Dr Nils Henrik Halberg
Dr

Nils Henrik Halberg

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Background

The Cancer Metabolism Group is keenly interested in how the physiological state of a person affects cancers.

Over a person’s lifetime, somatic cells will accumulate spontaneously occurring gene mutations, the majority of which do not cause disease. The global incidence of cancer has more than doubled over the past 30 years – primarily due to increasing living standards, modern lifestyles, and an aging population.

The common denominator for these is alterations to the physiological homeostasis of the individual at risk rather than a change in mutational burden. This strongly implies that the interaction of physiological conditions with cells harboring oncogenic mutations governs cancer risk.

The Cancer Metabolism lab utilizes systems biology technologies to both clinical biobank and mouse models to dissect the molecular drivers of the intersect between physiology and tumorigenesis.

Availability

Dr Nils Henrik Halberg is:
Available for supervision
Media expert

Qualifications

  • Doctor of Philosophy of Cell Metabolism, University of Copenhagen

Research interests

  • Cancer cell plasticity

    Cancer cells are adaptive. My key interest is how and why they adapt when exposed to physiological stressors as obesity, exercise and fasting.

  • Cellular interaction networks

    Wihtin the tumor ecosystems cells interact in niches. This might be closeness to blood vessels to support cellular functions or interacting with specific cells to enable adaption. Spatial technologies allow us to understand these at cellular resultion.

Research impacts

Key Publications

  1. C/EBPB-dependent adaptation to palmitic acid promotes tumor formation in hormone receptor negative breast cancer. Liu XZ, Rulina A, Choi MH, Pedersen L, Lepland J, Takle ST, Madeleine N, Peters SD, Wogsland CE, Grøndal SM, Lorens JB, Goodarzi H, Lønning PE, Knappskog S, Molven A, Halberg N. Nat Commun. 2022 Jan 10;13(1):69. doi: 10.1038/s41467-021-27734-2. PMID: 35013251
  2. High-dimensional immunotyping of tumors grown in obese and non-obese mice. Wogsland CE, Lien HE, Pedersen L, Hanjra P, Grondal SM, Brekken RA, Lorens JB, Halberg N. Dis Model Mech. 2021 Apr 1;14(4):dmm048977. doi: 10.1242/dmm.048977. Epub 2021 Mar 30. PMID: 33653826
  3. PITPNC1 Recruits RAB1B to the Golgi Network to Drive Malignant Secretion. Halberg N, Sengelaub CA, Navrazhina K, Molina H, Uryu K, Tavazoie SF. Cancer Cell. 2016 Mar 14;29(3):339-353. doi: 10.1016/j.ccell.2016.02.013. PMID: 26977884
  4. Cellular mechanisms linking cancers to obesity. Liu XZ, Pedersen L, Halberg N. Cell Stress. 2021 Apr 12;5(5):55-72. doi: 10.15698/cst2021.05.248. PMID: 33987528
  5. A microRNA regulon that mediates endothelial recruitment and metastasis by cancer cells. Png KJ, Halberg N, Yoshida M, Tavazoie SF. Nature. 2011 Dec 14;481(7380):190-4. doi: 10.1038/nature10661. PMID: 22170610
  6. Hypoxia-inducible factor 1alpha induces fibrosis and insulin resistance in white adipose tissue. Halberg N, Khan T, Trujillo ME, Wernstedt-Asterholm I, Attie AD, Sherwani S, Wang ZV, Landskroner-Eiger S, Dineen S, Magalang UJ, Brekken RA, Scherer PE. Mol Cell Biol. 2009 Aug;29(16):4467-83. doi: 10.1128/MCB.00192-09. Epub 2009 Jun 22. PMID: 19546236

In the news:

https://onkologisktidsskrift.no/sykdommer/13-brystkreft/194-norsk-studie-derfor-oker-overvekt-risikoen-for-brystkreft.html

https://cancerworld.net/study-unveils-how-obesity-raises-cancer-risk/

https://www.forskning.no/kreft-overvekt/1-av-5-som-dor-av-kreft-har-fedme-na-vet-forskere-mer-om-hvorfor/1965262#:~:text=Kreftceller%20blir%20tvunget%20til%20%C3%A5%20bli%20mer%20aggressive&text=Kreftceller%20har%20ti%20ganger%20%C3%B8kt,mindre%20fettrikt%20milj%C3%B8%2C%20forteller%20Halberg.&text=Annonse-,%E2%80%93%20Vi%20fant%20at%20kreftceller%20i%20lipid%2Drike%20milj%C3%B8er%20blir%20mer,lettere%20danner%20kreftsvulster%2C%20sier%20Halberg.

https://www.tv2.no/nyheter/utenriks/forskere-kan-ha-funnet-nokkelen-til-et-lengre-liv/15812692/

Search Professor Nils Henrik Halberg’s works on UQ eSpace

22 works between 2007 and 2024
All (22) Journal Article (20) Conference Publication (2)

21 - 22 of 22 works

2008

Journal Article

Plasma adiponectin complexes have distinct biochemical characteristics

Schraw, Todd, Wang, Zhao V., Halberg, Nils, Hawkins, Meredith and Scherer, Philipp E. (2008). Plasma adiponectin complexes have distinct biochemical characteristics. Endocrinology, 149 (5), 2270-2282. doi: 10.1210/en.2007-1561

Plasma adiponectin complexes have distinct biochemical characteristics

2007

Journal Article

Paradoxical elevation of high-molecular weight adiponectin in acquired extreme insulin resistance due to insulin receptor antibodies

Semple, Robert K., Halberg, Nils H., Burling, Keith, Soos, Maria A., Schraw, Todd, Luan, Jian'an, Cochran, Elaine K., Dunger, David B., Wareham, Nicholas J., Scherer, Philipp E., Gorden, Phillip and O'Rahilly, Stephen (2007). Paradoxical elevation of high-molecular weight adiponectin in acquired extreme insulin resistance due to insulin receptor antibodies. Diabetes, 56 (6), 1712-1717. doi: 10.2337/db06-1665

Paradoxical elevation of high-molecular weight adiponectin in acquired extreme insulin resistance due to insulin receptor antibodies

Availability

Dr Nils Henrik Halberg is:
Available for supervision

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Available projects

  • What are the properties of cancer cells adapted to aberrant physiological environments?

    Background

    Obesity increases the risk of developing thirteen types of cancer that normal weight individuals may not develop despite of harbouring the same cancer risk loci. Globally, overweight/obesity may account for 544 300 cancer cases every year and is currently implicated in 15-20% of cancer-related mortalities. This places obesity second only to smoking as the most prevalent preventable cause of cancer. We have previously demonstrated that obesity is not associated with additional oncogenic genetic alterations that could explain the increased cancer risk. Instead, we demonstrate that cancer cells undergo adaptive epigenetic remodelling and gain tumour initiating properties when exposed to prolonged periods of obese conditions. This interaction between metabolic, epigenetic, and tumorigenic events currently represents significant knowledge gaps.

    The aims are to:

    • Uncover the relationship between systemic metabolic challenge as induced by physiological stressors and intracellular metabolite dynamics in cancer cells.

    • Identification of the metabolites that are sufficient to drive tumour initiation – and how this is achieved.

    • Determine how metabolite-driven epigenetic changes can display loci specificity.

    • Discover the epigenetic, transcriptional and translational machinery required to that link physiological stressor to tumour initiation.

  • How is the tumor ecosystem affected by obesity and how does that affect tumor outcomes?

    Background:

    Obesity increases the risk of developing thirteen types of cancer that normal weight individuals may not develop despite of harbouring the same cancer risk loci. Globally, overweight/obesity may account for 544 300 cancer cases every year and is currently implicated in 15-20% of cancer-related mortalities. This places obesity second only to smoking as the most prevalent preventable cause of cancer. We have previously demonstrated that obesity is not associated with additional oncogenic genetic alterations that could explain the increased cancer risk. Instead, we demonstrate that cancer cells undergo adaptive epigenetic remodelling and gain tumour initiating properties when exposed to prolonged periods of obese conditions. This interaction between metabolic, epigenetic, and tumorigenic events currently represents significant knowledge gaps.

    The aims are to:

    • Use spatial technologies to specify obesity dependent changes to the cancer ecosystem
    • Develop appropriate mouse models of the cancer ecosystem in obese and non-obese condidtions.

Enquiries

Contact Dr Nils Henrik Halberg directly for media enquiries about:

  • Cancer
  • Epigenetics
  • Metabolism
  • Metabolites
  • obesity
  • systems biology

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