A prospective endocrine and metabolic therapy (ET) trial can optimize patients’ treatment with an injectable marker designed to appear closely to the patient’s blood or liver cells, thereby helping more people survive than otherwise would have been possible.
Leukemia is a serious and often fatal immune system disease in which the blood and lymph system, comprising a nucleus of hiPSCs, proliferate uncontrollably and cause impaired cell cycle followed by a dramatic decrease in normal blood cell numbers.
In half of patients, the core of the disease is triggered in the late stages of the disease. These patients are overtreated, and there is high risk of acute and intensive toxicity.
The clinical benefit and tolerability of ET is currently not even considered clinically relevant. However, its use in research clinical trials reflects a novel, efficacious marker that can influence ET survival and match or even surpass the clinical relevance of other markers.
In a new study published in The Lancet, a team of researchers led by Dr. Alfonso Villarreal, of the Spanish National Cancer Research Centre (CNIO), has explored the potential of glycoprotein ELISA as a further valuable marker of ET survival in a small population of ET patients. The study, carried out at the ESIC PV biobank and Nanociès OB/CRISIS 1.0, is the result of a two-year follow-up with this population.
Treatment.
The ETE trial involves a single, phase II ET study and with an expected follow-up of about 12 months, it could be a sea change in immunotherapy and democracy, providing a final impact of about 31-45% efficacy in the first two years, and a fraction of clinical efficacy by year 5.
“The overall aim of the study was to study the immunological and biochemical functions of the cytokines generated in ETE patients. This analysis, nonetheless, showed that not only the peptides and water molecules of the cytokine family, but also leukotrienes from lipids, activators of non-receptor functional properties and potential micromodulators of membrane permeability, were up-regulated only in the first stage of ET disease,” said Villarreal.
Metabolic.
The results of the trial have not only shown that one can be almost certain to be cured of ET, but also that the immune and metabolic dysfunction of these patients can be optimized by ET stimulators.
“Our study revealed that the dysbiosis, or imbalance of the human leukocyte population, strongly factors into ET disease processes and that ET patients suffer from metabolic activation and fatty liver disease, as well as other vascular diseases, suggesting a strong role for the immune system in ET pathogenesis,” said Villarreal.
Reference.
The National Cancer Research Centre and the institute of Neurosciences of the University of Barcelona, led by Dr. Alfonso Villarreal, has been funding the study. The authorities funded the study at the almost 100% grant rate of the grant fund announced by the National Institute for Health (RURY)-Medical Research Competitiveness Algorithm (RURY-MAP).