Current Size: 100%


New annual report proves LBI-CR performs research at a very high level

The Ludwig Boltzmann Institute for Cancer Research (LBI-CR) consolidates scientific success with outstanding achievements. 2016 was again with respect to publications and the acquisition of external research funds at an unusually high level. Furthermore, the staff of the LBI-CR, together with partner institutions, were able to put significant emphasis on applied and clinically translational cancer research, which was also very popular in the media.

Review on Natural Killer Cell Regulation in Cancer

Interplay of type I interferons (IFNs) and natural killer (NK) cell activation during antitumor response. Type I IFNs either impact on maturation, homeostasis, and activation of NK cells, or indirectly influence NK cells to kill tumor cells via other immune cells or cells of the tumor microenvironment. Dendritic cells (DCs), in particular, are essential for NK cell priming via production of IL15. Another indirect effect of type I IFNs on NK cell function in cancer might result from modulation of surface mol

Type I interferons (IFNs) are known to mediate antitumor effects against several tumor types and have therefore been commonly used in clinical anticancer treatment. However, how IFN signaling exerts its beneficial effects is only partially understood. The clinically relevant activity of type I IFNs has been mainly attributed to their role in tumor immune surveillance. Different mechanisms have been postulated to explain how type I IFNs stimulate the immune system. On the one hand, they modulate innate immune cell subsets such as natural killer (NK) cells.

Expression of EGFR by myeloid cells of the colorectal tumor stroma contributes to tumor development

EGFR in tumor-associated myeloid cells promotes development of colorectal cancer in mice and associates with outcomes of patients. Inhibitors of the epidermal growth factor receptor (EGFR) are the first-line therapy for patients with metastatic colorectal tumors without RAS mutations. However, EGFR inhibitors are ineffective in these patients, and tumor level of EGFR does not associate with response to therapy. 

New paper out on JAK2/STAT5 signaling as therapeutic target

The JAK2/STAT5 pathway is a novel potential target of therapy in canine mastocytoma, which is a frequently diagnosed cutaneous neoplasms in dogs. In non-resectable mastocytoma patients, novel targeted drugs are often applied. The transcription factor STAT5 has been implicated in the survival of human neoplastic mast cells. We have now reported the JAK2/STAT5 pathway as a novel target in canine mastocytoma.

New paper out on prognostic marker DCLK1 in head and neck cancer

New paper out on expression of DCLK1 in 127 patients being associated with poor survival. In particular, DCLK1 expression had a significant impact on survival of oropharyngeal carcinoma patients. Specifically, DCLK1+/HPV- patients had the worst prognosis after simultaneous assessment of DCLK1 and HPV status in comparison to the other three possible DCLK1/HPV constellations. Higher levels of DCLK1 mRNA were also associated with poor clinical outcome. Inhibition of DCLK1 in our HNSCC cell lines led to growth arrest and induction of apoptosis.

Metabolism drives growth and division of cancer cells

 The metabolic status of the cell and its supply of nutrients is signaled, amongst other, by the O-linked N-acetylglucosamine (GlcNAc) transferase (OGT). This enzyme links GlcNAc (orange squares) as a mark to STAT5 at the OH groups of threonine 92 (T). Cytokine receptors activate the kinase JAK2, which phosphorylates STAT5 on tyrosine 694 (Y) (red circles).

The metabolic state of tumor cells contributes to signals that control the proliferation of tumor cells. Already the German biochemist and Nobel Prize laureate Otto H. Warburg observed in the 1920s that tumor cells radically change their metabolism. This process was termed "Warburg Effect", however neglected until recently by cancer research, but the latest results show it is indeed of fundamental importance for the development of aggressive tumors.

Researchers of LBI-CR raised a record breaking 1.8 Mio € of external funds in 2016

In 2016 keyresearchers of the LBI-CR succeeded in raising more funds for their research than ever before. We are proud to report an outstanding success rate of 60%, as of ten proposals we received funding for six projects totalling an overall volume of € 1.8 Mio. With the renewal of one SFB and the intitiation of a new one Richard Moriggl maintains outstanding financial support by the Austrian Science Fund (FWF).