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Nils Halberg's picture

Nils Halberg

Researcher , 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.

 

Journal articles
  • Halberg, Nils; Sengelaub, Caitlin A.; Navrazhina, Kristina; Molina, Henrik; Uryu, Kunihiro; Tavazoie, Sohail F. 2016. PITPNC1 recruits RAB1B to the Golgi network to drive malignant secretion. Cancer Cell. 29: 339-353. doi: 10.1016/j.ccell.2016.02.013
  • Jun, JC; Devera, R; Unnikrishnan, D; Shin, MK; Bevans-Fonti, S; Yao, Q; Rathore, A; Younas, H; Halberg, Nils; Scherer, PE; Polotsky, VY. 2016. Adipose HIF-1α causes obesity by suppressing brown adipose tissue thermogenesis. Journal of Molecular Medicine.

More information in national current research information system (CRIStin)

For a fully updated publication list and citations see google schoolar or Orcid