Evidence map›Paper›PMID 17941951›Full record

ReviewBritish journal of haematology2007

Murine models of chronic lymphocytic leukaemia: role of microRNA-16 in the New Zealand Black mouse model.

Brian J Scaglione, Erica Salerno, Murugabaskar Balan, Frederick Coffman, Pablo Landgraf, Fatima Abbasi, Sergei Kotenko, Gerald E Marti, Elizabeth S Raveche

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of haematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Knockout of both miR-15/16 loci induces acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  7. Review
  8. Animal Models to Study MicroRNA Function.Advances in cancer research · 2017
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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 4 institutions in 1 country.

Brian J ScaglioneNew Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
Erica Salerno
Murugabaskar Balan
Frederick Coffman
Pablo Landgraf
Fatima Abbasi
Sergei Kotenko
Gerald E Marti
Elizabeth S Raveche
Rutgers New Jersey Medical SchoolCenter for Biologics Evaluation and Research · USRutgers, The State University of New Jersey · USRockefeller University · US

Funding

Studies of the role of microRNA miR-16-1 in the NZB mouse model of CLLR01CA129826 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RAVECHE, ELIZABETH S · 2010 to 2012
$938k
IMMUNOREGULATION BY UNIQUE AUTOIMMUNE LY1+ B CELLSR01CA071478 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RAVECHE, ELIZABETH S · 1997 to 2000
$198k
NCI NIH HHS R01 CA071478NCI NIH HHS R01 CA129826
6 · The paper itself

Abstract

Mouse models are valuable tools in the study of human chronic lymphocytic leukaemia (CLL). The New Zealand Black (NZB) strain is a naturally occurring model of late-onset CLL characterized by B-cell hyperproliferation and autoimmunity early in life, followed by progression to CLL. Other genetically engineered models of CLL that have been developed include (NZB x NZW) F1 mice engineered to express IL5, mice expressing human TCL1A, and mice overexpressing both BCL2 and a tumour necrosis factor receptor-associated factor. The applicability to human CLL varies with each model, suggesting that CLL is a multifactorial disease. Our work with the de novo NZB model has revealed many similarities to the human situation, particularly familial CLL. In NZB, the malignant clones express CD5, zap-70, and have chromosomal instability and germline Ig sequence. We also identified a point mutation in the 3'-flanking sequence of Mirn16-1, which resulted in decreased levels of the microRNA, miR-16 in lymphoid tissue. Exogenous restoration of miR-16 to an NZB malignant B-1 cell line resulted in cell cycle alterations, suggesting that the altered expression of Mirn15a/16-1 is an important molecular lesion in CLL. Future studies utilizing the NZB mouse could ascertain the role of environmental triggers, such as low dose radiation and organic chemicals in the augmentation of a pre-existing propensity to develop CLL.

Indexed as

Disease Models, AnimalAnimalsBase SequenceLeukemia, Lymphocytic, Chronic, B-CellMiceMice, Inbred NZBMice, TransgenicMicroRNAsMolecular Sequence DataPoint MutationRNA, NeoplasmMicroRNAsRNA, Neoplasm

Identifiers

PMID17941951
PMCPMC2692662
OpenAlexW2026139605

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.