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LBG Health Sciences Meeting great success

The LBG Meeting for Health Sciences provides an important meeting point for the LBG Life Sciences community and provides young scientists an excellent opportunity to present their work. This conference focuses on the translation of research results from theory into practice. Therefore, abstracts on preclinical, clinical or implementation research were welcome in four thematic sessions:

European consortia are stepping up the development of state-of-the-art treatment for aggressive blood cancer with € 3 million in funding

New cancer therapies are now being developed specifically against oncogenic cell signals. But for rare diseases, these new drugs are often not approved. Two EU-consortia with Austrian participation have now received funding from the ERA-NET TRANSCAN-2 to develop modern treatments for rare but very aggressive peripheral T-cell lymphomas and leukemias.

Survival signalling mediated by Tyk2 is the Achilles’ heel of Anaplastic Large Cell Lymphomas

Anaplastic Large Cell Lymphomas (ALCL) are rare tumors of white blood cells, which fall into at least four categories. New research by the international ERIA consortium led by scientists in Vienna have now identified that all types of ALCL rely on the same signaling pathway for survival. TYK2 prevents apoptotic cell death by increasing the expression of the BCL2 family member Mcl1. Therefore TYK2 represents an attractive drug target due to its unique enzymatic domain, and TYK2-specific inhibitors show promise as novel targeted inhibitors for ALCL.


The LBG Meeting for Health Sciences encourages and supports young scientists by offering them an opportunity to present their work. Moreover, it is a chance for early career researchers to establish themselves within the scientific setting. The conference focuses on the translation of research results from theory into practice. Therefore, abstracts on preclinical, clinical or implementation research are welcome. The thematic sessions will include key-note lectures by international experts and oral presentations of the best submitted abstracts.

+++ Call for abstracts now open! +++

STAT3 isoforms: Alternative fates in cancer?

Signal transducer and activator of transcription (STAT) 3 is an important mediator of cytokine signaling and transcriptional regulator of cell proliferation, maturation and survival. It has been described as a key player in cancer development and progression. However, under certain circumstances, STAT3 is also considered a potent tumor suppressor. This contradiction is partially explained by its expression as different isoforms. Alternative splicing gives rise to two STAT3 isoforms, STAT3α and its truncated version STAT3β.

Cross-Talk of Hedgehog and Interleukin-6 Signaling in Cancer

Persistent activation of Hedgehog (HH)/GLI signaling accounts for the development of basal cell carcinoma (BCC), a very frequent non-melanoma skin cancer with rising incidence. Targeting HH/GLI signaling by approved pathway inhibitors can provide significant therapeutic benefit to BCC patients. However, limited response rates, development of drug resistance and severe side effects of HH pathway inhibitors call for improved treatment strategies such as rational combination therapies simultaneously inhibiting HH/GLI and cooperative signals promoting the oncogenic activity of HH/GLI.

Afatinib might be rational treatment for many lung cancer patients

Lung cancer remains a serious health threat with less than one in five patients still alive 5 years after diagnosis. This is mainly due to the lack of modern treatment options for the majority of patients, which still receive classical chemotherapy. However, Emilio Casanova and Herwig Moll from the Ludwig Boltzmann Institute of Cancer Research (LBI-CR) and Medical University of Vienna (MUV) now describe in the journal Science Translational Medicine that the established drug Afatinib may prove an unexpected therapeutic option for many patients.

New paper on Targeting STAT5B in T-Cell Neoplasia.

STAT5BN642H-driven proliferation in T-cell leukemia/lymphoma via common γ-chain (γc)-receptor signaling. STAT5BN642H is activated by Janus kinase (JAK) upon cytokine stimulation such as interleukin 2 (IL-2). Subsequently, phosphorylated STAT5BN642H translocates into the nucleus and initiates transcription. (1) STAT5BN642H exhibits prolonged activation and enhanced DNA binding leading to (2) increased transcription of STAT5 target genes and enhanced proliferation.

The somatic hot spot mutation in STAT5B was found in many T cell leukemia/lymphoma patients. The team of  Moriggl generated and analyzed a transgenic mouse model with hematopoietic STAT5BN642H expression that caused aggressive T-cell leukemia/lymphomas. Herein, we discuss the scientific merit of our model and its relevance for pre-clinical studies.

Now published in Molecular & Cellular Oncology Volume 5, 2018 - Issue 3