Publications by authors named "M Lasa"

Apoptosis is a type of programmed cell death which can be induced by thyroid hormone in pituitary and other cell models. This process is characterized by several biochemical changes, including modifications in plasma membrane lipid composition, mitochondrial membrane dysfunction, and DNA fragmentation, among others. These cellular alterations can be measured using western blotting and flow cytometry techniques.

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  • - In a study of 138 multiple myeloma (MM) patients, researchers explored the benefits of monitoring peripheral residual disease (PRD) in blood instead of relying solely on more invasive bone marrow (BM) assessments.
  • - Positive PRD results from next-generation flow (NGF) indicated a significantly higher risk of disease progression/death, and those with undetectable PRD had excellent survival rates.
  • - The findings suggest that PRD monitoring is a valuable and less cumbersome method for identifying patients at risk of relapse during maintenance treatment in transplant-eligible MM patients.
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There is accumulating evidence of BCMA and GPRC5D loss after treatment with T-cell redirecting therapies in patients with relapsed/refractory multiple myeloma (RRMM). While complete CD38 loss is not observed upon relapses after treatment with anti-CD38 monoclonal antibodies (mAb), there is downregulation of surface CD38 expression and decreased number and function of NK cells, which renders these patients resistant to retreatment with anti-CD38 mAb. Here, we provide preclinical evidence that RRMM patients previously exposed to anti-CD38 mAb could benefit from T-cell-based immunotherapy that depend less on CD38 antigen density and NK-cell activity, such as the novel CD38/CD3xCD28 trispecific T-cell engager, SAR442257.

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Background: Inferior vena cava agenesis (IVCA) is a rare anomaly predisposing affected people to lower-limb venous thrombosis with low frequency of pulmonary embolism. Antenatal thrombosis and inherited thrombophilia have been suggested as causes of IVCA. However, there is little evidence on the clinical course and management of this condition.

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  • BRAF mutations are common in thyroid cancer and lead to poor treatment outcomes, prompting research into alternative survival mechanisms.
  • Cells from thyroid tumors rely heavily on fatty acid oxidation for energy, which is regulated by autophagy, highlighting potential therapeutic targets.
  • Inhibiting autophagy or fatty acid oxidation triggers a shift to increased glycolysis, which is crucial for the survival of certain thyroid cancer cells and may enhance sensitivity to the BRAF inhibitor, vemurafenib.
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