Sentences with phrase «myeloid cell leukemia»
Mar. 14, 2018 — New agreement will pursue therapies targeting MCL1 (myeloid cell leukemia 1), which is highly prevalent in many difficult - to - treat cancers.
https://news.vanderbilt.edu/ Not exact matches
«Stem - cell researchers solve mystery of relapse in acute myeloid leukemia.»
Targeting exhausted immune cells may change the prognosis for patients with acute myeloid leukemia (AML) relapse after a stem cell transplant, according to Penn State College of Medicine researchers.
Chronic myeloid leukemia (CML) develops through chromosomal alterations in blood - forming cells of the bone marrow and usually occurs in older persons.
Several factors newly discovered to be phosphorylated by GSK - 3 are also known to be mutated in acute myeloid leukemia, a condition in which aberrant splicing causes uncontrolled white blood cell proliferation.
Chronic myeloid leukemia (CML) is a form of blood cancer based on a genetic disorder that leads to the overproduction of white blood cells.
In acute myeloid leukemia, undifferentiated bone marrow cells grow uncontrollably in the blood and bone marrow, crowding out and destroying healthy cells.
The scientists discovered that dinaciclib, by interfering with UPR activation, caused multiple myeloma and myeloid leukemia cells to initiate a form of cell suicide known as apoptosis when exposed to agents that induced ER stress.
Researchers at Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center have found a chemical «signature» in blood - forming stem cells that predicts whether patients with acute myeloid leukemia (AML) will respond to chemotherapy.
Leukemia researchers at Princess Margaret Cancer Centre have developed a 17 - gene signature derived from leukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trLeukemia researchers at Princess Margaret Cancer Centre have developed a 17 - gene signature derived from leukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trleukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trleukemia (AML) will respond to standard treatment.
«Chemical stem cell signature predicts treatment response for acute myeloid leukemia.»
Researchers at University of California San Diego School of Medicine and Moores Cancer Center have identified RNA - based biomarkers that distinguish between normal, aging hematopoietic stem cells and leukemia stem cells associated with secondary acute myeloid leukemia (sAML), a particularly problematic disease that typically afflicts older patients who have often already experienced a bout with cancer.
The production of healthy red blood cells is critical for those with acute myeloid leukemia but is sometimes overlooked as conventional treatments focus on killing the leukemia cells alone.
«We are now investigating chromosome fragile site formation in various human cell lines, including the chronic myeloid leukemia and Fragile X cells,» said Feng.
Dr Xu showed that for BET inhibitors to successfully kill lymphoma and myeloid leukemia cells the presence of a protein called BIM, which brings on apoptosis, was critical.
But as the blood stem cells age, their ability to regenerate blood declines, potentially contributing to anemia and the risk of cancers like acute myeloid leukemia and immune deficiency.
Self - renewal of blast crisis chronic myeloid leukemia cells was reduced by approximately 40 percent when treated with the small molecule, called 8 - Aza, as compared to untreated cells.
«Prostaglandin EI inhibits leukemia stem cells: Targeting leukemia stem cells in combination with standard chemotherapy may improve treatment for chronic myeloid leukemia.»
ANAHEIM, CALIFORNIA — Chronic myeloid leukemia (CML) cells invade the bone marrow and spleen by destroying healthy cells with a toxic protein, according to a new study.
Researchers can now tag individual malignant cells in the bone marrow of patients with acute myeloid leukemia.
In cancer, a state marked by increased protein translation and biomass expansion, HSF1 is activated and binds to numerous genes throughout the genome, as seen in the heat map of HSF1 ChIP - Seq read density in M0 - 91acute myeloid leukemia cells (DMSO, far left).
(TORONTO, Canada — Dec. 7, 2016)-- Leukemia researchers at Princess Margaret Cancer Centre have developed a 17 - gene signature derived from leukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trLeukemia researchers at Princess Margaret Cancer Centre have developed a 17 - gene signature derived from leukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trleukemia stem cells that can predict at diagnosis if patients with acute myeloid leukemia (AML) will respond to standard trleukemia (AML) will respond to standard treatment.
A Phase 3 Open - Label Randomized Study of Quizartinib (AC220) Monotherapy Versus Salvage Chemotherapy in Subjects with FLT3 - ITD Positive Acute Myeloid Leukemia (AML) Refractory To or Relapsed After First - line Treatment With or Without Hematopoietic Stem Cell Transplantation (HSCT) Consolidation
Based on empirical data obtained in cases of chronic myeloid leukemia, a myeloproliferative syndrome controlled by the immune system, and in solid tumors, we observe both the possible contribution of innate CD8 (+) T cells to cancer disease control and their susceptibility to tumor immune subversion.
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells).
Acute myeloid leukemia (AML) is characterized by a rapidly - developing cancer in the myeloid line of blood cells, which is responsible for producing red blood cells, platelets and several types of white blood cells called granulocytes.
Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell.
CT - 011, developed by Israel - based Curetech Ltd, is also being tested in phase II trials in metastatic melanoma, colorectal cancer in combination with chemotherapy, advanced renal cell and prostate cancers, as well as in acute myeloid leukemia.
«Remissions of Acute Myeloid Leukemia and Blastic Plasmacytoid Dendritic Cell Neoplasm Following Treatment with CD123 - Specific CAR T Cells: A First - in - Human Clinical Trial» is presented at the ASH Annual Meeting Dec. 9 to 12, 2017.
Locafaro G *, Andolfi G *, Russo F, Camisa B, Ciceri F, Bondanza A, Roncarolo MG *, Gregori S. HLA class I - dependent targeting of myeloid leukemia by IL -10-engineered human CD4 + Tr1 cells.
In addition to being integral to cell biology, tyrosine kinases also present targets for new anticancer therapies: One of the most highly touted, rationally designed anticancer compounds, Gleevec, inhibits an oncogenic tyrosine kinase whose aberrant activity fuels the rampant growth of cells in patients with chronic myeloid leukemia.
Allogeneic Sibling Donor Peripheral Blood Stem Cells Transplantation With Myeloablative Conditioning for Chronic Myeloid Leukemia in Blast Crisis - Successful Treatment Despite Severe Phase of the Disease
Her thesis was entitled «Function and inhibition of BRD9 in acute myeloid leukemia cells.»
Rac2 - MRC - cIII — generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors.
Induction of Differentiation and Cellular Manipulation of Human Myeloid HL - 60 Leukemia Cells.
AST - VAC1 (antigen - presenting autologous dendritic cells) is an autologous cancer immunotherapy with promising efficacy and safety data from a Phase 2 study in Acute Myeloid Leukemia (AML).
(Chronic myeloid leukemia, a deadly blood cancer, for example, is caused when two chromosomes in white blood cells exchange fragments, resulting in a hapless fusion of genes that are normally kept apart.)
To evaluate the impact of VPA treatment on the preservation of GVL activity, we challenged BALB / c recipients with host - type GFP + acute myeloid leukemia cells (H - 2d) to mimic residual leukemia in patients receiving allogeneic BMT.
St. Jude Children's Research Hospital scientists have found that cells of a deadly acute myeloid leukemia can be killed by blocking production of a molecular «battery.»
Low - dose donor CD8 + cells in the CD4 - depleted graft prevent allogeneic marrow graft rejection and severe graft - versus - host disease for chronic myeloid leukemia patients in first chronic phase.
In GVL experiments, acute myeloid leukemia cells that were developed in our institute were administered on the day of transplantation (31).
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.
Leukemia is a cancer of the bone marrow and blood and is classified by cell type and rate of growth: acute lymphocytic, chronic lymphocytic, acute myeloid, and chronic myeloid.
We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML) / atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B - lineage acute lymphoblastic leukemia (ALL), T - cell ALL, and chronic lymphocytic leukemia (CLL).
Ponatinib Extends Survival Over Transplant in Chronic Phase CML: The results of a new study that included patients from the PACE trial and the European Bone Marrow Transplant registry revealed that treatment with ponatinib yielded better overall survival (OS) compared with allogeneic stem cell transplantation (allo - SCT) in patients with chronic phase chronic myeloid leukemia (CP - CML) with a T315I mutation.
Inhibiting a protein called BRD4 critical to the survival of acute myeloid leukemia (AML) cells has shown to be an effective therapeutic strategy...
ONC201 demonstrated (GI50 1 - 8 µM) dose - and time - dependent efficacy in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), chronic lymphocytic leukemia (CLL), diffuse large B - cell lymphoma (DLBCL), mantle cell lymphoma (MCL), Burkitt's lymphoma, anaplastic large cell lymphoma (ALCL), cutaneous T - cell lymphoma (CTCL), Hodgkin's lymphoma (nodular sclerosis) and multiple myeloma (MM) cell lines including cells resistant to standard of care (dexamethasone in MM) and primary samples.
Elevated numbers of circulating CD34 (+) cells were found in p.P214L and p.Y401N carriers, and two patients from different families suffered from refractory anemia with excess blasts, while one patient from a third family was successfully treated for acute myeloid leukemia.
Acute myeloid leukemia (AML) is the leading cause of leukemia mortality in the United States.1 Curative treatment involves intensive induction chemotherapy, before proceeding to either consolidation chemotherapy or allogeneic stem cell transplantation based on the patient's risk for relapse.2 This approach has been employed for > 4 decades and, although most individuals achieve complete remissions with front - line therapy, 3 the majority of patients ultimately relapse with drug - resistant disease, and overall survival rates remain disappointingly poor.4 The limited ability of many patients to tolerate the intense chemotherapy - based treatments, in particular hematological toxicity, further contributes to the poor outcomes noted in this disease.
These include imatinib, sold under the brand name Gleevec for chronic myeloid leukemia; gefitinib, sold as Iressa for metastatic non-small cell lung cancer; and sunitinib, marketed as Sutent, for renal cell cancer and gastrointestinal stromal tumors.