Sentences with phrase «controls hematopoietic»

Marie - Dominique Filippi, PhD, PhD Cincinnati Children's Hospital Medical Center Cincinnati, OH Mitochondrial Morphology Controls Hematopoietic Stem Cell Self - Renewal and Confers Them Divisional Memory

The team has shown that the microenvironment that controls hematopoietic stem cells can be targeted for the treatment of a set of disorders called myeloproliferative neoplasias, the most prominent of which are chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), and atypical chronic myelogenous leukemia (CML).

The findings, published today in Nature, demonstrate that these myeloproliferative neoplasias only appear after damage to the microenvironment that sustains and controls the hematopoietic stem cells — the cells that produce the cells of the blood and the immune system.

Not exact matches

«The ability to control autoimmunity by autologous HSCT [hematopoietic stem cell transplantation] has been demonstrated in other treatment - refractory autoimmune conditions, including neurologic diseases.

«A large number of quiescent hematopoietic stem cells was activated simultaneously when the epigenetic control provided by genomic imprinting was removed,» explains Venkatraman.

«In normal conditions, the microenvironment is able to control the proliferation, differentiation and migration of the hematopoietic stem cell.

To gauge the effect off the loss of imprinting control on the maintenance of the quiescent hematopoietic stem cell pool, Venkatraman analyzed the numbers of quiescent, active and differentiated hematopoietic stem cells in mouse bone marrow.

The Stowers study is the first to show that hematopoietic stem cells (the parent cells) can be directly controlled by their own progeny (megakaryocytes).

They also expressed lower levels of an RNA message that controls the expression of a family of proteins called SOC, known to inhibit the migration of hematopoietic stem cells.

Finally, I will show how we have combined our results to generate a model of hematopoietic differentiation where specific transcription factors control lineage regulatory regions; our model predicts many already known lineage - controlling factors as well as finds new potential regulators of hematopoietic differentiation such as ATF3 in monocytes and Tcf7l2 and Runx2 in NK cells.

Platelets (or thrombocytes) control the process of blood clotting and transfusions are common to prevent bleeding in treatments involving hematopoietic stem cell (HSC) and bone marrow (BM) transplantation [1].

The FLT3 - signaling pathway controls cell proliferation and survival, particularly of hematopoietic progenitor cells.

Professor Kyurkchiev's group is currently developing a project on the controlled differentiation of human induced pluripotent stem cells into hematopoietic stem cells and lymphoid cells.

He has been interested in differentiation and growth control throughout his career and is an expert on hematopoietic stem cells, macrophage differentiation, hematopoietic and Maf family transcription factors.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.