Stem cell replication, somatic mutations and role of randomness in the development of cancer

Vittorio Perduca; Ludmil B. Alexandrov; Michelle Kelly-Irving; Cyrille Delpierre; Hanane Omichessan; Mark P. Little; Paolo Vineis; Gianluca Severi

doi:10.1007/s10654-018-0477-6

Stem cell replication, somatic mutations and role of randomness in the development of cancer

Vittorio Perduca, Ludmil B. Alexandrov, Michelle Kelly-Irving, Cyrille Delpierre, Hanane Omichessan, Mark P. Little, Paolo Vineis, Gianluca Severi

Research output: Contribution to journal › Review article › peer-review

12 Citations (Scopus)

Abstract

An intense scientific debate has recently taken place relating to the “bad luck” hypothesis in cancer development, namely that intrinsic random, and therefore unavoidable, mutagenic events would have a predominant role in tumorigenesis. In this article we review the main contributions to this debate and explain the reasons why the claim that cancer is mostly explained by intrinsic random factors is unsupported by data and theoretical models. In support of this, we present an analysis showing that smoking-induced mutations are more predictive of cancer risk than the lifetime number of stem cell cellular divisions.

Original language	English
Pages (from-to)	439-445
Number of pages	7
Journal	European Journal of Epidemiology
Volume	34
Issue number	5
DOIs	https://doi.org/10.1007/s10654-018-0477-6
Publication status	Published - 15 May 2019
Externally published	Yes

Keywords

Cancer
Environment
Epidemiology
Risk factors
Somatic mutations

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10.1007/s10654-018-0477-6

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title = "Stem cell replication, somatic mutations and role of randomness in the development of cancer",

abstract = "An intense scientific debate has recently taken place relating to the “bad luck” hypothesis in cancer development, namely that intrinsic random, and therefore unavoidable, mutagenic events would have a predominant role in tumorigenesis. In this article we review the main contributions to this debate and explain the reasons why the claim that cancer is mostly explained by intrinsic random factors is unsupported by data and theoretical models. In support of this, we present an analysis showing that smoking-induced mutations are more predictive of cancer risk than the lifetime number of stem cell cellular divisions.",

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AU - Perduca, Vittorio

AU - Alexandrov, Ludmil B.

AU - Kelly-Irving, Michelle

AU - Delpierre, Cyrille

AU - Omichessan, Hanane

AU - Little, Mark P.

AU - Vineis, Paolo

AU - Severi, Gianluca

PY - 2019/5/15

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N2 - An intense scientific debate has recently taken place relating to the “bad luck” hypothesis in cancer development, namely that intrinsic random, and therefore unavoidable, mutagenic events would have a predominant role in tumorigenesis. In this article we review the main contributions to this debate and explain the reasons why the claim that cancer is mostly explained by intrinsic random factors is unsupported by data and theoretical models. In support of this, we present an analysis showing that smoking-induced mutations are more predictive of cancer risk than the lifetime number of stem cell cellular divisions.

AB - An intense scientific debate has recently taken place relating to the “bad luck” hypothesis in cancer development, namely that intrinsic random, and therefore unavoidable, mutagenic events would have a predominant role in tumorigenesis. In this article we review the main contributions to this debate and explain the reasons why the claim that cancer is mostly explained by intrinsic random factors is unsupported by data and theoretical models. In support of this, we present an analysis showing that smoking-induced mutations are more predictive of cancer risk than the lifetime number of stem cell cellular divisions.

KW - Cancer

KW - Environment

KW - Epidemiology

KW - Risk factors

KW - Somatic mutations

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M3 - Review article

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EP - 445

JO - European Journal of Epidemiology

JF - European Journal of Epidemiology

IS - 5

ER -

Stem cell replication, somatic mutations and role of randomness in the development of cancer

Abstract

Keywords

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