Evidence map›Paper›PMID 11438662›Full record

ArticleMolecular and cellular biology2001

Apoptosis triggered by Myc-induced suppression of Bcl-X(L) or Bcl-2 is bypassed during lymphomagenesis.

C M Eischen, D Woo, M F Roussel, J L Cleveland

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

112 citing papers in PubMed, 213 citations in OpenAlex.

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  13. FTO Alleviates CdClInternational journal of molecular sciences · 2022
    Article
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52 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

C M EischenDepartment of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
D Woo
M F Roussel
J L Cleveland
St. Jude Children's Research Hospital · USUniversity of California, Los Angeles · USUniversity of Tennessee Health Science Center · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
PAX3/FKHR IN ALVEOLAR RHABDOMYOSARCOMAP01CA071907 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI DOWNING, JAMES R · 1996 to 2005
$10.8M
The Bcl-2/Bcl-X Pathway in Myc-Induced LymphomagenesisR01CA076379 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1998 to 2012
$3.5M
Myc Role in Hematopoiesis, Vasculogenesis &AgiogenesisR01DK044158 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1991 to 2009
$2.8M
FMS TRANSFORMATION/CSF-1 RECEPTOR SIGNAL TRANSDUCTIONR01CA056819 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ROUSSEL, MARTINE F · 1992 to 2001
$594k
MOLECULAR CHARACTERIZATION OF THE MURINE PCY MUTATIONR01DK045663 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WOO, DAVID D · 1992 to 1996
–
DIFFERENTIAL GENE EXPRESSION IN POLYCYSTIC KIDNEYSR01DK040700 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WOO, DAVID D · 1990 to 1992
–
MEDIATORS OF MYC INDUCED MYELOID LEUKEMIA AND APOPTOSISF32CA081695 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI EISCHEN, CHRISTINE M · 1999 to 1999
–
NCI NIH HHS CA-21765NCI NIH HHS CA56819NCI NIH HHS CA71907NCI NIH HHS CA76379NCI NIH HHS CA81695NCI NIH HHS F32 CA081695NCI NIH HHS P01 CA071907NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA076379NIDDK NIH HHS DK40700NIDDK NIH HHS DK44158NIDDK NIH HHS DK45663NIDDK NIH HHS R01 DK044158
6 · The paper itself

Abstract

Enforced Bcl-2 expression inhibits Myc-induced apoptosis and cooperates with Myc in transformation. Here we report that the synergy between Bcl-2 and Myc in transforming hematopoietic cells in fact reflects a Myc-induced pathway that selectively suppresses the expression of the Bcl-X(L) or Bcl-2 antiapoptotic protein. Myc activation suppresses Bcl-X(L) RNA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-X(L) and Bcl-2 expression is inhibited by Myc in precancerous B cells from Emu-myc transgenic mice. The suppression of bcl-X RNA levels by Myc requires de novo protein synthesis, indicating that repression is indirect. Importantly, the suppression of Bcl-2 or Bcl-X(L) by Myc is corrupted during Myc-induced tumorigenesis, as Bcl-2 and/or Bcl-X(L) levels are markedly elevated in over one-half of all lymphomas arising in Emicro-myc transgenic mice. Bcl-2 and/or Bcl-X(L) overexpression did not correlate with loss of ARF or p53 function in tumor cells, indicating that these two apoptotic pathways are inactivated independently. Therefore, the suppression of Bcl-X(L) or Bcl-2 expression represents a physiological Myc-induced apoptotic pathway that is frequently bypassed during lymphomagenesis.

Indexed as

ApoptosisADP-Ribosylation Factor 1Animalsbcl-X ProteinBlotting, NorthernBlotting, WesternCells, CulturedCell SurvivalLymph NodesMiceMice, KnockoutMice, TransgenicMyeloid CellsProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycRNAADP-Ribosylation Factor 1Bcl2l1 protein, mousebcl-X ProteinProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycRNATumor Suppressor Protein p53

Identifiers

PMID11438662
PMCPMC87232
OpenAlexW2126393916

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.