It was approved for medical use in the European Union in December 2020.Each dose of brexucabtagene autoleucel is a customized treatment created using the recipients own immune system to help fight the lymphoma. The recipients T cells, a type of white blood cell, are collected and genetically modified to include a new gene that facilitates the targeting and killing of the lymphoma cells. These modified T cells are then infused back into the recipient. Prognosis
Recent clinical advances in mantle cell lymphoma (MCL) have seen standard‐of‐care treatment algorithms transformed. Frontline rituximab combination therapy, high dose cytarabine‐based induction in younger patients and, more recently, Bruton Tyrosine Kinase (BTK) inhibitors in the relapse setting have all demonstrated survival advantage in clinical trials (Wang et al., 2013; Eskelund et al., 2016; Rule et al., 2016). Over the last 15 years these practices have gradually become embedded in clinical practice and real‐world data has observed corresponding improvements in patient survival (Abrahamsson et al., 2014; Leux et al., 2014).The overall 5-year survival rate for MCL is generally 50% (advanced stage MCL) to 70% (for limited-stage MCL). Prognosis for individuals with MCL is problematic and indexes do not work as well due to patients presenting with advanced stage disease. Staging is used but is not very informative, since the malignant B-cells can travel freely though the lymphatic system and therefore most patients are at stage III or IV at diagnosis.
Infants from diabetic mothers usually have several blastogenic malformations. Diabetic embryopathy is therefore an etiological subgroup of defects of blastogenesis that present different monotopic and polytopic developmental defects. Abortion and perinatal deaths
Diabetic embryopathy may result in early or late spontaneous abortion and stillbirth. In maternal diabetes, 90% of pregnancy losses happen in the first trimester due to oxidative stress. Diabetic embryopathy abortions in the second-trimester are most likely due to severe birth defect, maternal metabolic derangement, placental insufficiency and fetal hypoxia due to membrane rupture. Pathogenesis
The development of birth defects associated with maternal hyperglycemia is multi-factorial. Environmental factors and genetic predisposition (paternal, maternal and offspring genome) are important in diabetic embryopathy. The diets of diabetic mothers impacts the rate at which malformations form in their offspring. Furthermore, there is evidence that resistance to certain malformations caused by diabetes is genetic. Epigenetics and its relationship with various environmental factors such as metabolism and diet play a significant role in teratogenesis. Hyperglycemia and associated teratogenic mediators influence DNA methylation, non-coding RNA expression, histone modifications and other epigenetic regulation mechanisms. Research is focused on exploring the impact of diabetic embryopathy on methylation signatures, which could potentially serve as a diagnostic biomarker for the condition. Prevention
Preconception
The probability of major birth defects in offspring of mothers with diabetes is 0.7-4.4% for glycohemoglobin levels <7%. For glycohemoglobin levels >10% the probability of major birth defects is 16.1-100% with an average of 26.6%.