Evidence map›Paper›PMID 20058155›Full record

ArticleRadiation and environmental biophysics2010

Modeling progression in radiation-induced lung adenocarcinomas.

Hatim Fakir, Werner Hofmann, Rainer K Sachs

Abstract read
In one paragraph

Article in Radiation and environmental biophysics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

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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.

Hatim FakirLondon Regional Cancer Program, 790 Commissioners Rd. E., London, ON, N6A 4L6, Canada. hatim.fakir@lhsc.on.ca
Werner Hofmann
Rainer K Sachs

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quantitative multistage carcinogenesis models are used in radiobiology to estimate cancer risks and latency periods (time from exposure to clinical cancer). Steps such as initiation, promotion and transformation have been modeled in detail. However, progression, a later step during which malignant cells can develop into clinical symptomatic cancer, has often been approximated simply as a fixed lag time. This approach discounts important stochastic mechanisms in progression and evidence on the high prevalence of dormant tumors. Modeling progression more accurately is therefore important for risk assessment. Unlike models of earlier steps, progression models can readily utilize not only experimental and epidemiological data but also clinical data such as the results of modern screening and imaging. Here, a stochastic progression model is presented. We describe, with minimal parameterization: the initial growth or extinction of a malignant clone after formation of a malignant cell; the likely dormancy caused, for example, by nutrient and oxygen deprivation; and possible escape from dormancy resulting in a clinical cancer. It is shown, using cohort simulations with parameters appropriate for lung adenocarcinomas, that incorporating such processes can dramatically lengthen predicted latency periods. Such long latency periods together with data on timing of radiation-induced cancers suggest that radiation may influence progression itself.

Indexed as

Disease ProgressionModels, BiologicalAdenocarcinomaCohort StudiesHumansLung NeoplasmsNeoplasm InvasivenessNeoplasms, Radiation-InducedStochastic Processes

Identifiers

PMID20058155
PMCPMC2855436

What OpenQuestion holds

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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.