Evidence map›Paper›PMID 21757645›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Asymmetric cancer cell division regulated by AKT.

Ipsita Dey-Guha, Anita Wolfer, Albert C Yeh, John G Albeck, Revati Darp, Eduardo Leon, Julia Wulfkuhle, Emanuel F Petricoin, Ben S Wittner, Sridhar Ramaswamy

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. HumaneLife · 2025
    Article
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  16. Review
  17. Asymmetric Cell Division and Tumor Heterogeneity.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Review
  20. Article

21 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

10 authors at 6 institutions in 2 countries.

Ipsita Dey-GuhaCenters for Cancer Research, Regenerative Medicine, Human Genetics Research, and Systems Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Anita Wolfer
Albert C Yeh
John G Albeck
Revati Darp
Eduardo Leon
Julia Wulfkuhle
Emanuel F Petricoin
Ben S Wittner
Sridhar Ramaswamy
Harvard University · USGeorge Mason University · USHarvard University Press · USCenter for Cancer Research · USHarvard Stem Cell Institute · USMassachusetts General Hospital · US

Funding

Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
Variation in Receptor Tyrosine Kinases and Breast Cancer RiskP50CA089393 · NCI · DANA-FARBER CANCER INSTITUTE · PI HARRIS, LYNDSAY NORINE · 2000 to 2009
$28.8M
(PQC6) Molecular Determinants of Quiescent Cancer CellsR01CA185086 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI VASUDEVAN, SHOBHA · 2014 to 2017
$1.8M
Molecular Signatures of Cancer MetastasisK08CA100339 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI RAMASWAMY, SRIDHAR · 2003 to 2007
$679k
Howard Hughes Medical InstituteNCI NIH HHS K08 CA100339NCI NIH HHS P50 CA089393NCI NIH HHS P50 CA127003NCI NIH HHS P50CA127003NCI NIH HHS P50 CA89393NCI NIH HHS R01 CA185086
6 · The paper itself

Abstract

Human tumors often contain slowly proliferating cancer cells that resist treatment, but we do not know precisely how these cells arise. We show that rapidly proliferating cancer cells can divide asymmetrically to produce slowly proliferating "G0-like" progeny that are enriched following chemotherapy in breast cancer patients. Asymmetric cancer cell division results from asymmetric suppression of AKT/PKB kinase signaling in one daughter cell during telophase of mitosis. Moreover, inhibition of AKT signaling with small-molecule drugs can induce asymmetric cancer cell division and the production of slow proliferators. Cancer cells therefore appear to continuously flux between symmetric and asymmetric division depending on the precise state of their AKT signaling network. This model may have significant implications for understanding how tumors grow, evade treatment, and recur.

Indexed as

Cell DivisionBlotting, WesternBreast NeoplasmsCell Line, TumorCell SurvivalDose-Response Relationship, DrugFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHCT116 CellsHeterocyclic Compounds, 3-RingHumansLuminescent ProteinsMicroscopy, ConfocalModels, BiologicalMolecular StructureHeterocyclic Compounds, 3-RingLuminescent ProteinsMK 2206Proto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID21757645
PMCPMC3150943
OpenAlexW2057449864

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.