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Dr Nils Henrik Halberg
Dr

Nils Henrik Halberg

Email: 

Overview

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/

Works

Search Professor Nils Henrik Halberg’s works on UQ eSpace

22 works between 2007 and 2024

1 - 20 of 22 works

2024

Conference Publication

Interplay of the proteotoxic CEL-MODY protein and oncogenic Kras in pancreatic cancer development

Fjeld, Karianne, Alam, Jahedul, López, Diego Iglesias, Kuznetsova, Ksenia, Seierstad, Renate V., Verbeke, Caroline, Vaudel, Marc, Regel, Ivonne, Halberg, Nils and Molven, Anders (2024). Interplay of the proteotoxic CEL-MODY protein and oncogenic Kras in pancreatic cancer development. 56th European Pancreatic Club Meeting 2024, Santiago de Compostela, Spain, 26 - 29 June 2024. Amsterdam, Netherlands: Elsevier. doi: 10.1016/j.pan.2024.05.010

Interplay of the proteotoxic CEL-MODY protein and oncogenic Kras in pancreatic cancer development

2024

Conference Publication

Detection of epigenetic priming in acinar cells after recovering from pancreatitis or metabolic stress

Wolff, Julia, Zhou, Quan, Schreiner, Nicole, Fahr, Lisa, Straub, Tobias, Mahajan, Ujjwal M., Holt, Eric, Bozdag, Beyza, Imhof, Axel, Mayerle, Julia, Halberg, Nils and Regel, Ivonne (2024). Detection of epigenetic priming in acinar cells after recovering from pancreatitis or metabolic stress. 56th European Pancreatic Club Meeting 2024, Santiago de Compostela, Spain, 26 - 29 June 2024. Amsterdam, Netherlands: Elsevier. doi: 10.1016/j.pan.2024.05.309

Detection of epigenetic priming in acinar cells after recovering from pancreatitis or metabolic stress

2024

Journal Article

PAQR4 regulates adipocyte function and systemic metabolic health by mediating ceramide levels

Zhu, Qingzhang, Chen, Shiuhwei, Funcke, Jan-Bernd, Straub, Leon G., Lin, Qian, Zhao, Shangang, Joung, Chanmin, Zhang, Zhuzhen, Kim, Dae-Seok, Li, Na, Gliniak, Christy M., Lee, Charlotte, Cebrian-Serrano, Alberto, Pedersen, Line, Halberg, Nils, Gordillo, Ruth, Kusminski, Christine M. and Scherer, Philipp E. (2024). PAQR4 regulates adipocyte function and systemic metabolic health by mediating ceramide levels. Nature Metabolism, 6 (7), 1347-1366. doi: 10.1038/s42255-024-01078-9

PAQR4 regulates adipocyte function and systemic metabolic health by mediating ceramide levels

2023

Journal Article

Correction: The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer (Molecular Cancer, (2023), 22, 1, (86), 10.1186/s12943-023-01788-w)

Entrialgo‑Cadierno, Rodrigo, Cueto‑Ureña, Cristina, Welch, Connor, Feliu, Iker, Macaya, Irati, Vera, Laura, Morales, Xabier, Michelina, Sandra Vietti, Scaparone, Pietro, Lopez, Ines, Darbo, Elodie, Erice, Oihane, Vallejo, Adrian, Moreno, Haritz, Goñi‑Salaverri, Ainhoa, Lara‑Astiaso, David, Halberg, Nils, Cortes‑Dominguez, Ivan, Guruceaga, Elizabeth, Ambrogio, Chiara, Lecanda, Fernando and Vicent, Silve (2023). Correction: The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer (Molecular Cancer, (2023), 22, 1, (86), 10.1186/s12943-023-01788-w). Molecular Cancer, 22 (1) 97. doi: 10.1186/s12943-023-01795-x

Correction: The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer (Molecular Cancer, (2023), 22, 1, (86), 10.1186/s12943-023-01788-w)

2023

Journal Article

Limiting mitochondrial plasticity by targeting DRP1 induces metabolic reprogramming and reduces breast cancer brain metastases

Parida, Pravat Kumar, Marquez-Palencia, Mauricio, Ghosh, Suvranil, Khandelwal, Nitin, Kim, Kangsan, Nair, Vidhya, Liu, Xiao-Zheng, Vu, Hieu S., Zacharias, Lauren G., Gonzalez-Ericsson, Paula I., Sanders, Melinda E., Mobley, Bret C., McDonald, Jeffrey G., Lemoff, Andrew, Peng, Yan, Lewis, Cheryl, Vale, Gonçalo, Halberg, Nils, Arteaga, Carlos L., Hanker, Ariella B., DeBerardinis, Ralph J. and Malladi, Srinivas (2023). Limiting mitochondrial plasticity by targeting DRP1 induces metabolic reprogramming and reduces breast cancer brain metastases. Nature Cancer, 4 (6), 893-907. doi: 10.1038/s43018-023-00563-6

Limiting mitochondrial plasticity by targeting DRP1 induces metabolic reprogramming and reduces breast cancer brain metastases

2022

Journal Article

C/EBPB-dependent adaptation to palmitic acid promotes tumor formation in hormone receptor negative breast cancer

Liu, Xiao-Zheng, Rulina, Anastasiia, Choi, Man Hung, Pedersen, Line, Lepland, Johanna, Takle, Sina T., Madeleine, Noelly, Peters, Stacey D’mello, Wogsland, Cara Ellen, Grøndal, Sturla Magnus, Lorens, James B., Goodarzi, Hani, Lønning, Per E., Knappskog, Stian, Molven, Anders and Halberg, Nils (2022). C/EBPB-dependent adaptation to palmitic acid promotes tumor formation in hormone receptor negative breast cancer. Nature Communications, 13 (1) 69, 69. doi: 10.1038/s41467-021-27734-2

C/EBPB-dependent adaptation to palmitic acid promotes tumor formation in hormone receptor negative breast cancer

2022

Journal Article

Carbon dot therapeutic platforms: administration, distribution, metabolism, excretion, toxicity, and therapeutic potential

Truskewycz, Adam, Yin, Hong, Halberg, Nils, Lai, Daniel T. H., Ball, Andrew S., Truong, Vi Khanh, Rybicka, Agata Marta and Cole, Ivan (2022). Carbon dot therapeutic platforms: administration, distribution, metabolism, excretion, toxicity, and therapeutic potential. Small, 18 (16) 2106342, 16. doi: 10.1002/smll.202106342

Carbon dot therapeutic platforms: administration, distribution, metabolism, excretion, toxicity, and therapeutic potential

2021

Journal Article

High-dimensional immunotyping of tumors grown in obese and non-obese mice

Wogsland, Cara E., Lien, Hilde E., Pedersen, Line, Hanjra, Pahul, Grondal, Sturla M., Brekken, Rolf A., Lorens, James B. and Halberg, Nils (2021). High-dimensional immunotyping of tumors grown in obese and non-obese mice. DMM Disease Models and Mechanisms, 14 (4) dmm.048977, 1-18. doi: 10.1242/dmm.048977

High-dimensional immunotyping of tumors grown in obese and non-obese mice

2021

Journal Article

Cellular mechanisms linking cancers to obesity

Liu, Xiao-Zheng, Pedersen, Line and Halberg, Nils (2021). Cellular mechanisms linking cancers to obesity. Cell Stress, 5 (5), 55-72. doi: 10.15698/CST2021.05.248

Cellular mechanisms linking cancers to obesity

2020

Journal Article

AXL Is a driver of stemness in normal mammary gland and breast cancer

Engelsen, Agnete S. T., Wnuk-Lipinska, Katarzyna, Bougnaud, Sebastien, Pelissier Vatter, Fanny A., Tiron, Crina, Villadsen, René, Miyano, Masaru, Lotsberg, Maria L., Madeleine, Noëlly, Panahandeh, Pouda, Dhakal, Sushil, Tan, Tuan Zea, Peters, Stacey D'mello, Grøndal, Sturla, Aziz, Sura M., Nord, Silje, Herfindal, Lars, Stampfer, Martha R., Sørlie, Therese, Brekken, Rolf A., Straume, Oddbjørn, Halberg, Nils, Gausdal, Gro, Thiery, Jean Paul, Akslen, Lars A., Petersen, Ole W., LaBarge, Mark A. and Lorens, James B. (2020). AXL Is a driver of stemness in normal mammary gland and breast cancer. iScience, 23 (11) 101649, 1-19. doi: 10.1016/j.isci.2020.101649

AXL Is a driver of stemness in normal mammary gland and breast cancer

2020

Journal Article

Golgi-localized PAQR4 mediates antiapoptotic ceramidase activity in breast cancer

Pedersen, Line, Panahandeh, Pouda, Siraji, Muntequa I., Knappskog, Stian, Lønning, Per Eystein, Gordillo, Ruth, Scherer, Philipp E., Molven, Anders, Teigen, Knut and Halberg, Nils (2020). Golgi-localized PAQR4 mediates antiapoptotic ceramidase activity in breast cancer. Cancer Research, 80 (11), 2163-2174. doi: 10.1158/0008-5472.CAN-19-3177

Golgi-localized PAQR4 mediates antiapoptotic ceramidase activity in breast cancer

2019

Journal Article

Upregulated PDK4 expression is a sensitive marker of increased fatty acid oxidation

Pettersen, Ina Katrine Nitschke, Tusubira, Deusdedit, Ashrafi, Hanan, Dyrstad, Sissel Elisabeth, Hansen, Lena, Liu, Xiao-Zheng, Nilsson, Linn Iren Hodneland, Løvsletten, Nils Gunnar, Berge, Kjetil, Wergedahl, Hege, Bjørndal, Bodil, Fluge, Øystein, Bruland, Ove, Rustan, Arild Christian, Halberg, Nils, Røsland, Gro Vatne, Berge, Rolf Kristian and Tronstad, Karl Johan (2019). Upregulated PDK4 expression is a sensitive marker of increased fatty acid oxidation. Mitochondrion, 49, 97-110. doi: 10.1016/j.mito.2019.07.009

Upregulated PDK4 expression is a sensitive marker of increased fatty acid oxidation

2019

Journal Article

Human endotrophin as a driver of malignant tumor growth

Bu, Dawei, Crewe, Clair, Kusminski, Christine M., Gordillo, Ruth, Ghaben, Alexandra L., Kim, Min, Park, Jiyoung, Deng, Hui, Xiong, Wei, Liu, Xiao-Zheng, Lønning, Per Eystein, Halberg, Nils, Rios, Adan, Chang, Yujun, Gonzalez, Anneliese, Zhang, Ningyan, An, Zhiqiang and Scherer, Philipp E. (2019). Human endotrophin as a driver of malignant tumor growth. JCI Insight, 4 (9) e125094, 9. doi: 10.1172/jci.insight.125094

Human endotrophin as a driver of malignant tumor growth

2017

Journal Article

Adipose HIF-1α causes obesity by suppressing brown adipose tissue thermogenesis

Jun, Jonathan C., Devera, Ronald, Unnikrishnan, Dileep, Shin, Mi-Kyung, Bevans-Fonti, Shannon, Yao, Qiaoling, Rathore, Aman, Younas, Haris, Halberg, Nils, Scherer, Philipp E. and Polotsky, Vsevolod Y. (2017). Adipose HIF-1α causes obesity by suppressing brown adipose tissue thermogenesis. Journal of Molecular Medicine, 95 (3), 287-297. doi: 10.1007/s00109-016-1480-6

Adipose HIF-1α causes obesity by suppressing brown adipose tissue thermogenesis

2016

Journal Article

PITPNC1 Recruits RAB1B to the Golgi Network to Drive Malignant Secretion

Halberg, Nils, Sengelaub, Caitlin A., Navrazhina, Kristina, Molina, Henrik, Uryu, Kunihiro and Tavazoie, Sohail F. (2016). PITPNC1 Recruits RAB1B to the Golgi Network to Drive Malignant Secretion. Cancer Cell, 29 (3), 339-353. doi: 10.1016/j.ccell.2016.02.013

PITPNC1 Recruits RAB1B to the Golgi Network to Drive Malignant Secretion

2016

Journal Article

PTPRN2 and PLCβ1 promote metastatic breast cancer cell migration through PI(4,5)P2-dependent actin remodeling

Sengelaub, Caitlin A., Navrazhina, Kristina, Ross, Jason B., Halberg, Nils and Tavazoie, Sohail F. (2016). PTPRN2 and PLCβ1 promote metastatic breast cancer cell migration through PI(4,5)P2-dependent actin remodeling. EMBO Journal, 35 (1), 62-76. doi: 10.15252/embj.201591973

PTPRN2 and PLCβ1 promote metastatic breast cancer cell migration through PI(4,5)P2-dependent actin remodeling

2013

Journal Article

Chronic intermittent hypoxia induces atherosclerosis via activation of adipose angiopoietin-like 4

Drager, Luciano F., Yao, Qiaoling, Hernandez, Karen L., Shin, Mi-Kyung, Bevans-Fonti, Shannon, Gay, Jason, Sussan, Thomas E., Jun, Jonathan C., Myers, Allen C., Olivecrona, Gunilla, Schwartz, Alan R., Halberg, Nils, Scherer, Philipp E., Semenza, Gregg L., Powell, David R. and Polotsky, Vsevolod Y. (2013). Chronic intermittent hypoxia induces atherosclerosis via activation of adipose angiopoietin-like 4. American Journal of Respiratory and Critical Care Medicine, 188 (2), 240-248. doi: 10.1164/rccm.201209-1688OC

Chronic intermittent hypoxia induces atherosclerosis via activation of adipose angiopoietin-like 4

2013

Journal Article

Selective inhibition of Hypoxia-inducible factor 1α ameliorates adipose tissue dysfunction

Sun, Kai, Halberg, Nils, Khan, Mahmood, Magalang, Ulysses J. and Scherer, Philipp E. (2013). Selective inhibition of Hypoxia-inducible factor 1α ameliorates adipose tissue dysfunction. Molecular and Cellular Biology, 33 (5), 904-917. doi: 10.1128/MCB.00951-12

Selective inhibition of Hypoxia-inducible factor 1α ameliorates adipose tissue dysfunction

2012

Journal Article

MicroRNA regulation of cancer-endothelial interactions: Vesicular microRNAs on the move

Halberg, Nils, Alarcón, Claudio and Tavazoie, Sohail F. (2012). MicroRNA regulation of cancer-endothelial interactions: Vesicular microRNAs on the move. EMBO Journal, 31 (17), 3509-3510. doi: 10.1038/emboj.2012.198

MicroRNA regulation of cancer-endothelial interactions: Vesicular microRNAs on the move

2009

Journal Article

Hypoxia-inducible factor 1α induces fibrosis and insulin resistance in white adipose tissue

Halberg, Nils, Khan, Tayeba, Trujillo, Maria E., Wernstedt-Asterholm, Ingrid, Attie, Alan D., Sherwani, Shariq, Wang, Zhao V., Landskroner-Eiger, Shira, Dineen, Sean, Magalang, Ulysses J., Brekken, Rolf A. and Scherer, Philipp E. (2009). Hypoxia-inducible factor 1α induces fibrosis and insulin resistance in white adipose tissue. Molecular and Cellular Biology, 29 (16), 4467-4483. doi: 10.1128/MCB.00192-09

Hypoxia-inducible factor 1α induces fibrosis and insulin resistance in white adipose tissue

Supervision

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.

Media

Enquiries

Contact Dr Nils Henrik Halberg directly for media enquiries about:

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

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