In patients with cancer, IGFBP-1 acts by binding IGF-1, therefore decreasing free levels of IGF-1 in serum; this process interferes with the proliferative effect of IGF-1 while also promoting apoptosis.12 There is scientific evidence that IGFBP-1 levels are lowered in persons with cancer.12

Studies have shown that IGF-1 levels are lower and IGFBP-1 levels are higher in serum taken from subjects who are more physically active.14,15 In addition, when lymph node cancer of the prostate (LNCaP) cell lines are exposed to this serum in vitro, cell proliferation is significantly decreased.16,17 Researchers are still examining the complex relationship between this family of proteins and neoplasia, but their work may provide an early insight into how exercise has an effect on cancer. 

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The protein p53 is also crucial to regulation of the cell cycle. It plays a role in the transcription of numerous genes, which means that p53 is intimately linked to apoptosis, cell growth and arrest, protein translation, and DNA repair.18 Normally, p53 functions by stimulating cell cycle arrest and DNA repair or inducing apoptosis in cells with damaged DNA.18 Loss of this “wild-type function” has been implicated in most cancers.19

It has been demonstrated in an animal model that levels of p53 are significantly higher in subjects that are more physically active and that this protein may play a direct role in slowing the growth of tumor cells.19 Similar results were obtained in another study, in which prostate cancer cell lines were exposed to serum from fasting blood samples collected from men who exercised or who were sedentary; cells exposed to exercise serum exhibited a 27% reduction in growth and a 37% increase in apoptosis in comparison with cells from the same line cultured in serum from the sedentary group.14 Researchers attributed this difference to a 100% increase in p53 in the LNCaP cells exposed to exercise serum.14 

Key take-aways

  • Physical activity reduces the risk for a variety of ailments, including cancer, and it may also reduce the risk for death after a diagnosis of cancer.
  • Studies have demonstrated that exercise both before and after a cancer diagnosis reduces cancer-specific mortality.
  • The ideal level of physical activity is 9 MET-hours per week, which is the equivalent of 150 minutes of moderate-intensity exercise or 75 minutes of vigorous-intensity exercise per week.
  • The biological mechanisms are poorly understood, but the insulin-like growth factor family and p53 protein may play a crucial role in halting cancer growth.
  • Practitioners should encourage their patients to exercise as much as possible as a supplement to their cancer treatment.


The current recommendation that individuals should expend at least 9 MET-hours per week by exercising extends not only to the prevention of cancer but also to the reduction of cancer mortality.1 Although some research has demonstrated that higher levels of activity are required to reduce one’s risk for dying of cancer, the nationally recommended figure was more than enough to make a difference in many instances.5 This seems to indicate that practitioners should urge their patients not only to exercise to stave off the development of chronic illnesses but also to make every effort to continue being physically active after receiving a diagnosis of a disease such as cancer.

Although it may be more difficult for patients undergoing treatment for cancer to expend the energy required to improve their chances of survival, the importance of increasing heart and respiratory rates should not be forgotten. Physical activity should be promoted as a supplement to traditional treatments, such as chemotherapy and radiation, and could be as simple as going outdoors or getting on a treadmill and walking for a half-hour 5 days a week.

Many studies have had the advantage of being able to follow patients over long periods; however, the specific length of time that the protective benefits of exercise last remains unclear. Nevertheless, based on the most recent data, patients with cancer may benefit from regular physical activity, which leads to a more favorable prognosis.2-4

Bradley Weiler, PAS-II, is a physician assistant student, SUNY Upstate Medical University, and Sandra Banas, MST, PA-C, is the founding chairperson and PA program director, SUNY Upstate Medical University, Syracuse, New York.


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  3. Meyerhardt JA, Heseltine D, Niedzwiecki D, et al. Impact of physical activity on cancer recurrence and survival in patients with stage III colon cancer: findings from CALGB 89803. J Clin Oncol. 2006;24(22):3535-3541.
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  5. World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007.
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  9. Irwin ML, Smith AW, McTiernan A, et al. Influence of pre- and postdiagnosis physical activity on mortality in breast cancer survivors: the health, eating, activity, and lifestyle study. J Clin Oncol. 2008;26(24):3958-3964.
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  13. Muller PA, Vousden KH. Mutant p53 in cancer: new functions and therapeutic opportunities. Cancer Cell. 2014;25(3):304-317.
  14. Leung PS, Aronson WJ, Ngo TH, Golding LA, Barnard RJ. Exercise alters the IGF axis in vivo and increases p53 protein in prostate tumor cells in vitro. J Appl Physiol. 2004;96(2):450-454.
  15. Ngo TH, Barnard RJ, Leung PS, Cohen P, Aronson WJ. Insulin-like growth factor 1 (IGF-1) and IGF binding protein-1 modulate prostate cancer cell growth and apoptosis: possible mediators for the effects of diet and exercise on cancer cell survival. Endocrinology. 2003;144(6):2319-2324.
  16. Barnard RJ, Leung PS, Aronson WJ, Cohen P, Golding LA. A mechanism to explain how regular exercise might reduce the risk for clinical prostate cancer. Eur J Cancer Prev. 2007;16(5):415-421.
  17. Rundqvist H, Augsten M, Strömberg A, et al. Effect of acute exercise on prostate cancer cell growth. PLoS ONE. 2013;8(7):e67579.
  18. Hasty P, Christy BA. p53 as an intervention target for cancer and aging. Pathobiol Aging Age Relat Dis. 2013;3. doi: 10.3402/pba.v3i0.22702 
  19. Higgins KA, Park D, Lee GY, Curran WJ, Deng X. Exercise-induced lung cancer regression: mechanistic findings from a mouse model. Cancer. 2014;120(21):3302-3310.

All electronic documents accessed August 10, 2016.