Evidence map›Paper›PMID 21340093›Full record

ReviewIntegrative biology : quantitative biosciences from nano to macro2011

Apoptotic cell signaling in cancer progression and therapy.

Jessica Plati, Octavian Bucur, Roya Khosravi-Far

Open access · greenAbstract readReview
In one paragraph

Review in Integrative biology : quantitative biosciences from nano to macro, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

125 citing papers in PubMed, 311 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Ubiquitin-Specific Protease 49 Interacts with Bax to Modulate Apoptosis.International journal of molecular sciences · 2026
    Article
  7. Article
  8. Review
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  12. Article
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  14. Observational
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  17. Article
  18. Article
  19. Article
  20. Review

65 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

3 authors at 3 institutions in 2 countries.

Jessica PlatiDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA.
Octavian Bucur
Roya Khosravi-Far
Beth Israel Deaconess Medical Center · USHarvard University · USInstitute of Biochemistry · RO

Funding

Training Program in Angiogenesis &InflammationT32HL007893 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 1998 to 2017
$5.5M
Tumor Selective Apoptosis by TRAILR01HL080192 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2010
$3.6M
Novel Strategies for Treatment of Myeloproliferative DisordersR01CA131664 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2008 to 2012
$1.8M
Oncogene-Induced Evasion from ApoptosisR01CA105306 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2009
$1.6M
NCI NIH HHS CA105306NCI NIH HHS CA131664NCI NIH HHS R01 CA105306NCI NIH HHS R01 CA131664NHLBI NIH HHS HL007893NHLBI NIH HHS HL080192NHLBI NIH HHS R01 HL080192NHLBI NIH HHS T32 HL007893
6 · The paper itself

Abstract

Apoptosis is a tightly regulated cell suicide program that plays an essential role in the development and maintenance of tissue homeostasis by eliminating unnecessary or harmful cells. Impairment of this native defense mechanism promotes aberrant cellular proliferation and the accumulation of genetic defects, ultimately resulting in tumorigenesis, and frequently confers drug resistance to cancer cells. The regulation of apoptosis at several levels is essential to maintain the delicate balance between cellular survival and death signaling that is required to prevent disease. Complex networks of signaling pathways act to promote or inhibit apoptosis in response to various cues. Apoptosis can be triggered by signals from within the cell, such as genotoxic stress, or by extrinsic signals, such as the binding of ligands to cell surface death receptors. Various upstream signaling pathways can modulate apoptosis by converging on, and thereby altering the activity of, common central control points within the apoptotic signaling pathways, which involve the BCL-2 family proteins, inhibitor of apoptosis (IAP) proteins, and FLICE-inhibitory protein (c-FLIP). This review highlights the role of these fundamental regulators of apoptosis in the context of both normal apoptotic signaling mechanisms and dysregulated apoptotic pathways that can render cancer cells resistant to cell death. In addition, therapeutic strategies aimed at modulating the activity of BCL-2 family proteins, IAPs, and c-FLIP for the targeted induction of apoptosis are briefly discussed.

Indexed as

Disease ProgressionAnimalsApoptosisHumansNeoplasmsSignal Transduction

Identifiers

PMID21340093
PMCPMC3130501
OpenAlexW2133575920

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.