Evidence map›Paper›PMID 20863894›Full record

ReviewSeminars in cancer biology2010

Molecular basis of CLL.

Yuri Pekarsky, Nicola Zanesi, Carlo M Croce

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Expression signature of human endogenous retroviruses in chronic lymphocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Non-Coding RNAs: The "Dark Side Matter" of the CLL Universe.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Yuri PekarskyHuman Cancer Genetics Program and Department of Molecular Virology, Immunology and Medical Genetics, OSU School of Medicine, Ohio State University, Columbus, OH 43210, USA. Pekarsky.Yuri@osumc.edu
Nicola Zanesi
Carlo M Croce
Cancer Genetics (United States) · US

Funding

Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
NCI NIH HHS P01 CA081534
6 · The paper itself

Abstract

B-cell chronic lymphocytic leukemia (CLL), the most common leukemia in the Western world, results from an expansion of a rare population of CD5+ mature B-lymphocytes. CLL occurs in two forms, aggressive and indolent. For the most part indolent CLL is characterized by low ZAP-70 expression and mutated IgH V(H); aggressive CLL shows high ZAP-70 expression and unmutated IgH V(H). Although clinical features and genomic abnormalities in CLL have been studied extensively, molecular mechanisms underlying disease development are still emerging. In the last few years, several important insights were reported in this area. MiR-15/16 targeting BCL2 and MCL1 and DLEU7 targeting TNF pathway were proposed as tumor suppressors at 13q14, a commonly deleted region in indolent CLL. Molecular details of how activation of TCL1, a critical oncogene in aggressive CLL, results in the initiation of this malignancy were clarified. Importance of these pathways was supported by investigations of several mouse models of CLL. Here, we present what has been learned from these new pathways, discuss mouse CLL models and how these mouse models recapitulate the molecular mechanisms of this common leukemia.

Indexed as

AnimalsChromosomes, Human, Pair 13HumansLeukemia, Lymphocytic, Chronic, B-CellMicroRNAsProto-Oncogene ProteinsTumor Suppressor ProteinsMicroRNAsProto-Oncogene ProteinsTumor Suppressor Proteins

Identifiers

PMID20863894
PMCPMC2997849
OpenAlexW2058831176

What OpenQuestion holds

Textmetadata
LicenceTDM
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.