Hypermethylation of the alternative AWT1 promoter in hematological malignancies is a highly specific marker for acute myeloid leukemias despite high expression levels.
The Wilms' tumor 1 (WT1) antigen is expressed in solid and hematological malignancies, but not healthy tissues, making it a promising target for cancer immunotherapies.
The Wilm's tumor 1 (WT1) gene, which is highly expressed in >80% of patients with acute myeloid leukemia (AML) and its increased expression level may cause poor clinical outcomes, is a potential MRD marker of hematological neoplasms.
Heightened co-expression and dysregulated signaling associated with Toll-like receptor 3 (TLR3) and Wnt5a is an integral component of solid tumors and hematological malignancies.
The data demonstrate that overexpression of MDR1 and MRP genes in hematological malignancies elevates in patients after chemotherapy and correlates with poor clinic prognosis and more frequent recurrences of the malignancies.
Group 3 comprises the tumors with predominantly low levels of MRP mRNA, comparable to the levels found in normal tissues (e.g., other hematological malignancies, soft tissue sarcomas, melanoma, and cancers of the prostate, breast, kidney, bladder, testis, ovary, and colon).
To date, there are clinical studies for the evaluation of WEE1 inhibitors in the treatment of solid tumors and studies on cell lines of non-MM hematological tumors.
This study is a prospective observational cohort study; Hypercoagulability and inflammatory biomarkers including:(1) Coagulation and fibrinolysis activation Markers (D-dimer, Fibrinogen, Antithrombin, plasminogen activator inhibitor 1 [PAI-1]);(2) Endothelium and platelet activation Markers (von Willebrand Factor [vWF], soluble P-selectin); and (3) Inflammation Markers (Tumor necrosis factor alpha [TNF-α], Interleukin-6 [IL-6]) were assayed on a group of 171 patients with hematological malignancies at time of diagnosis.
Dysregulation of VEGF expression and signaling pathways therefore plays an important role in the pathogenesis and clinical features of hematologic malignancies, in particular multiple myeloma.
Overexpression of vascular endothelial growth factor (VEGF) is associated with increased angiogenesis, growth and invasion in solid tumors, and hematologic malignancies.
Perturbation in the expression and signaling pathways of vascular endothelial growth factor (VEGF) has been linked to pathogenesis of hematologic malignancies.
Alterations in the expression and signalling pathways of vascular endothelial growth factor (VEGF) have been linked to the clinical features and pathogenesis of hematologic malignancies.
Efficient modulation of aberrant vascular endothelial growth factor (VEGF) and its receptor-1 (Flt-1) expressions have become a potential therapeutic strategy for hematologic malignancies including myeloid leukemia.
Usp9x has emerged as a potential therapeutic target in some hematologic malignancies and a broad range of solid tumors including brain, breast, and prostate.
Together, these results identify USP7 as a promising therapeutic target for the treatment of hematological malignancies with DDR defects, where ATM/p53-dependent apoptosis is compromised.
These BACs have been mapped to 19q12-19q13.1 and 19q11-19q13.1, respectively, and are predicted to contain the markers D19S409 and D19S919 and the gene for ubiquinol-cytochrome C reductase, Rieske iron-sulfur polypeptide1 (UQCRFS1). dmin originating from chromosome 19 have not been reported previously in hematologic malignancies.
UHRF1 overexpression is observed in a number of solid tumors and hematological malignancies, and is considered a primary mechanism in inhibiting apoptosis.