Evidence map›Paper›PMID 16247448›Full record

ArticleOncogene2006

The fate of irradiated tumor cells.

C Belka

Abstract readComment
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

C BelkaDepartment of Radiation Oncology, University Tübingen, Tübingen, Germany. claus.belka@uni-tuebingen.de
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy remains a key component of modern multimodal anticancer treatment approaches. Although most clinically relevant improvements in radiation oncology are based on optimized radiation technology, it now becomes obvious that biology-based approaches will further boost the efficacy of modern radiation oncology. Of relevance to this is the question of the ultimate fate of an irradiated cell and the mechanistic basis of the induced cell death or inactivation observed. Research bearing on this question is reported in this issue of Oncogene by Wendt et al. (2005), who show that the levels of p21CIP/WAF1 play a key role in determining whether an irradiated tumour cell is arrested in the G2 phase of the cell cycle, rather than apoptosing. The demonstration that caffeine treatment can abrogate this G2 arrest, and that the cells go on to die, has implications for overcoming treatment resistance imposed by radiation-induced upregulation of p21CIP/WAF1.

Indexed as

CaffeineCell DeathCyclin-Dependent Kinase Inhibitor p21G2 PhaseHumansNeoplasmsRadiation ToleranceUp-RegulationCaffeineCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21

Identifiers

PMID16247448
OpenAlexW1979814659

What OpenQuestion holds

Textmetadata
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.