9 documents found, page 1 of 1

Influence of genetic variants of oxidative stress related genes on prognosis an...

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of BCR-ABL1 oncogene. Oxidative stress conditions are crucial in tumor development and progression. The NRF2, codified by NFE2L2 gene, plays a central role in redox balance, promoting the transcription of cytoprotective and antioxidant genes such as SOD2, GPX1 and CAT. The action of this transcription factor is regulat...

Genetic variants in oxidative stress-related genes and their impact on prognosi...

Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasia characterized by the BCR::ABL1 fusion gene, which codifies the BCR-ABL protein with increased tyrosine kinase activity. Despite the clinical results for the outstanding tyrosine kinase inhibitors (TKIs), drug resistance is a problem in CML management. Genetic variants that alter redox homeostasis by changing antioxidant enzyme expression or...

Diagnosis and Laboratory Follow-Up of Patients with Multiple Myeloma: Guideline...

Multiple myeloma is a neoplasm of plasma cells that in most cases is associated with the secretion of monoclonal immunoglobulins and can involve multiple organs. Its timely diagnosis is essential to limit or avoid irreversible damage and dysfunction of target organs. Appropriate initial stratification of patients allows for optimization in the selection and sequence of therapy, as well as proper follow-up durin...

Diagnosis and laboratory follow-up of patients with multiple myeloma: guideline...

Multiple myeloma is a neoplasm of plasma cells that in most cases is associated with the secretion of monoclonal immunoglobulins and can involve multiple organs. Its timely diagnosis is essential to limit or avoid irreversible damage and dysfunction of target organs. Appropriate initial stratification of patients allows for optimization in the selection and sequence of therapy, as well as proper follow-up durin...

CD20+ T cells in monoclonal B cell lymphocytosis and chronic lymphocytic leukem...

Introduction: In monoclonal B cell lymphocytosis (MBL) and chronic lymphocytic leukemia (CLL), the expansion of malignant B cells disrupts the normal homeostasis and interactions between B cells and T cells, leading to immune dysregulation. CD20+ T cells are a subpopulation of T cells that appear to be involved in autoimmune diseases and cancer. Methods: Here, we quantified and phenotypically characterized CD20...

Genetic variants of ABC and SLC transporter genes and chronic myeloid leukaemia...

Solute carrier (SLC) and ATP-binding cassette (ABC) transporters comprise a variety of proteins expressed on cell membranes responsible for intrusion or extrusion of substrates, respectively, including nutrients, xenobiotics, and chemotherapeutic agents. These transporters mediate the cellular disposition of tyrosine kinase inhibitors (TKIs), and their genetic variants could affect its function, potentially pre...

Negative MR4·0 chronic myeloid leukaemia and its possible implications for trea...

ABL1 tyrosine kinase inhibitors (TKI) have dramatically improved the outcome for chronic myeloid leukaemia (CML) patients, resulting in a life expectancy that approaches that of the general population. Nevertheless, lifelong TKI therapy may have consequences, including chronic adverse events that can substantially impact patients’ quality of life, adherence to therapy and treatment success. Recently, several cl...

Combined study of ADAMTS13 and complement genes in the diagnosis of thrombotic ...

Background: The 2 main forms of thrombotic microangiopathy (TMA) are thrombotic thrombocytopenic purpura (TTP) and atypical hemolytic uremic syndrome (aHUS). Deficiency of ADAMTS13 and dysregulation of the complement pathway result in TTP and aHUS, respectively; however, overlap of their clinical characteristics makes differential diagnosis challenging. Objectives and Methods: We aimed to develop a TMA diagnosi...

JAK2V617F allele burden is associated with thrombotic mechanisms activation in ...