Long non-coding RNA deleted in lymphocytic leukaemia 1 promotes hepatocellular carcinoma progression by sponging miR-133a to regulate IGF-1R expression.
In conclusion, miR-31 may exert an anticancer role in B-ALL in children and may be a potential marker to assist in diagnosis and prognostic prediction.
Mechanistically, we demonstrate that GATA3-driven nucleosome eviction dynamically modulates N-Me enhancer activity and is strictly required for NOTCH1-induced T-ALL initiation and maintenance.
Besides, we found that silenced DLEU1 significantly decreased insulin-like growth factor 1 receptor (IGF-1R) expression (a target of miR-133a) and its downstream signal PI3K/AKT pathway in HCC cells, while miR-133a inhibitor partially reversed this trend.
The coinciding loss of CD52 membrane expression may contribute to the development of resistance to alemtuzumab (ALM) treatment in B-ALL patients resulting in the outgrowth of CD52-negative escape variants.
In P210 (+) chronic myelogenous leukemia (CML), down-regulated PAK1 gene expressions may lead to the suppression of cell proliferation and promotion of apoptosis through phosphorylation of STAT5, with a reverse effect in P190 (+) acute lymphoblastic leukemia(ALL), especially acute B lymphoblastic leukemia (B-ALL).
Cortactin is an actin-binding protein involved in cell adhesion and migration that is overexpressed in many solid tumors and in adult B-cell chronic lymphocytic leukemia.
A qRT-PCR assay was used to examine the levels of lncRNA GAS5 and miR-222 in leukomonocytes of patients with B lymphocytic leukaemia and in healthy donors.
Here, we assessed the MCL1-antagonist S63845, the MDM2-inhibitor HDM201, and the MEK1/2-inhibitor trametinib as single agents and in combination in a variety of AML cell lines and mononuclear cells isolated from patients with hematological malignancies centered on myeloid leukemia, some lymphatic leukemia, as well as some lymphomas, for their ability to induce apoptosis and cell death.
In P210 (+) chronic myelogenous leukemia (CML), down-regulated PAK1 gene expressions may lead to the suppression of cell proliferation and promotion of apoptosis through phosphorylation of STAT5, with a reverse effect in P190 (+) acute lymphoblastic leukemia(ALL), especially acute B lymphoblastic leukemia (B-ALL).
Tumor antigen-redirected chimeric antigen receptor (CAR) T-cell immunotherapies have induced remarkable responses in patients with relapsed or chemorefractory B-lymphoblastic leukemia, and similar strategies are now under early clinical study in adults with relapsed/refractory AML.
Expression and role of granulocyte macrophage colony-stimulating factor receptor (GM-CSFR) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia.
The ectopic expression of CDX2 has been frequently observed in acute myeloid and lymphoid leukemia which in most cases is concomitant with poor prognosis.
Expression of IRX3 alone was sufficient to immortalize hematopoietic stem and progenitor cells (HSPCs) in myeloid culture and induce lymphoid leukemias in vivo.
BCL6 is overexpressed in the bone marrow of methotrexate-resistant children with B-ALL, which is capable of attenuating the sensitivity of B-ALL to methotrexate via promoting ZEB1 expression.