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Nils Henrik Halberg's picture

Nils Henrik Halberg

Associate Professor, NCMM Young Associate Investigator
  • E-mailNils.Halberg@uib.no
  • Phone+47 55 58 64 42+47 414 72 368
  • Visitor Address
    Department of Biomedicine, University of Bergen
    Jonas Lies Vei 91
    5020 Bergen
    Room 
    5B116B
  • Postal Address
    Postboks 7804
    5020 Bergen

Dr. Halberg completed his graduate studies at the University of Copenhagen in 2009. Working in the laboratory of Dr. Philipp Scherer at the UT Southwestern Medical Center he studied the functional role of hypoxia and fibrosis in obese white adipose tissue. He did postdoctoral work in the laboratory of Dr. Sohail Tavazoie at the Rockefeller University studying the mechanisms of metastatic secretory programs in breast cancer. In 2015, he moved the University of Bergen to start his academic laboratory in the Department of Biomedicine. His laboratory seeks to better our understanding of the mechanistic connection between obesity and cancer.

Metastatic colonization, the spread of cancer cells from the primary tumor to secondary organ sites, is the major cause of death in patients with solid tumors. While its impact on human health has been recognized for years, the mechanistic framework that drives the colonization has only recently begun to be understood. Such mechanisms include intrinsic cellular pathways and interactions between cancer cells with neighboring cell types in the tumor microenvironment as immune cells, endothelial cells and fibroblast.

A critical health issue facing our society today is the connection between obesity and cancer. Extensive epidemiological evidence indicates that obesity is a driving factor for cancer development and spread—in particular for breast, endometrial and colon cancer. In spite of this clear connection, no unbiased in-depth mechanistic studies have been undertaken to establish how tumor cells take advantage of the altered energy state present in obese individuals. Without this mechanistic insight we are unable to develop effective therapeutic strategies to tackle this growing clinical problem.

Our laboratory utilizes in vitro and in vivo experimental cancer systems and metabolic analysis combined with contemporary molecular biology and clinical bioinformatics approaches to systemically elucidate the mechanisms by which cancer cells exploit an altered metabolic environment to promote metastatic colonization.

Metastatic colonization, the spread of cancer cells from the primary tumor to secondary organ sites, is the major cause of death in patients with solid tumors. While its impact on human health has been recognized for years, the mechanistic framework that drives the colonization has only recently begun to be understood. Such mechanisms include intrinsic cellular pathways and interactions between cancer cells with neighboring cell types in the tumor microenvironment as immune cells, endothelial cells and fibroblast.

A critical health issue facing our society today is the connection between obesity and cancer. Extensive epidemiological evidence indicates that obesity is a driving factor for cancer development and spread—in particular for breast, endometrial and colon cancer. In spite of this clear connection, no unbiased in-depth mechanistic studies have been undertaken to establish how tumor cells take advantage of the altered energy state present in obese individuals. Without this mechanistic insight we are unable to develop effective therapeutic strategies to tackle this growing clinical problem.

Our laboratory utilizes in vitro and in vivo experimental cancer systems and metabolic analysis combined with contemporary molecular biology and clinical bioinformatics approaches to systemically elucidate the mechanisms by which cancer cells exploit an altered metabolic environment to promote metastatic colonization.

 

Academic article
  • Show author(s) 2020. Golgi-Localized PAQR4 Mediates Antiapoptotic Ceramidase Activity in Breast Cancer. Cancer Research. 2163-2174.
  • Show author(s) 2020. AXL is a driver of stemness in normal mammary gland and breast cancer. iScience. 1-40.
  • Show author(s) 2019. Upregulated PDK4 expression is a sensitive marker of increased fatty acid oxidation. Mitochondrion (Amsterdam. Print). 97-110.
  • Show author(s) 2019. Human endotrophin as a driver of malignant tumor growth. JCI Insight. 1-17.
  • Show author(s) 2016. PITPNC1 recruits RAB1B to the Golgi network to drive malignant secretion. Cancer Cell. 339-353.
  • Show author(s) 2016. Adipose HIF-1α causes obesity by suppressing brown adipose tissue thermogenesis. Journal of Molecular Medicine.
Masters thesis
  • Show author(s) 2021. Obesity-Induced Breast Cancer Stemness Through Epigenetic Regulation.
  • Show author(s) 2020. High Dimensional and Spatial Analysis of Solid Tumors.
  • Show author(s) 2019. Making in vivo models viable again: Synthetic lethality between DNA repair factors Xlf and Paxx is rescued by inactivation of Trp53.
  • Show author(s) 2019. High dimensional analysis of immune infiltrate in cancers associated with obesity.
  • Show author(s) 2019. Development of an in vivo selection-based model system to study PDAC liver colonization in obese and non-obese microenvironments.
  • Show author(s) 2019. Cancer subpopulation dynamics in obese environments.
  • Show author(s) 2017. Malignant Exploitation of the Altered Metabolic Landscape in Obese Hormone Receptor Negative Breast Cancer Patients.
Doctoral dissertation
  • Show author(s) 2019. Discovery and Targeting of the Cellular Functions of PAQR4 in Breast Cancer.

More information in national current research information system (CRIStin)

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