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.
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.
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 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.
Lukas Kenner contributed to "Absence of PD-L1 on tumor cells is associated with reduced MHC I expression and PD-L1 expression increases in recurrent serous ovarian cancer" recently published in Science Reports.
Seeking to exploit some of his recent discoveries Florian Grebien now launched a new project in cooperation with CeMM and the Structural Genomics Consortium, Toronto, Canada. With the financial support of the FFG "Industrianahe Dissertationen" PhD student Jessica Ebner will aim to target the epigenetic regulator WDR5 with an innovative approach.
Richard Moriggl and colleagues published their view on steering of carcinoma progression by the YIN/YANG interaction of STAT1/STAT3.
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.
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).
For the third time the LBG Health Sciences Meeting awarded the best research contributions with a prize. In the category "Cancer Research" Luisa Schmidt of the research group Florian Grebien at the LBI-CR was selected with her research on "Acute Myeloide Leukemia with CEBPA Mutations is sensitive against Blockade of Menin-MLL Interaction". We congratulate Luisa to this fine success.