Evidence map›Paper›PMID 32632094›Full record

ArticleLeukemia2020

Is cancer latency an outdated concept? Lessons from chronic myeloid leukemia.

Manuel Abecasis, Nicholas C P Cross, Manuel Brito, Isabelina Ferreira, Kathleen M Sakamoto, Nobuko Hijiya, Joannah Score, Robert Peter Gale

Abstract read
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In one paragraph

Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  7. Cell Phone Radiation Exposure Limits and Engineering Solutions.International journal of environmental research and public health · 2023
    Review
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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

8 authors at 5 institutions in 3 countries.

Manuel AbecasisDepartment of Hematology, Instituto Portugues de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal.
Nicholas C P CrossSchool of Medicine, University of Southampton, Southampton, UK.ORCID http://orcid.org/0000-0001-5481-2555
Manuel BritoServiço de Hematologia, Hospital Pediátrico de Coimbra, Coimbra, Portugal.
Isabelina FerreiraDepartment of Hematology, Instituto Portugues de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal.
Kathleen M SakamotoDepartment of Pediatrics, Division of Hematology/Oncology, Stanford University, Palo Alto, CA, USA.
Nobuko HijiyaDepartment of Pediatrics, Division of Hematology Oncology and Stem Cell Transplant, Columbia University, Irving Medical Center, New York, NY, USA.
Joannah ScoreSchool of Medicine, University of Southampton, Southampton, UK.
Robert Peter GaleDepartment of Immunology and Inflammation, Haematology Research Centre, Imperial College London, London, UK. robertpetergale@alumni.ucla.edu.ORCID http://orcid.org/0000-0002-9156-1676
University of Southampton · GBCentre for Inflammation Research · GBColumbia University Irving Medical Center · USHospitais da Universidade de Coimbra · PTStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our concept of cancer latency, the interval from when a cancer starts until it is diagnosed, has changed dramatically. A prior widely-used definition was the interval between an exposure to a cancer-causing substance and cancer diagnosis. However, this definition does not accurately reflect current knowledge of how most cancers develop assuming, mostly incorrectly, one exposure is the sole cause of a cancer, ignoring the possibility the cancer being considered would have developed anyway but that the exposure accelerated cancer development and eliding the randomness in when a cancer is diagnosed. We show, using chronic myeloid leukaemia as a model, that defining cancer latency is not as simple as it once seemed. It is difficult or impossible to know at which event or mutation to start to clock to measure cancer latency. It is equally difficult to know when to stop the clock given the stochastic nature of when cancers are diagnosed. Importantly, even in genetically-identical twins with the same driver mutation intervals to develop cancer vary substantially. And we discuss other confonders. Clearly we need a new definition of cancer latency or we need to abandon the concept of cancer latency in the modern era of cancer biology.

Indexed as

Disease ProgressionHumansLeukemia, Myelogenous, Chronic, BCR-ABL Positive

Identifiers

PMID32632094
OpenAlexW3039335298

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.