Solid epidemiological data demonstrate that exercise training can reduce disease risk and mortality for several cancer diagnoses. In addition to improving the functional capacity of cancer patients, exercise training may directly regulate tumor physiology and metabolism. Exercise training has the potential to be a beneficial and integrated component of cancer management, yet to fully elucidate its potential, understanding of the mechanistic effects of exercise on tumor physiology is warranted. We focus on gaining such insight into the mechanistic effects of exercise on tumor biology and physiology through a translational approach that includes cell culture studies, animal models and clinical exercise interventions in cancer patients.

The core of our pre-clinical studies is based on the idea that during acute bouts of exercise, marked systemic changes occur with induction of stress-related hormones, release of myokines and other peptides, and mobilization of immune cells. Each of these factors may directly or indirectly control cancer cell growth. In cell culture studies, we are working on characterizing the role of these exercise-induced factors on intracellular signalling response and metabolism in breast and prostate cancer cells.

In animal models we have shown that voluntary exercise by wheel running inhibits tumor growth across various cancer diagnoses, including malignant melanoma, breast, liver and lung cancer. Moreover, we are pursuing studies to gain insight into the effect of exercise on intratumoral immune cell infiltration and intratumoral metabolism.

In addition to our preclinical work, we are conducting randomized controlled exercise intervention trials in cancer patients before tumor resection. Our primary hypothesis is that physical training before and during cancer treatment may prevent loss of physical function, and thus:

  • Improve survival and decrease the risk of disease recurrence.
  • Reduce post-operative complications after tumor resection, which may among others decrease hospitalization.
  • Reduce toxicities to neoadjuvant chemotherapy, improving treatment tolerability.
  • Prevent worsening of comorbidities.
  • Regulate systemic factors, which we have identified to directly control cancer cell viability and metabolism.


For further reading, please see:

  1. Pernille Hojman, Julie Gehl, Jesper F. Christensen and Bente K. Pedersen. Molecular mechanisms linking exercise to cancer prevention and treatment. Cell Metab, pii: S1550-4131(17)30567-3.
  2. Christine Dethlefsen, Louise Seier Hansen, Christian Lillelund, Christina Andersen, Julie Gehl, Jesper Frank Christensen, Bente Klarlund Pedersen, and Pernille Hojman. 2017. Exercise-induced catecholamines activate the Hippo tumor suppressor pathway to reduce risks of breast cancer development. Cancer Res, 77(18):4894-4904.
  3. Christine Dethlefsen, Christian Lillelund, Julie Midtgaard, Christina Andersen, Bente Klarlund Pedersen, Jesper Frank Christensen, Pernille Hojman. 2016. Exercise Regulates Breast Cancer Cell Viability - Systemic Training Adaptations versus Acute Exercise Responses. Breast Cancer Res Treat, 159 (3):469-79.
  4. Line Pedersen, Manja Idorn, Gitte H. Olofsson, Britt Lauenborg, Intawat Nookaew, Rasmus Hvass Hansen, Helle Hjorth Johannesen, Jürgen C. Becker, Katrine S. Pedersen, Christine Dethlefsen, Jens Nielsen, Julie Gehl, Bente K. Pedersen, Per thor Straten, Pernille Hojman. 2016. Voluntary running suppresses tumor growth through epinephrine- and IL-6-dependent NK cell mobilization and redistribution. Cell Metabolism, 23(3):554-62. doi: 10.1016/j.cmet.2016.01.011. 

Figure from Hojman et al, Cell Metab 2018