Evidence map›Paper›PMID 26160835›Full record

ReviewOncotarget2015

RB1 dual role in proliferation and apoptosis: cell fate control and implications for cancer therapy.

Paola Indovina, Francesca Pentimalli, Nadia Casini, Immacolata Vocca, Antonio Giordano

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
7.5field-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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
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  17. Proteogenomic discovery ofScience advances · 2025
    Article
  18. Retinocytoma: understanding pathogenesis, diagnosis, and treatment approaches.International journal of retina and vitreous · 2025
    Review
  19. Article
  20. Article

43 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 2 countries.

Paola IndovinaSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA, USA.
Francesca PentimalliOncology Research Center of Mercogliano (CROM), Istituto Nazionale Tumori "Fodazione G. Pascale" - IRCCS, Naples, Italy.
Nadia CasiniDepartment of Medicine, Surgery and Neuroscience, University of Siena and Istituto Toscano Tumori (ITT), Siena, Italy.
Immacolata VoccaOncology Research Center of Mercogliano (CROM), Istituto Nazionale Tumori "Fodazione G. Pascale" - IRCCS, Naples, Italy.
Antonio GiordanoSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA, USA.
University of Siena · ITIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inactivation of the retinoblastoma (RB1) tumor suppressor is one of the most frequent and early recognized molecular hallmarks of cancer. RB1, although mainly studied for its role in the regulation of cell cycle, emerged as a key regulator of many biological processes. Among these, RB1 has been implicated in the regulation of apoptosis, the alteration of which underlies both cancer development and resistance to therapy. RB1 role in apoptosis, however, is still controversial because, depending on the context, the apoptotic cues, and its own status, RB1 can act either by inhibiting or promoting apoptosis. Moreover, the mechanisms whereby RB1 controls both proliferation and apoptosis in a coordinated manner are only now beginning to be unraveled. Here, by reviewing the main studies assessing the effect of RB1 status and modulation on these processes, we provide an overview of the possible underlying molecular mechanisms whereby RB1, and its family members, dictate cell fate in various contexts. We also describe the current antitumoral strategies aimed at the use of RB1 as predictive, prognostic and therapeutic target in cancer. A thorough understanding of RB1 function in controlling cell fate determination is crucial for a successful translation of RB1 status assessment in the clinical setting.

Indexed as

ApoptosisCell ProliferationAnimalsAntineoplastic AgentsBiomarkers, TumorGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplasmsPhosphorylationRetinoblastoma ProteinSignal TransductionTreatment OutcomeAntineoplastic AgentsBiomarkers, TumorRetinoblastoma Proteinapoptosiscancer therapyCDK inhibitorsE2FRB family

Identifiers

PMID26160835
PMCPMC4627222
OpenAlexW2101615610

What OpenQuestion 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 OpenQuestion graph.