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A person taps the tablet to control where the beam of light appears on a floor. The swarm robots then roll toward the illumination, constantly communicating…
Rydberg atoms, atoms whose outermost electrons are highly excited but not ionized, might be just the thing for processing quantum information.
The test results are in. All in all, they are positive, along with a couple of suggestions for improvement: StreetPong, the world’s first traffic-light game,…
The formation and onset of the prevalent form of acute myeloid leukemia (AML, FAB subtype M2) requires RUNX1/ETO, the product of the t(8;21) chromosomal translocation. Tetramerization through the nervy homology region 2 (NHR2) of ETO is essential for the RUNX1/ETO-mediated transformation. The inventors demonstrated that inhibition of NHR2 tetramerization by first-in-class small molecules is a viable entry point for the treatment of AML. Drug candidates have been identified by a small-molecule in silico screening and have been validated in cellular assays. Several compounds proved to be successful in
inhibiting NHR2 tetramerization. Preferred compound 7.44 was able to slow tumor growth in a xenograft mouse model (SKNO 1 xenograft). The pending patent application covers claims directed to a variety of chemotypes that proved activity against AML.
The present invention provides a novel susceptibility gene for hereditary cancers. RAD51C, which encodes for a protein involved in DNA repair, has been found to be mutated in families with breast and ovarian cancer, but not in healthy control subjects. In addition, the patients were all selected from pedigrees negative for mutations of BRCA1 and BRCA2 to particularly identify genetic mutations causing a cancer predisposition independently of already known determinants. All analyzed mutations were identified as mono-allelic germline mutations. Besides gynecological cancers, mutations of RAD51C were also detected in patients suffering from head and neck squamous cell carcinomas (HNSSC). Thus, the presence of mutations in RAD51C is associated with an increased predisposition of developing cancer and positions RAD51C as a high-risk cancer susceptibility gene. Furthermore, an abnormal RAD51C gene status correlates with an increased probability for response to a DNA-damaging therapeutic agent and therefore represents an ideal companion diagnostic.
This invention enables an easy and economical way for the stratification of patients (e.g. for treatment with tyrosine-kinase-inhibitors) with a state-of-the-art sensitivity, which might be even be more sensitive than mutation detection by next-generation-sequencing technologies. In addition this detection technology is based on the established and worldwide accessible RT-PCR-platform. It can even be used – in combination with suitable enrichment strategies – for the non-invasive analysis of CTCs or free DNA from plasma/serum samples to facilitate continuous monitoring of treatment response.
Currently, the inventors are establishing strategies for detecting a panel of the most common oncogenic mutations with similar impressive sensitivities.