Evidence map›Paper›PMID 16855632›Full record

ArticleLeukemia2006

Aberrant stabilization of c-Myc protein in some lymphoblastic leukemias.

S Malempati, D Tibbitts, M Cunningham, Y Akkari, S Olson, G Fan, R C Sears

Open access · bronzeAbstract read
In one paragraph

Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.3field-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

55 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.International journal of biological sciences · 2026
    Review
  3. Review
  4. Fueling the fire-a pan-cancer analysis of MYC-regulated lipid metabolism.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Mission Possible: Advances in MYC Therapeutic Targeting in Cancer.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2019
    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

7 authors at 1 institution in 1 country.

S MalempatiDepartment of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
D Tibbitts
M Cunningham
Y Akkari
S Olson
G Fan
R C Sears
Oregon Health & Science University · US

Funding

Cellular Mechanisms Controlling Myc Protein StabilityR01CA100855 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2003 to 2014
$3.6M
Integration of Ras, Myc and E2F Signaling PathwaysK01CA086957 · NCI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2001 to 2005
$700k
NCI NIH HHS K01 CA086957NCI NIH HHS R01 CA100855
6 · The paper itself

Abstract

Overexpression of the c-Myc oncoprotein is observed in a large number of hematopoietic malignancies, and transgenic animal models have revealed a potent role for c-Myc in the generation of leukemias and lymphomas. However, the reason for high c-Myc protein levels in most cases is unknown. We examined whether aberrant protein stabilization could be a mechanism of c-Myc overexpression in leukemia cell lines and in primary bone marrow samples from pediatric acute lymphoblastic leukemia (ALL) patients. We found that c-Myc protein half-life was prolonged in the majority of leukemia cell lines and bone marrow samples tested. There were no mutations in the c-myc gene in any of the leukemia cell lines that could account for increased c-Myc stability. However, abnormal phosphorylation at two conserved sites, Threonine 58 and Serine 62, was observed in leukemia cell lines with stabilized c-Myc. Moreover, stabilized c-Myc from the ALL cell lines showed decreased affinity for glycogen synthase kinase3beta, the kinase that phosphorylates c-Myc at Threonine 58 and facilitates its degradation. These findings reveal that deregulation of the c-Myc degradation pathway controlled by Serine 62 and Threonine 58 phosphorylation is a novel mechanism for increased expression of a potent oncoprotein known to be involved in hematopoietic malignancies.

Indexed as

Amino Acid SequenceBlotting, WesternCell LineChildEnzyme ActivationGene AmplificationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansImmunoprecipitationIn Situ Hybridization, FluorescenceMolecular Sequence DataPhosphatidylinositol 3-KinasesPhosphorylationPrecursor Cell Lymphoblastic Leukemia-LymphomaProteasome Endopeptidase ComplexATP dependent 26S proteaseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mycSerineThreonine

Identifiers

PMID16855632
PMCPMC2322939
OpenAlexW2051025473

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.