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Established cancer therapeutics are effective against aggressive blood cancer with mutations in STAT5

Research teams from Vienna investigated a typical mutation in STAT5 that renders tumors more aggressive but susceptible to established drugs.

The prestigious Journal of Clinical Investigation is now publishing an important contribution to leukemia and lymphoma research. This study by scientists at the Veterinary University of Vienna, the Medical University of Vienna, the Research Center for Molecular Medicine of the Academy of Sciences, and the Ludwig Boltzmann Institute for Cancer Research focused on the mutated form of the STAT5B oncogene.

SR-BI is crucial for the metastatic phenotype in melanoma

Metastatic melanoma is characterised by metabolic abnormalities. But how aggressive tumor behaviour is altered by metabolic state remains ill understood.  Researchers from Vienna in collaboration with the LBI-CR now report high-density lipoprotein (HDL) receptor SR-BI expression can predict melanoma progression in patients. The metastasis-associated epithelial-to-mesenchymal transition (EMT) was perturbed by SR-BI knockdown, but not functional inhibition of its cholesterol transporting capacity.

First evidence of single agent activity of BCL-2 inhibitor venetoclax

T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive T-lymphoid malignancy usually refractory to current treatment strategies and associated with a short overall survival. A group of researchers from Vienna led by CeMM and in collaboration with colleagues from the LBI-CR pursued to identify novel effective treatments for T-PLL patients by functional testing of primary patient-derived lymphoma cells using a library of 106 FDA-approved anti-cancer drugs or compounds currently in clinical development.

Is reactivation of the p53 pathway a new cancer therapy?

The p53 tumor suppressor is inactivated in most cancers, thus suggesting that loss of p53 is a prerequisite for tumor growth. Therefore, its reintroduction through different means bears great clinical potential. Kenner and colleagues review small molecules, which are currently developed and able to reactivate specific, frequently observed mutant forms of p53 or that inhibit the negative regulator MDM2.

Stem cells regulate invasion of somatic cells

Stem cells have the property to induce the invasion of primary somatic cells through insulin-like growth factor I (IGF-I)- or II (IGF-II)-mediated activation of mechanistic target of rapamycin complex 1 (mTORC1). We propose downstream of mTORC1 stem cell-induced invasion is mediated by hypoxia-inducible factor 1-alpha (HIF-1α)-regulated matrix metalloproteinases. Human stem cells use this mechanism to induce invasion and thereby attract cells from the microenvironment in vivo.

Novel strategy to control STAT signalling axis

Signal transducers and activators of transcription (STATs) are latent, cytoplasmic transcription factors. Janus kinases (JAKs) and activated CDC42-associated kinase-1 (ACK1/TNK2) catalyse the phosphorylation of STAT1 and the expression of its target genes. Here we demonstrate that catalytically active ACK1 promotes the phosphorylation and nuclear accumulation of STAT1 in transformed kidney cells.

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