Evidence map›Paper›PMID 27019364›Full record

ReviewAging2016

Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies.

Giuseppa Pistritto, Daniela Trisciuoglio, Claudia Ceci, Alessia Garufi, Gabriella D'Orazi

Open access · hybridAbstract readReview
In one paragraph

Review in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 842 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
842citing papers in PubMed, 5 pooled it
23.5field-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

842 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,619 citations in OpenAlex.

  1. Prognostic Value of Bcl-xL in Head and Neck Squamous Cell Carcinoma: A Systematic Review and Meta-Analysis.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
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  11. International journal of molecular sciences · 2026
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  12. Oral vitamin DPoultry science · 2026
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782 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.

Giuseppa PistrittoDepartment of Systems Medicine, University "Tor Vergata", 00133 Rome, Italy.
Daniela TrisciuoglioDepartment of Research, Advanced Diagnostics, and Technological Innovation, Regina Elena National Cancer Institute, 00158 Rome, Italy.
Claudia CeciDepartment of Systems Medicine, University "Tor Vergata", 00133 Rome, Italy.
Alessia GarufiDepartment of Research, Advanced Diagnostics, and Technological Innovation, Regina Elena National Cancer Institute, 00158 Rome, Italy.
Gabriella D'OraziDepartment of Research, Advanced Diagnostics, and Technological Innovation, Regina Elena National Cancer Institute, 00158 Rome, Italy.
University of Chieti-Pescara · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells, such as those resulting from DNA damage or during development. 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. Deregulation in apoptotic cell death machinery is an hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression but also for tumor resistance to therapies. Most anticancer drugs currently used in clinical oncology exploit the intact apoptotic signaling pathways to trigger cancer cell death. Thus, defects in the death pathways may result in drug resistance so limiting the efficacy of therapies. Therefore, a better understanding of the apoptotic cell death signaling pathways may improve the efficacy of cancer therapy and bypass resistance. This review will highlight the role of the fundamental regulators of apoptosis and how their deregulation, including activation of anti-apoptotic factors (i.e., Bcl-2, Bcl-xL, etc) or inactivation of pro-apoptotic factors (i.e., p53 pathway) ends up in cancer cell resistance to therapies. In addition, therapeutic strategies aimed at modulating apoptotic activity are briefly discussed.

Indexed as

AnimalsAntineoplastic AgentsApoptosisDisease ProgressionHumansNeoplasmsSignal TransductionAntineoplastic Agentsapoptosiscancerdefective apoptotic pathwaysmiRNAsp53small molecules

Identifiers

PMID27019364
PMCPMC4925817
OpenAlexW2408954743

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.