Publications by authors named "C Cobaleda"
B-cell Acute Lymphoblastic Leukemia (B-ALL) is the most common pediatric cancer, arising most often in children aged 2-5 years. This distinctive age distribution hints at an association between B-ALL development and disrupted immune system function during a susceptible period during childhood, possibly triggered by early exposure to infection. While cure rates for childhood B-ALL surpass 90% in high-income nations, survivors suffer from diminished quality of life due to the side effects of treatment.
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- There has been a significant increase in understanding the genetic factors that make individuals susceptible to hematopoietic malignancies over the past decade, challenging the belief that these conditions only affect younger people.
- Research shows that cancers in people of all ages can arise from germline mutations, with the age of onset linked to different biological pathways.
- Recent genome-wide studies have identified new germline variants associated with hematopoietic cancers, leading to advancements in genetic counseling, treatment strategies, and the potential prevention of these malignancies.
Article Synopsis
- B-cell acute lymphoblastic leukemia (B-ALL) often starts quietly in children without obvious symptoms.
- Researchers found that stress to the immune system can cause changes in certain B cells, pushing them towards developing leukemia.
- The study shows that a protein called Myd88 is important in preventing leukemia; when its levels drop, more leukemia cases happen, but triggering a different immune signal can delay the disease.
The historical lack of preclinical models reflecting the genetic heterogeneity of multiple myeloma (MM) hampers the advance of therapeutic discoveries. To circumvent this limitation, we screened mice engineered to carry eight MM lesions (NF-κB, KRAS, MYC, TP53, BCL2, cyclin D1, MMSET/NSD2 and c-MAF) combinatorially activated in B lymphocytes following T cell-driven immunization. Fifteen genetically diverse models developed bone marrow (BM) tumors fulfilling MM pathogenesis.
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