Accurate and early diagnosis is crucial to select an optimal treatment and to increase the chances for survival. A research team at Lund University has now found a novel way to diagnose mantle cell lymphomas (MCL).

The novel approach that will be tested in the routine diagnosis of lymphoma in the Department of Pathology is based on a new biomarker, i.e., a factor that is specific for a certain disease. The discovery is a result of research within CREATE Health, a Center for Translational Cancer Research supported by the Foundation for Strategic Research and the Wallenberg Foundation.

CREATE Health has integrated investigators from the faculties of medicine, engineering, and natural sciences together with clinical oncologists from the university hospital. The overall aim is to identify proteins and genes that can be used as biomarkers for cancer, using emerging advanced technologies. Several very promising projects are under development, but the novel diagnostic approach for MCL has advanced the furthest. Scientist Sara Ek and colleagues have by studying more than 50,000 gene fragments found those that are specifically overexpressed in this disease. She has also identified the corresponding proteins and it is one of these proteins that serves as a specific biomarker.

- In a collaboration with pathologists, we are now studying the biomarker to see if it can be used as a novel routine test for this aggressive blood cancer. In a longer perspective, knowledge about the function of these disease-specific proteins can also lead to novel therapeutic modalities for blood cancer, explains professor Carl Borrebaeck, program director for CREATE Health.

Dr. Michael Dictor, pathologist at Lund University Hospital agrees.- The biomarker Sox11 has shown to be a very sensitive and specific marker for MCL in addition to providing new information on how the disease might arise.

lu.se

The researchers then used a sophisticated genetic technique to repair the mutated dystrophin gene in the isolated DMD CD133+ cells so that dystrophin synthesis was restored. Importantly, intramuscular or intra-arterial delivery of the genetically corrected muscle cell progenitors resulted in significant recovery of muscle morphology, function, and dystrophin expression in a mouse model of muscular dystrophy.

These data demonstrate that genetically engineered blood or muscle-derived CD133+ cells represent a possible tool for future stem cell-based autograft applications in humans with DMD, says Dr. Torrente. The authors caution that significant additional work needs to be done prior to using this technology in humans. Additional research will substantially enhance our understanding of the mechanisms underlying this effect and may lead to the improvement of gene and cell therapy strategies for DMD.

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