Evidence map›Paper›PMID 27125204›Full record

ArticleLeukemia2016

CDKN2A-independent role of BMI1 in promoting growth and survival of Ph+ acute lymphoblastic leukemia.

S A Mariani, V Minieri, M De Dominici, I Iacobucci, L F Peterson, B Calabretta

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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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

6 authors at 4 institutions in 2 countries.

S A MarianiDepartment of Cancer Biology and Sydney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
V MinieriDepartment of Cancer Biology and Sydney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
M De DominiciDepartment of Cancer Biology and Sydney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
I IacobucciDepartment of Hematology, University of Bologna, Bologna, Italy.
L F PetersonDivision of Hematology and Oncology, University of Michigan, Ann Arbor, MI, USA.
B CalabrettaDepartment of Cancer Biology and Sydney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
Sidney Kimmel Cancer Center · USThomas Jefferson University · USUniversity of Bologna · ITUniversity of Michigan–Ann Arbor · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Targeting the C/EBPalpha-Gfi-pathway in CML stem cellsR01CA167169 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CALABRETTA, BRUNO · 2013 to 2017
$1.6M
NCI NIH HHS P30 CA056036NCI NIH HHS R01 CA167169
6 · The paper itself

Abstract

BMI1 is a key component of the PRC1 (polycomb repressive complex-1) complex required for maintenance of normal and cancer stem cells. Its aberrant expression is detected in chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia (ALL), but no data exist on BMI1 requirement in ALL cells. We show here that BMI1 expression is important for proliferation and survival of Ph+ ALL cells and for leukemogenesis of Ph+ cells in vivo. Levels of BIM, interferon-α (IFNα)-regulated genes and E2F7 were upregulated in BMI1-silenced cells, suggesting that repressing their expression is important for BMI1 biological effects. Consistent with this hypothesis, we found that: (i) downregulation of BIM or E2F7 abrogated apoptosis or rescued, in part, the reduced proliferation and colony formation of BMI1 silenced BV173 cells; (ii) BIM/E2F7 double silencing further enhanced colony formation and in vivo leukemogenesis of BMI1-silenced cells; (iii) overexpression of BIM and E2F7 mimicked the effect of BMI1 silencing in BV173 and SUP-B15 cells; and (iv) treatment with IFNα suppressed proliferation and colony formation of Ph+ ALL cells. These studies indicate that the growth-promoting effects of BMI1 in Ph+ ALL cells depend on suppression of multiple pathways and support the use of IFNα in the therapy of Ph+ ALL.

Indexed as

AnimalsApoptosisCell LineCell ProliferationCell SurvivalCyclin-Dependent Kinase Inhibitor p16Gene Expression RegulationGene Transfer TechniquesHumansInterferon-alphaMicePolycomb Repressive Complex 1Precursor Cell Lymphoblastic Leukemia-LymphomaBMI1 protein, humanCyclin-Dependent Kinase Inhibitor p16Interferon-alphaPolycomb Repressive Complex 1

Identifiers

PMID27125204
PMCPMC4972639
OpenAlexW2317035559

What OpenQuestion holds

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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.