Understanding cancer MMoA

A recently published paper in Nature Communications describes drugs targeting cancerous stem cells in blood of myelofibrosis patients and molecular mechanisms driving these drug responses. The paper was written as a collaboration of the following labs: Wollscheid (ITM), Snijder (IMSB), Theocharides (USZ), Lopes (UZH), and Skoda (USB).

Myelofibrosis (MF), a blood cancer with bone marrow scarring, is often caused by JAK2 or CALR gene mutations in over 90% of patients. Researchers, including Wildschut et al., employed pharmacoscopy to identify effective drugs from other diseases for MF patients. They screened blood samples to target disease-driving mutations in hematopoietic stem cells while sparing healthy cells. Individualized drug prioritization using this method, coupled with proteomics and clinical data, revealed that CALR mutation patients responded well to BET inhibitors, especially without RAS pathway upregulation. The study also identified patient subgroups linked to disease advancement and high CALR mutation burden, facilitating specific drug targeting. This research unveils the drug response landscape in MF patients and actionable disease mechanisms in subgroups.

More Information and recently published papers by Wollscheid Lab

external pageProteogenetic drug response profiling elucidates targetable vulnerabilities of myelofibrosis

external pageEx Vivo Image-based Drug Profiling for Discovery and Personalization of Myelofibrosis Treatments

external pageProtein Guard Mechanism May Be Used against Infectious Disease and Cancer

external pageTesting hundreds of existing therapeutics to fight blood cancer more effectively

 

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