well as antibody-dependent cellular cytotoxicity. Since autologous cell therapy will not be complicated by graft-versus-host disease, our results show that expanded CD56+ cells could be applied for treatment of pre-B ALL without transplantation, or for purging of bone marrow in the setting of autologous bone marrow transplants.

Indexed as

Cytotoxicity, ImmunologicAntibodies, MonoclonalAntineoplastic AgentsB-LymphocytesBone Marrow CellsCD3 ComplexCD56 AntigenCell ProliferationChildCoculture TechniquesGene ExpressionHumansInterleukin-15K562 CellsKiller Cells, NaturalPrecursor B-Cell Lymphoblastic Leukemia-LymphomaAntibodies, MonoclonalAntineoplastic AgentsCD3 ComplexCD56 AntigenIL15 protein, humanInterleukin-15NCAM1 protein, human

Identifiers

PMID25134458
PMCPMC4334757
OpenAlexW2062374367

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.