Evidence map›Paper›PMID 22249027›Full record

ReviewThe international journal of biochemistry & cell biology2012

Breast cancer stem cells.

Marco A Velasco-Velázquez, Nora Homsi, Marisol De La Fuente, Richard G Pestell

Abstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Ropivacaine as a novel AKT1 specific inhibitor regulates the stemness of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. CD24: A Novel Target for Cancer Immunotherapy.Journal of personalized medicine · 2022
    Review
  20. Article

23 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 4 institutions in 2 countries.

Marco A Velasco-VelázquezDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA. marcovelasco@unam.mx
Nora Homsi
Marisol De La Fuente
Richard G Pestell
Sidney Kimmel Cancer Center · USTemple University · USThomas Jefferson University · USUniversidad Nacional Autónoma de México · MX

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Initiation and Maintenance In Mammary TumorigenesisR01CA075503 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 1998 to 2011
$4.6M
CYCLIN D1 FUNCTION IN PROSTATE CANCERR01CA086072 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2001 to 2013
$3.3M
REGULATION OF CYCLIN D1 EXPRESSIONR01CA070896 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2000 to 2010
$3.2M
DACH1/Eya Cell fate determination factor and mammary tumorigenesisR01CA132115 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2009 to 2018
$3.1M
Cyclin D1 Regulation of Nuclear Receptor Function in Breast CancerR01CA107382 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2004 to 2008
$1.6M
NCI NIH HHS P30 CA056036NCI NIH HHS P30CA56036NCI NIH HHS R01 CA070896NCI NIH HHS R01CA070896NCI NIH HHS R01 CA075503NCI NIH HHS R01CA075503NCI NIH HHS R01 CA086072NCI NIH HHS R01CA086072NCI NIH HHS R01 CA107382NCI NIH HHS R01CA107382NCI NIH HHS R01 CA132115NCI NIH HHS R01CA132115
6 · The paper itself

Abstract

Breast cancer stem cells (BCSCs) constitute a subpopulation of tumor cells that express stem cell-associated markers and have a high capacity for tumor generation in vivo. Identification of BCSCs from tumor samples or breast cancer cell lines has been based mainly on CD44(+)/CD24(-/low) or ALDH(+) phenotypes. BCSCs isolation has allowed the analysis of the molecular mechanisms involved in their origin, self-renewal, differentiation into tumor cells, resistance to radiation therapy and chemotherapy, and invasiveness and metastatic ability. Molecular genetic analysis using knockout animals and inducible transgenics has identified NF-κB, c-Jun, p21(CIP1), and Forkhead-like-protein Dach1 involvement in BCSC expansion and fate. Clinical analyses of BCSCs in breast tumors have found a correlation between the proportion of BCSCs and poor prognosis. Therefore, new therapies that specifically target BCSCs are an urgent need. We summarize recent evidence that partially explain the biological characteristics of BCSCs.

Indexed as

Neoplastic Stem CellsAnimalsBreast NeoplasmsCell DifferentiationDrug Resistance, NeoplasmHumansNeoplasm Metastasis

Identifiers

PMID22249027
PMCPMC3294043
OpenAlexW2111984765

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.