China
Africa
Explore chapters and articles related to this topic
T-Lymphoblastic Leukemia/Lymphoma
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
FLT3 mutations are rare in T-ALL (1%–2%). FLT3- internal tandem duplication (ITD)+ T-ALL shows the phenotype of ETP T-ALL (negative CD3, CD4, CD5, and CD8; positive CD117, CD34, CD2, CD7, TdT, CD13, CD135, and cytoplasmic CD3) [45]. Occasional cases with this phenotype are positive for MPO, representing mixed phenotype acute leukemia (MPAL).
Increased synthesis of pro-inflammatory cytokines in C9ORF72 patients
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Gabriel Pinilla, Anupama Kumar, Mary Kay Floaters, Carlos A. Pardo, Jeffrey Rothstein, Hristelina Ilieva
Fms-like tyrosine kinase 3 ligand is a cytokine and growth factor that increases the number of T and B lymphocytes by activating the hematopoietic progenitors. It binds to CD135 on hematopoietic progenitors and is considered crucial for plasmocytoid and classical dendritic cell development (31). CSF levels of Fms-like tyrosine kinase 3 ligand levels have been reported elevated in ALS patients (32). GM-CSF is produced by macrophages, T cells, fibroblasts, endothelial cells and stimulates stem cells to produce granulocytes, monocytes, and macrophages. GM-CSF levels were found decreased with longer duration of ALS disease (33). CCL5 or RANTES (regulated on activation, normal T cell expressed and secreted) has T-cell chemotactic properties and was also found different between the two ALS groups. While CCL5 levels increase with age (34), there is no statistically difference between the ages of the two ALS groups (58.2 IQR 10.8 vs. 62.0 IQR 8.0), thus the effect of age is an unlikely explanation. It is quite possible that the detected changes in growth factor levels specific for the C9+ group are a compensatory type of change. In the future, it will be interesting to obtain a detailed analysis of lymphocyte counts and subtypes in this patient group in parallel with the growth factor analysis.
Therapy of acute myeloid leukemia: therapeutic targeting of tyrosine kinases
Published in Expert Opinion on Investigational Drugs, 2019
The RTK ‘Fms-like Tyrosine kinase 3’ FLT3 is a surface protein designated CD135 and is expressed on many hematopoietic progenitors and 70–100% of AMLs [13,14]. FLT3 mutations are seen in all cytogenetic classes of AML. Tumor-associated mutations of FLT3 include Juxta-membrane (JM) domain internal tandem duplications (ITDs or ITRs) and kinase domain (TKD) mutations [7,8,15,16]. Both of these types of mutations result in some degree of autonomy from or increased reactivity to ligand binding for activation and autophosphorylation of the receptor FLT3 molecule, but their signaling is different, as ITDs but not TKDs activate STAT5 [10]. The FLT3-ITDs represent activation markers associated with poor prognosis (early relapse and shorter survival) when identified in human acute myeloid leukemia and are seen in 20–30% of cases [8,17]. FLT3-ITD allelic ratio (AR) or variant allele frequency varies greatly in mutated cases, with increasing AR associated with poorer outcomes at diagnosis [18]. Additionally, the length of the ITD has been shown to affect the sensitivity to FLT3 inhibitors, with longer ITDs that extend closer to the JM domain being associated with poorer prognoses and worse responses to induction chemotherapy [19,20].
A Purification Technique for Adipose-Derived Stromal Cell Cultures Leads to a More Regenerative Cell Population
Published in Journal of Investigative Surgery, 2019
Renee F. Conway, Kevin M. Okarski, John A. Szivek
FCER1α is expressed in low quantities in monocytes and dendritic cells and in high quantities in most granulocytes (eosinophils, basophils, and mast cells but not neutrophils).28 CD135 is expressed in lymphoid, hematopoietic, granulocyte, and macrophage progenitor cells.29 These two biomarkers should not be expressed in MSCs.30 FCER1α and CD135 were expressed at low levels in cell populations given just the primary extraction and were not expressed in TS and TR cell populations. Therefore, FCER1α-expressing granulocytes and progenitor cells committed to non-mesenchymal lineages were eliminated during the purification.