Evidence map›Paper›PMID 10498879›Full record

ReviewOncogene1999

Transgenic models of lymphoid neoplasia and development of a pan-hematopoietic vector.

J M Adams, A W Harris, A Strasser, S Ogilvy, S Cory

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. ROS-Induced CXCR4 Signaling Regulates Mantle Cell Lymphoma (MCL) Cell Survival and Drug Resistance in the Bone Marrow Microenvironment via Autophagy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Pathogenesis of human B cell lymphomas.Annual review of immunology · 2012
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Micromanagement of lymphomas.PLoS biology · 2008
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

J M AdamsThe Walter and Eliza Hall Institute of Medical Research, P.O. Royal Melbourne Hospital, Melbourne, Victoria 3050, Australia.
A W Harris
A Strasser
S Ogilvy
S Cory
The Royal Melbourne Hospital · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

ONCOGENE-INDUCED LEUKEMOGENESIS IN TRANSGENIC MICER01CA043540 · NCI · WALTER AND ELIZA HALL INST MEDICAL RES · PI CORY, SUZANNE · 1987 to 2009
$1.7M
MECHANISMS IN THE REGULATION OF APOPTOSISR01CA080188 · NCI · WALTER AND ELIZA HALL INST MEDICAL RES · PI ADAMS, JERRY M · 1999 to 2006
$1.1M
NCI NIH HHS CA43540NCI NIH HHS CA80188
6 · The paper itself

Abstract

The pathways to lymphoid neoplasia have been explored in a number of transgenic models. Because B lymphoid malignancies often involve translocation of an oncogene (e.g. myc, bcl-2, cyclin D1) to an immunoglobulin locus, resulting in its deregulated expression, the consequences of oncogene overexpression in lymphocytes can be evaluated with transgenes driven by an immunoglobulin regulatory element, such as an enhancer from the IgH locus. Mice bearing such transgenes have provided insight into the preneoplastic state, including alterations in the control of cellular proliferation, differentiation or apoptosis. They have also allowed studies on oncogene cooperation in vivo and the modulating effect of genetic background. Briefly reviewed here are the models studied in the authors' laboratories. Mice bearing myc and bcl-2 transgenes have received most attention but others studied include abl, ras, cyclin D1 and bmi-1 oncogenes. Also discussed is a new transgenic vector that should facilitate transgenic approaches to non-lymphoid leukemias. The vector bears elements from the promoter region of the vav gene, which is expressed almost exclusively in hematopoietic cells. It has proven capable of driving transgene expression throughout the hematopoietic compartment, including progenitor cells and their precursors. This novel vector should aid studies on many aspects of hematopoiesis, including the modeling of leukemogenesis.

Indexed as

Disease Models, AnimalGenetic VectorsAnimalsHematopoietic Stem CellsHumansLymphomaMiceMice, TransgenicOncogenes

Identifiers

PMID10498879
OpenAlexW2116905501

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.