Evidence map›Paper›PMID 21673068›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2011

ERK1/2 and p38α/β signaling in tumor cell quiescence: opportunities to control dormant residual disease.

Maria Soledad Sosa, Alvaro Avivar-Valderas, Paloma Bragado, Huei-Chi Wen, Julio A Aguirre-Ghiso

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

155 citing papers in PubMed, 223 citations in OpenAlex.

  1. Review
  2. Review
  3. Mechanisms of breast cancer dormancy in bone metastasis.Clinical & experimental metastasis · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Unlocking Lung Cancer Cell Dormancy: An Epigenetic Perspective.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Cancer Cell Dormancy in the Bone Microenvironment.Current osteoporosis reports · 2025
    Review
  18. Review
  19. Review
  20. Enter sandman: how to tackle dormant breast cancer cells.Medical oncology (Northwood, London, England) · 2025
    Review

95 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

5 authors at 2 institutions in 1 country.

Maria Soledad SosaDepartment of Medicine, Division of Hematology and Oncology, Tisch Cancer Institute at Mount Sinai, New York, New York, USA.
Alvaro Avivar-Valderas
Paloma Bragado
Huei-Chi Wen
Julio A Aguirre-Ghiso
Icahn School of Medicine at Mount Sinai · USUniversity at Albany, State University of New York · US

Funding

Functional Determinants of Metastatic DormancyR01CA109182 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI AGUIRRE-GHISO, JULIO A. · 2005 to 2025
$8.3M
Translational Machinery in Stress Signaling and Tumor SuppressionR21ES017146 · NIEHS · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI AGUIRRE-GHISO, JULIO A., BEGLEY, THOMAS J · 2009 to 2010
$454k
NCI NIH HHS CA109182NCI NIH HHS R01 CA109182NIEHS NIH HHS ES017146NIEHS NIH HHS R21 ES017146
6 · The paper itself

Abstract

Systemic minimal residual disease after primary tumor treatment can remain asymptomatic for decades. This is thought to be due to the presence of dormant disseminated tumor cells (DTC) or micrometastases in different organs. DTCs lodged in brain, lungs, livers, and/or bone are a major clinical problem because they are the founders of metastasis, which ultimately kill cancer patients. The problem is further aggravated by our lack of understanding of DTC biology. In consequence, there are almost no rational therapies to prevent dormant DTCs from surviving and expanding. Several cancers, including melanoma as well as breast, prostate, and colorectal carcinomas, undergo dormant periods before metastatic recurrences develop. Here we review our experience in studying the cross-talk between ERK1/2 and p38α/β signaling in models of early cancer progression, dissemination, and DTC dormancy. We also provide some potential translational and clinical applications of these findings and describe how some currently used therapies might be useful to control dormant disease. Finally, we draw caution on the use of p38 inhibitors currently in clinical trials for different diseases as these may accelerate metastasis development.

Indexed as

MAP Kinase Signaling SystemResting Phase, Cell CycleBreast NeoplasmsExtracellular Signal-Regulated MAP KinasesFemaleHumansMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14Mitogen-Activated Protein Kinase 3Neoplasm, ResidualNeoplasmsp38 Mitogen-Activated Protein KinasesStress, PhysiologicalExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein Kinases

Identifiers

PMID21673068
PMCPMC3226348
OpenAlexW1979964863

What OpenQuestion holds

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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.