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Cited by 981Cancer, Stress, Anesthesia, and Immune ResponseStress Responses and CortisolTryptophan and brain disorders

The influence of bio-behavioural factors on tumour biology: pathways and mechanisms

Open access
Antoni, Michael H., Lutgendorf, Susan K., Cole, Steven W., Dhabhar, Firdaus S., Sephton, Sandra E., McDonald, Paige Green, Stefanek, Michael, Sood, Anil K.·2006·Nature Reviews Cancer
DOI 10.1038/nrc1820PMC PMC3146042
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Abstract

Epidemiological studies indicate that stress, chronic depression and lack of social support might serve as risk factors for cancer development and progression. Recent cellular and molecular studies have identified biological processes that could potentially mediate such effects. This review integrates clinical, cellular and molecular studies to provide a mechanistic understanding of the interface between biological and behavioural influences in cancer, and identifies novel behavioural or pharmacological interventions that might help improve cancer outcomes.

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Crossref · 10.1038/nrc1820

Cites

153 of 153 references verified0 citation errors · 0 not checkable

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  • The same cortisol-cytokine negative relationship has been found in response to other psychosocial interventions in oncology.

    “Furthermore, the same cortisol-cytokine negative relationship has been found in response to other psychosocial interventions in oncology [4–5].”

    From Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers (2016) · cites this paper as [5]

    The Abstract reports that psychosocial interventions in cancer patients can alter neuroendocrine and immune function, and separately describes reduced cortisol alongside improved immune indicators. It does not report a negative cortisol–cytokine relationship in response to oncology interventions; the immune outcomes it names are lymphocyte proliferation and NK-cell activity. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Inflammation is a proposed mechanism mediating ELA effects on later depression, age-related diseases, neurodevelopmental changes, cancers, and other systemic effects.

    “Inflammation is also a proposed mechanism mediating ELA effects on later depression, age-related diseases [3], neurodevelopmental changes [40], cancers [49], and other systemic effects discussed.”

    From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [49]

    The paper discusses inflammatory and immune pathways in cancer: its section on pharmacological interventions links an inflammatory response to certain cancers, and its discussion of immune function describes stress-related changes in tumour incidence and progression. It does not establish that inflammation mediates the effects of early-life adversity (ELA) on later cancer. The citation [49] is attached to “cancers,” not to the sentence’s separate claims about depression, age-related disease, or neurodevelopmental changes. (LLM, conf=0.83)

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  • Glucocorticoid dysregulation may promote oncogenic tumor cell microenvironments, fostering growth, migration, invasiveness, and angiogenesis, potentially contributing to links between ELA and cancers.

    “Glucocorticoid dysregulation may also promote oncogenic tumor cell microenvironments (in part via pro-inflammatory effects, as discussed below), fostering growth, migration, invasiveness, and angiogenesis [49], thus potentially contributing to observed links between ELA and cancers [7].”

    From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [49]

    The ‘Glucocorticoids and other mediators’ passage (indexed as Abstract; page unavailable) says glucocorticoids may facilitate cancer growth alongside catecholamines. The review attributes tumour-cell migration and invasion, and VEGF-related angiogenesis, chiefly to stress or catecholamines rather than specifically to glucocorticoid dysregulation. The ELA–cancer link has a separate citation in the citing sentence and is not assessed here. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Negative psychological states and limited social interactions have been linked to lower white blood cell activity, reduced numbers of antibodies and increased stress hormone response.

    “In contrast, negative psychological states and limited social interactions have been linked to lower white blood cell activity, reduced numbers of antibodies and increased stress hormone response [2, 4–5].”

    From Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers (2016) · cites this paper as [5]

    The paper links psychological distress to reduced natural-killer-cell activity in patients with breast or ovarian cancer and associates social support with higher activity. It also reports that chronic stress suppresses humoral immunity and that catecholamine levels rise with stress. It does not establish reduced numbers of antibodies or show that limited social interactions are linked to all three outcomes as stated. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Positive psychological states have been linked to optimised immune responses including lowering inflammation, enhanced cellular function and other longer term health outcomes.

    “These positive states have, in turn, been linked to optimised immune responses including the lowering of inflammation, enhanced cellular function and other longer term health outcomes [4–5].”

    From Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers (2016) · cites this paper as [5]

    The paper links positive psychosocial factors to enhanced cellular immune function in patients with cancer and reports that social support and optimism have predicted longer survival (Abstract; page not provided). It does not establish that positive states lower inflammation, and it cautions that studies of psychosocial interventions have not consistently shown a survival advantage. The claim is therefore broader than the evidence in this source. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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Cites

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Research works printed but not linked: 2

  1. [97]Cole SW, Jamieson BD, Zack J. A cAMP externalizes lymphocyte CXCR4: implications for chemotaxis and HIV infection. J Immunol. 1999;162:1392–1400. [PubMed] [Google Scholar]
  2. [108]Felten S, Felten D. In: Psychoneuroimmunology. Ader R, Felten D, Cohen N, editors. St. Louis; Montana: 1991. pp. 27–71. [Google Scholar]

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Authors
Antoni, M. H., Lutgendorf, S. K., Cole, S. W., Dhabhar, F. S., Sephton, S. E., McDonald, P. G., Stefanek, M., & Sood, A. K.
Affiliations
  • University of Miami (US)
  • University of Iowa (US)
  • Stanford Medicine (US)
  • University of Louisville (US)
  • National Institutes of Health (US)
  • The University of Texas MD Anderson Cancer Center (US)
ORCID
Venue
Nature Reviews Cancer
Publisher
Springer Science and Business Media LLC
Published
2006-03
Volume
6
Issue
3
Pages
240-248
ISSN
  • 1474-175X (ISSN-L)
  • 1474-1768
DOI
10.1038/nrc1820
PMC
PMC3146042
OpenAlex
W2025845020
Cited by
981
References
153
Citations by year
2026: 43 · 2025: 42 · 2024: 48 · 2023: 51 · 2022: 47 · 2021: 58 · 2020: 57 · 2019: 53 · 2018: 52 · 2017: 46 · 2016: 53 · 2015: 42 · 2014: 40 · 2013: 64 · 2012: 69
FWCI
5.32
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature reviews. Cancer (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (UH3TR000943)
  • National Cancer Institute (R01CA110793, R01CA109298, P50CA083639)
  • National Center for Advancing Translational Sciences
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
psychological stress, depression, social support, tumor progression, tumor biology, behavioral factors, cancer risk factors, molecular mechanisms, pharmacological interventions, oncological outcomes
MeSH terms
Animals, Depression, Humans, Neoplasms, Risk Factors, Social Support, Socioeconomic Factors, Stress, Psychological, Signal Transduction

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