• Acute lymphoblastic leukemia (ALL) is the most common malignancy diagnosed in children, representing more than a quarter of all pediatric cancers. (medscape.com)
  • The image below depicts bone marrow aspirate from a child with T-cell acute lymphoblastic leukemia. (medscape.com)
  • Also, see the Childhood Acute Lymphoblastic Leukemia: Diagnosis, Management, and Complications slideshow to help recognize and treat this disease and its associated complications. (medscape.com)
  • Children with acute lymphoblastic leukemia (ALL) often present with signs and symptoms that reflect bone marrow infiltration and/or extramedullary disease. (medscape.com)
  • See Acute Lymphoblastic Leukemia Staging for more complete information. (medscape.com)
  • Occasionally, people with PDGFRA -associated chronic eosinophilic leukemia develop other blood cell cancers, such as acute myeloid leukemia or B-cell or T-cell acute lymphoblastic leukemia or lymphoblastic lymphoma. (medlineplus.gov)
  • Clofarabine increases the eradication of minimal residual disease of primary B-precursor acute lymphoblastic leukemia compared to high-dose cytarabine without improvement of outcome. (uke.de)
  • Occasionally, the FIP1L1-PDGFRA fusion can be identified in patients with acute myeloid leukemia or B-cell or T-cell acute lymphoblastic leukemia or lymphoblastic lymphoma and sporadically in myeloid sarcoma (Metzgeroth et al. (atlasgeneticsoncology.org)
  • T-cell acute lymphoblastic leukemia (T-ALL) arises from leukemic transformation and expansion of immature T-cell precursors. (aacrjournals.org)
  • Virtually absent from normal pediatric and adult tissues, with the exception of low-level expression in a subset of immature b cell precursors known as hematogones and adipocytes, ROR1 is notably overexpressed, and considered a survival factor, in a number of B lymphoid and epithelial malignancies: including chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL), acute lymphoblastic leukemia (ALL), marginal zone lymphoma, lung adenocarcinoma. (peprotech.com)
  • I have expertise in novel therapies for acute myeloid leukemia, stem cell mobilization and homing, as well as stem cell transplantation. (rochester.edu)
  • Role of signal transduction inhibition in treatment of acute myelogenous leukemia/myelodysplasia. (rochester.edu)
  • This is a multicenter, open-label, Phase 1/2a dose escalation and expansion study of orally administered emavusertib (CA-4948) monotherapy in adult patients with Acute Myelogenous Leukemia (AML) or high risk Myelodysplastic Syndrome (MDS). (rochester.edu)
  • High risk of acute pulmonary toxicity with both myeloablative and non-myeloablative total body irradiation-based conditioning for allogeneic stem cell transplantation. (dukecancerinstitute.org)
  • Antineoplastic agents are used for induction, consolidation, and maintenance therapy and central nervous system (CNS) prophylaxis in patients with acute lymphoblastic leukemia (ALL). (medscape.com)
  • Corticosteroids may be used during induction, consolidation, and/or maintenance therapy for acute lymphoblastic leukemia (ALL). (medscape.com)
  • 3) We are defining the properties of cancer stem cells that initiate and sustain the unique disease features of acute leukemias through the use of various adoptive animal models. (stanford.edu)
  • Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation. (stanford.edu)
  • This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias. (stanford.edu)
  • To characterize gene expression signatures in acute lymphocytic leukemia (ALL) cells associated with known genotypic abnormalities in adult patients. (aacrjournals.org)
  • After more than four decades of intensive research, the cellular origins of acute lymphocytic leukemia (ALL) have been well defined, and several distinct genetic mechanisms that lead to malignant transformation of these cells have been identified ( 1 - 4 ). (aacrjournals.org)
  • Mouse monoclonal to CD10.COCL reacts with CD10, 100 kDa common acute lymphoblastic leukemia antigen (CALLA), which is expressed on lymphoid precursors, germinal center B cells, and peripheral blood granulocytes. (antiviralbiologic.com)
  • Although aberrant DNA methylation has been observed previously in acute lymphoblastic leukemia (ALL), the patterns of differential methylation have not been comprehensively determined in all subtypes of ALL on a genome-wide scale. (biomedcentral.com)
  • Pediatric acute lymphoblastic leukemia (ALL) originates from the malignant transformation of lymphocyte progenitor cells into leukemic cells in the B-cell and T-cell lineages. (biomedcentral.com)
  • In this paper, the bovine serum albumin protected gold nanozymes (BSA-Au nanozymes) were utilized as a novel nanodrug for treatment of acute T-type lymphoblastic leukemia (Jurkat) by production of excessive ROS and effect on the expression of anti-apoptotic genes. (springeropen.com)
  • Acute lymphoblastic leukemia termed as ALL is defined as a type of blood malignancy that is detectable through the accumulation of B and T lymphocyte progenitor cells in the bone marrow [ 4 ]. (springeropen.com)
  • Acute myeloid leukemia (AML) is a disease along with poor prognosis. (cancer-research-network.com)
  • Acute myeloid leukemia (AML) is a group of malignant diseases of the hematopoietic system. (cancer-research-network.com)
  • The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia. (harvard.edu)
  • In the majority of instances, this fusion appears in and promotes the proliferation and differentiation of myeloid precursor cells along the eosinophil linage. (wikipedia.org)
  • In other cases, however, the fusion, while occurring in myeloid precursor cells, promotes proliferation and differentiation of precursor cells along the neutrophil linage or, less commonly, occurs in lymphoid precursor cells to promote the proliferation and differentiation of precursor cells along the lymphoid lineage. (wikipedia.org)
  • Stability of Imprinting and Differentiation Capacity in Naïve Human Cells Induced by Chemical Inhibition of CDK8 and CDK19. (axonmedchem.com)
  • Our research focuses on developmental pathways that regulate hematopoietic cell growth and differentiation and are disrupted in the course of neoplastic transformation, particularly in leukemias and lymphomas. (stanford.edu)
  • Due to their secretory functions, differentiation capabilities, specific homing effects through chemotaxis, distinctive therapeutic potentials, and ex vivo expandability, cells have become an attractive reagent for advanced therapeutic strategies. (biomedcentral.com)
  • Applied to biological elements, such as the cell fronts bordering a wound, this approach makes it possible to identify the various interactions which play a defining role during tissue growth, differentiation, and healing, but above all to highlight their hierarchy at the different scales observed. (regenerativemedicine.net)
  • This suggests that the initial underlying genetic defect in these malignancies can begin in myeloid or lymphoid progenitor cells or in precursors to these myeloid and lymphoid progenitor cells. (wikipedia.org)
  • FIP1L1-PDGFRA rearrangement has been found in a variety of cell lineages (neutrophils, monocytes, eosinophils, CD34+ cells, mast cells and even lymphoid) consistent with an origin in an hematopoietic stem cells or early progenitors progenitor (Gotlib and Cools, 2008). (atlasgeneticsoncology.org)
  • Patients often present with hepatomegaly or splenomegaly hypercellular bone marrows with myelofibrosis, increased number of neutrophils and/or mast cells. (atlasgeneticsoncology.org)
  • Once migrated to the bone marrow, MM cells unbalance bone formation and resorption via the recruitment and maturation of osteoclast precursors. (oncotarget.com)
  • The Notch pathway plays a key role in different types of cancer and drives several biological processes relevant in MM, including cell localization within the bone marrow, proliferation, survival and pharmacological resistance. (oncotarget.com)
  • On the other hand, ALL is caused by excessive proliferation of B or T lymphocyte precursors and accumulation of blast cells in the bone marrow, resulting in the filling of the bone marrow space and finally the suppression of hematopoiesis in the bone marrow, which eventually leads to anemia, thrombocytopenia and becomes neutropenic [ 6 , 7 ]. (springeropen.com)
  • Regulation of hematopoietic stem cells in niche signaling]. (elsevierpure.com)
  • Stem Cells and Development. (elsevierpure.com)
  • His pioneering work spans discoveries in basic biology of blood stem cells and leukemia to first-in-human clinical trials for people with cancer and heart diseases, alongside shaping innovative policies in state health and healthcare financing. (ufl.edu)
  • In his early career Dr. Cogle discovered that blood stem cells make blood vessels and used that biology to invent new therapeutics and diagnostics for people with cancer and heart disease. (ufl.edu)
  • Efficient generation of embryonic stem cells from single blastomeres of cryopreserved mouse embryos in the presence of signalling modulators. (axonmedchem.com)
  • Chemical conversion of human conventional Pluripotent Stem Cells to Trophoblast Stem Cells. (axonmedchem.com)
  • Revealing cell populations catching the early stages of the human embryo development in naïve pluripotent stem cells. (axonmedchem.com)
  • In particular, stem cells, including mesenchymal stem cells (MSCs), hematopoietic stem cells (HSCs), and induced pluripotent stem cells (iPSCs), and immune cells, such as T-cells and Natural Killer (NK) cells, have been favored candidates for regenerative medicine and cell-based cancer immunotherapy, respectively. (biomedcentral.com)
  • Particularly, we have found that Wnt signaling dysregulates mammary stem cells, and that this precedes the formation of differentiated, bilineal tumors. (wisc.edu)
  • In the present study we provide a comprehensive, genome-wide map of de novo DNA methylation changes in ALL cells at diagnosis and relapse by interrogating the methylation levels of 435,941 CpG sites distributed genome-wide in a large collection of pediatric ALL cells of diverse cytogenetic backgrounds. (biomedcentral.com)
  • See Chronic Leukemias: 4 Cancers to Differentiate , a Critical Images slideshow, to help detect chronic leukemias and determine the specific type present. (medscape.com)
  • However, these circumstances do not account for the increased number of eosinophils in PDGFRA -associated chronic eosinophilic leukemia. (medlineplus.gov)
  • Another characteristic feature of PDGFRA -associated chronic eosinophilic leukemia is organ damage caused by the excess eosinophils. (medlineplus.gov)
  • People with PDGFRA -associated chronic eosinophilic leukemia can also have an enlarged spleen (splenomegaly) and elevated levels of certain chemicals called vitamin B12 and tryptase in the blood. (medlineplus.gov)
  • Some people with PDGFRA -associated chronic eosinophilic leukemia have an increased number of other types of white blood cells, such as neutrophils or mast cells. (medlineplus.gov)
  • PDGFRA -associated chronic eosinophilic leukemia is often grouped with a related condition called hypereosinophilic syndrome. (medlineplus.gov)
  • PDGFRA -associated chronic eosinophilic leukemia is caused by mutations in the PDGFRA gene. (medlineplus.gov)
  • The most common genetic abnormality in PDGFRA -associated chronic eosinophilic leukemia results from a deletion of genetic material from chromosome 4 , which brings together part of the PDGFRA gene and part of the FIP1L1 gene, creating the FIP1L1-PDGFRA fusion gene. (medlineplus.gov)
  • When the FIP1L1-PDGFRA fusion gene mutation or point mutations in the PDGFRA gene occur in blood cell precursors, the growth of eosinophils (and occasionally other blood cells, such as neutrophils and mast cells) is poorly controlled, leading to PDGFRA -associated chronic eosinophilic leukemia. (medlineplus.gov)
  • An interstitial deletion del(4)(q12q12) generating a FIP1L1-PDGFRA fusion gene is observed in diverse eosinophilia-associated hematologic disorders like hyperseosinophilic syndrome (HES), systemic mastocytosis (SM) and chronic eosinophilic leukemia (CEL). (atlasgeneticsoncology.org)
  • however chronic eosinophilic leukemia with FIP1L1-PDGFRA is likely to be responsive also to dasatinib, nilotinib, sorafenib and midostaurin (PKC412) (Lierman et al. (atlasgeneticsoncology.org)
  • Interestingly, the T674I mutation that is analogous to the T315I mutation of BCR-ABL1 in chronic myeloid leukemia also confers imatinib resistance (Cools et al. (atlasgeneticsoncology.org)
  • Hence, myeloid cells play a dual role in cancer as they can initiate antitumor responses and communicate with cells of the adaptive immune system, but also promote local inflammation leading to chronic cancer-associated inflammation ( 5 , 6 ). (frontiersin.org)
  • Chronic B cell activation may drive proliferation of antigen-selected B cell clones that accumulate genetic lesions and ultimately undergo neoplastic transformation. (biomedcentral.com)
  • In contrast, thymocytes that recognize self-peptide/MHC with high affinity undergo negative selection via TCR-mediated apoptosis, prompting Trinquand, dos Santos, Tran Quang, and colleagues to hypothesize that reactivation of this developmental checkpoint in T-ALL cells may have antileukemic activity. (aacrjournals.org)
  • Wnt-5a has since been suggested as a candidate ligand for ROR1, and ROR1 has been implicated to function as a pseudokinase, promoting proliferation and resistance to apoptosis in cancer cells through interaction with Wnt-5a, and TCL1-co-activation of AKT. (peprotech.com)
  • Cellular apoptosis (ie, programmed cell death) is another potential mechanism of many antineoplastic agents. (medscape.com)
  • Androgen deprivation therapy induces apoptosis or cell cycle arrest in prostate cancer (PCa) cells. (oncotarget.com)
  • Using constructs downregulating or overexpressing MCL1 we demonstrate that expression of MCL1 prevents induction of apoptosis when PCa cells are grown under steroid-deprived conditions. (oncotarget.com)
  • The BH3-mimetic Obatoclax induces apoptosis and decreases MCL1 expression in androgen-sensitive PCa cells, while castration-resistant PCa cells are less sensitive and react with an upregulation of MCL1 expression. (oncotarget.com)
  • JNK1 shRNA expressing INS1 cells demonstrated elevated apoptosis and cleaved caspase 9 and 3 in comparison to nonsense shRNA expressing control INS1 cells when subjected to palmitate and high blood sugar associated with elevated CHOP appearance, ROS development and mRNA appearance. (cgp60474.com)
  • JNK2 shRNA expressing INS1 cells didn't influence palmitate and high blood sugar induced apoptosis or ER tension markers, but increased appearance in comparison to non-sense shRNA expressing INS1 cells mRNA. (cgp60474.com)
  • Finally, JNK3 shRNA expressing INS1 cells didn't induce apoptosis in comparison to nonsense shRNA expressing INS1 cells when subjected to palmitate and high blood sugar but showed elevated caspase 9 and 3 cleavage connected with elevated and mRNA appearance. (cgp60474.com)
  • These data claim that JNK1 protects against palmitate and high glucose-induced -cell apoptosis connected with decreased ER and mitochondrial tension. (cgp60474.com)
  • Long term and extreme ER tension induced -cell apoptosis is certainly connected with c-jun N-terminal kinase (JNK) activation [9], [15]. (cgp60474.com)
  • In proinflammatory cytokine-induced -cell apoptosis JNK activation is quite transient and rapid [20]. (cgp60474.com)
  • Effects of oxygen metabolites/chemokines on hematopoietic stem cell expansion and preservation. (rochester.edu)
  • Effects of hematopoietic stem cell adhesion on marrow stromal cell cytokine p. (rochester.edu)
  • These signaling pathways control many important cellular processes, such as cell growth and division (proliferation) and cell survival. (medlineplus.gov)
  • As a result, the signaling pathways are constantly turned on (constitutively activated), which increases the proliferation and survival of cells. (medlineplus.gov)
  • Receptor-tyrosine-kinase-like orphan receptor 1 (ROR1) is a tumor-associated, surface protein predominantly expressed during embryogenesis, where it is involved in organ morphogenesis, nervous system development, and neural progenitor cell maintenance and survival. (peprotech.com)
  • Such defects are often associated with changes in cellular signal transduction pathways, such as the Ras-Raf-MEK-ERK kinase cascade, which promotes cell survival and growth. (wisc.edu)
  • Moreover, the cytotoxic effect of the developed nanodrug on the Jurkat cell line was evaluated which illustrated that survival rate in the studied cell line reaches its minimum value (100% lethality, 0.0% survival) after treatment for 48 h. (springeropen.com)
  • Overall, the BSA-Au nanozymes can be used as the nanodrug for treatment of T-type lymphoblastic leukemia via reducing the expression of anti-apoptotic genes, increasing the effect of common anticancer drugs such as Adriamycin and ara-C, and consequently increasing the survival of patients with leukemia. (springeropen.com)
  • However, alternative splicing of its Precursor mRNA results in multiple transcript variants encoding distinct FIP1L1 protein isoforms. (wikipedia.org)
  • FIP1L1 is a subunit of the cleavage and polyadenylation specificity factor subunit 1 (CPSF1) complex that polyadenylates the 3' end of precursor mRNAs (pre-mRNA) (see CPSF). (wikipedia.org)
  • mRNA microarray analyses of A549, PC14, and PC14CDDP cells that were transiently transfected with either pre-miR-197 or LNA-miR-197 and their controls. (nih.gov)
  • Analysis of MCL1 protein and mRNA expression in PCa tissue and primary cell culture specimens of luminal and basal origin, respectively, reveals higher expression in cancerous tissue compared to benign origin. (oncotarget.com)
  • In humans, an interstitial chromosomal deletion of about 800 kilobases at 4q12 deletes the CHIC2 gene (i.e.cysteine rich hydrophobic domain 2 gene) to create an in-frame fusion of the FIP1L1 gene with the platelet-derived growth factor receptor alpha gene (PGDFRA) gene. (wikipedia.org)
  • The product of PDGFRA, platelet-derived growth factor receptor alpha (PDGFRA), is a tyrosine kinase receptor of the RTK class III. (wikipedia.org)
  • FIP1L1 gene fusions between it and either the platelet-derived growth factor receptor, alpha (PGDFRA) or Retinoic acid receptor alpha (RARA) genes are causes of certain human diseases associated with pathologically increased levels of blood eosinophils and/or Leukemias. (wikipedia.org)
  • The PDGFRA gene provides instructions for making a receptor protein that is found in the cell membrane of certain cell types. (medlineplus.gov)
  • During normal thymic development, T cells mature via cell surface expression of the T-cell receptor (TCR) and positive selection of thymocytes that bind self-peptide/MHC complexes with low affinity. (aacrjournals.org)
  • First identified during PCR-based cloning of a human neuroblastoma cell line in search of tyrosine kinases similar to tropomyosin-receptor-kinase (Trk) neurotropic receptors, ROR1, along with the related receptor tyrosine kinase (RTK) ROR2, was catalogued as an "orphan" receptor due to the fact its related ligand remained elusive. (peprotech.com)
  • In turn, MM cells-derived RANKL causes the upregulation of its receptor, RANK, and Notch2 in pre-osteoclasts. (oncotarget.com)
  • The binding of a growth factor brings the multiple monomeric receptor chains into close proximity resulting into the trans-phosphorylation of their cytoplamic domains, which consequently activates downstream signaling cascades. (openrheumatologyjournal.com)
  • Altogether, our results suggest that MCL1 is a key molecule deciding over the fate of PCa cells upon inactivation of androgen receptor signaling. (oncotarget.com)
  • Fms-related tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase expresses on hematopoietic cells. (cancer-research-network.com)
  • KIT receptors belong to the Class III receptor tyrosine kinase (RTK) family, which also includes PDGFRA (platelet-derived growth factor receptor A) and CSF1R (colony stimulating factor 1 receptor). (cancer-research-network.com)
  • FIP1L1-PDGFRA fusion genes have been detected in the eosinophils, neutrophils, mast cells, monocytes, T lymphocytes, and B lymphocytes involved in hematological malignancies. (wikipedia.org)
  • characterized by an elevated number of cells called eosinophils in the blood. (medlineplus.gov)
  • Although tumor-promoting functions have been attributed to other granulocytes, like eosinophils ( 17 ), basophils ( 18 ) and mast cells ( 19 ), further research is required to fully elucidate their role in cancer, as antitumoral roles have also been described ( 20 , 21 ). (frontiersin.org)
  • TCR stimulation via antigen/MHC presentation or anti-CD3 mAb induces T-ALL cell death. (aacrjournals.org)
  • Chimeric antigen receptors (CAR) recognize specific proteins on the surface of tumor cells. (msdmanuals.com)
  • Although the efficacy of adoptive transfer of tumor infiltrating lymphocytes (TILs) was examined over several decades, genetically engineered T cells expressing chimeric antigen receptors (CARs) rapidly replaced the application of TILs due to their high specificity, non-MHC-restricted recognition of tumor antigen, superior potency, and improved in vivo persistency [ 9 , 13 , 14 ]. (biomedcentral.com)
  • However, these immunotherapeutic approaches are hampered by the tumor-promoting nature of myeloid cells, including monocytes, macrophages, and neutrophils. (frontiersin.org)
  • Despite the arsenal of defense strategies against foreign invaders, myeloid cells succumb to the instructions of an established tumor. (frontiersin.org)
  • Interestingly, the most primordial defense responses employed by myeloid cells against pathogens, such as complement activation, antibody-dependent cell cytotoxicity and phagocytosis, actually seem to favor cancer progression. (frontiersin.org)
  • In this review, we discuss how rudimentary defense mechanisms deployed by myeloid cells can promote tumor progression. (frontiersin.org)
  • Nevertheless, the majority of scientific discoveries points toward a more tumor-supporting role for myeloid cells in the TME. (frontiersin.org)
  • The innate immune response by myeloid cells occurs as a succession of events starting at signaling through cytosolic or surface PRRs, followed by effector responses including the release of cytokines, reactive oxygen species (ROS), reactive nitrogen species (RNS), antibacterial peptides and degranulation ( Figure 1 ). (frontiersin.org)
  • PRR on myeloid cells can be triggered by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs), but also indirectly by secondary mechanisms such as complement activation and circulating antibodies (Abs), resulting in cytolytic and phagocytic effector mechanisms. (frontiersin.org)
  • New abnormal growth of tissue. (lookformedical.com)
  • Two or more abnormal growths of tissue occurring simultaneously and presumed to be of separate origin. (lookformedical.com)
  • Abnormal growths of tissue that follow a previous neoplasm but are not metastases of the latter. (lookformedical.com)
  • Complete morphologic, immunologic, and genetic examination of the leukemic cells is necessary to establish the diagnosis of ALL. (medscape.com)
  • Lack of asparagine synthetase activity results in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine. (medscape.com)
  • Selective killing of leukemic cells it thought to be due to depletion of plasma asparagine, the amino acid required for protein synthesis. (medscape.com)
  • 90% leukemic cells. (aacrjournals.org)
  • In his mid career, as a Leukemia & Lymphoma Society Scholar in Clinical Research, he translated laboratory research discoveries into investigator-initiated clinical trials. (ufl.edu)
  • Leukemia Society of America, Clinical Scholar Award. (rochester.edu)
  • Clinical trials of LAK cells in humans are ongoing but this approach has not gained widespread use and is generally considered less effective than other cell therapies. (msdmanuals.com)
  • OBJECTIVES: To describe the morphologic characteristics of skin lesions, extent of extracutaneous disease, and outcomes in patients with neonatal presentation of Langerhans cell histiocytosis (LCH), and to examine clinical predictors of disease prognosis. (thedoctorsdoctor.com)
  • Primary interests include clinical trials design and the design and analysis of biomarker and imaging studies especially in the areas of GI cancer, lymphoma, melanoma, transplant and cancer immunotherapy. (dukecancerinstitute.org)
  • Multiple myeloma (MM) is a malignant plasma cell (PC) disorder accounting for approximately 10% of all hematological cancers. (oncotarget.com)
  • FIP1L1-PDGFRA fusion proteins retain PDGFRA-related Tyrosine kinase activity but, unlike PDGFRA, their tyrosine kinase is constitutive, i.e. continuously active: the fusion proteins lack the intact protein's 3'-end that includes its juxtamembrane domain which normally blocks tyrosine kinase activity unless PDGFRA is bound to its activating ligand, platelet-derived growth factor. (wikipedia.org)
  • Single-cell profiling of transcriptome and histone modifications with EpiDamID. (axonmedchem.com)
  • IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression. (harvard.edu)
  • Results: Multivariate analysis revealed controlling nutritional status (CONUT) score could independently predict OS (HR 10.247, P=0.001) and PFS (HR 5.587, P=0.001) in addition to prognostic index of natural killer lymphoma plus EBV (PINK-E). Herein, a reformative model, CONUT-PINK-E, was developed and further verified in external validation cohort. (bvsalud.org)
  • In this study, we reported that sterile alpha motif and HD domain-containing protein 1 (SAMHD1) deficiency induced STING expression and inhibited tumor growth in DLBCL. (bvsalud.org)
  • Concomitant use of interferon enhances the expression of major histocompatibility complex (MHC) antigens and TAAs on tumor cells, thereby augmenting the killing of tumor cells by the infused effector cells. (msdmanuals.com)
  • Here we present evidences that MM can efficiently drive osteoclastogenesis by contemporaneously activating Notch signaling on tumor cells and osteoclasts through the aberrant expression of Notch ligands belonging to the Jagged family. (oncotarget.com)
  • Finally, MM cells through Jagged ligands expression can also activate Notch signaling in pre-osteoclast by direct contact. (oncotarget.com)
  • The tumor cells are clonal and characterized by an increased expression of several cellular oncogenes. (biomedcentral.com)
  • Expression of B cell-stimulatory cytokines IL-1β, IL-6, IL-10, IL-12 p40 , IL-13 and TNFα and HIV proteins p17, gp120 and nef were elevated in the Tg mice with lymphoma. (biomedcentral.com)
  • Increased expression of HIV proteins and the B-cell stimulatory factors is consistent with the interpretation that one or more of these factors play a role in lymphoma development. (biomedcentral.com)
  • Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form. (nih.gov)
  • Using PCa cellular models in vitro and in vivo we show that MCL1 expression is upregulated in androgen-deprived PCa cells. (oncotarget.com)
  • The effect of BSA-Au nanozymes on the Bcl-2 expression and survivin in the Jurkat cell line was checked. (springeropen.com)
  • The results showed that the expression of anti-apoptotic genes was significantly reduced after treatment of the Jurkat cell line with the BSA-Au nanozymes (p-value of 0.001) as the potential nanodrug while their expression in the normal PBMC was not affected by the nanodrug. (springeropen.com)
  • Immune cells abundantly infiltrate tumors, creating a complex environment mediated by repetitive cycles of antitumor responses and immune evasion ( 1 ). (frontiersin.org)
  • Cell-division rates vary for different tumors. (medscape.com)
  • Here we report a phenotypic and molecular characterization of B cell tumors that develop in Tg26 mice. (biomedcentral.com)
  • As the sensor of cytosolic DNA, the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a critical role in regulating anti-tumor immunity and cell death. (bvsalud.org)
  • We also identified a set of 83 genes that were highly expressed in leukemia blasts from patients without known molecular abnormalities who subsequently relapsed following therapy. (aacrjournals.org)
  • Genetic rearrangements and point mutations affecting the PDGFRA gene are somatic mutations, which are mutations acquired during a person's lifetime that are present only in certain cells. (medlineplus.gov)
  • In addition to these basic issues concerning leukemia pathogenesis, we are devising new diagnostic procedures for detecting and monitoring leukemia patients based on molecular genetic abnormalities in the malignant cells. (stanford.edu)
  • Many innovative methods have been developed with genetic modification of cells being the most advanced cell surface engineering technique. (biomedcentral.com)
  • Although genetic modification is a powerful tool, it has a limited applicability due to the permanent modifications made on cells. (biomedcentral.com)
  • When bound by its proper ligand, Platelet-derived growth factor (PDGF), it tyrosine kinase becomes active in phosphorylating proteins that, among other functions, promote cell growth and proliferation. (wikipedia.org)
  • Growth factor cytokine receptors typically have intrinsic kinase activity. (openrheumatologyjournal.com)
  • Gene-drug level of sensitivity analyses and medication combination studies reveal synergism of BRD4 and kinase inhibition like a plausible reason behind the superior strength in cell eliminating. (antiviralbiologic.com)
  • Emerging evidence has indicated the involvement of ferroptosis in tumorigenesis through regulating various biological processes, including tumor growth, metastasis, stemness, drug resistance, and recurrence. (bvsalud.org)
  • It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. (lookformedical.com)
  • Using rat epithelial cells, they established flat colonies (2D) in which the cells grow around a silicone insert, subsequently removed to mimic an open lesion. (regenerativemedicine.net)
  • In addition, mtDNA stress in TFAM-deficient mouse melanoma cells produces tumours that are more resistant to doxorubicin in vivo. (regenerativemedicine.net)
  • Another myeloid population in the tumor microenvironment (TME) are DCs, that originate from different precursors and display various phenotypes, ranging from immunosuppressive monocyte-derived DCs (Mo-DCs) to immunocompetent cDC1 and cDC2 subsets ( 22 ). (frontiersin.org)
  • In vitro , MET overexpression activated ERK signaling and rendered BRAF-mutant colorectal cancer cells resistant to vemurafenib and panitumumab, and sensitivity was restored by treatment with the MET inhibitor crizotinib. (aacrjournals.org)
  • Animal studies have shown that LAK cells are more effective against cancer cells than are the original endogenous T cells, presumably because of their greater number. (msdmanuals.com)
  • Therefore CAR T cells and TCR T cells may represent complementary approaches to cancer therapy. (msdmanuals.com)
  • CAR T cell immunotherapy for human cancer. (msdmanuals.com)
  • Over the past decade, cancer immunotherapy has been steering immune responses toward cancer cell eradication. (frontiersin.org)
  • Myeloid innate immune cells, such as granulocytes, monocytes, macrophages and dendritic cells (DCs), play an important role in cancer-cell recognition, initiation of inflammation and antitumor responses ( 2 ). (frontiersin.org)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • The integrated stress response is a signaling pathway activated in cancer cells in response to both dysregulated growth and metabolism, and also following exposure to many therapies that appears one such targetable pathway for improved treatment of these diseases. (biomedcentral.com)
  • Targeted therapies exploit molecular vulnerabilities unique to cancer cells and typically alter cellular signaling pathways to inhibit tumorigenic growth and promote cell death. (biomedcentral.com)
  • Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. (medscape.com)
  • We are studying the role that normal chromatin structure plays in gene regulation in hematopoietic cells and how its disruption leads to altered development and cancer. (stanford.edu)
  • Cell-based therapy has expanded its influence in cancer immunotherapy, regenerative medicine, and tissue engineering. (biomedcentral.com)
  • Unfortunately, these breakthrough discoveries in both regenerative medicine and cancer immunotherapy using cells as therapeutic reagents soon faced a common problem: the inability to control cellular functions to maximize the therapeutic benefits. (biomedcentral.com)
  • The developmental story of cell-based cancer immunotherapy is not so different from MSCs in regenerative medicine. (biomedcentral.com)
  • It has an archaic metabolism similar to yeast, growing rapidly in low oxygen environments, and making only two ATP energy molecules from a molecule of sugar, then throwing off waste which creates a moat of toxicity and protects the cancer cells from the body's defenses. (dunphynunley.com)
  • This is an oxygen-based, highly efficient process, unlike cancer cell metabolism. (dunphynunley.com)
  • Cancer cells thrive where other cells suffer. (dunphynunley.com)
  • In cultured primary fibroblasts and cancer cells, the chemotherapeutic drug doxorubicin causes mtDNA damage and release, which leads to cGAS STING dependent ISG activation. (regenerativemedicine.net)
  • Patrycja Paruch, professor in the Department of Quantum Matter Physics at the UNIGE Faculty of Science, explains: "For cancer tumor invasion, or in the event of a wound, cell front proliferation is crucial, but the speed and morphology of the front is highly variable. (regenerativemedicine.net)
  • Therefore, we propose that damage to and subsequent release of mtDNA elicits a protective signalling response that enhances nDNA repair in cells and tissues, suggesting that mtDNA is a genotoxic stress sentinel. (regenerativemedicine.net)
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation. (stanford.edu)
  • Ferroptosis is a recently recognized form of cell death with distinct features in terms of morphology, biochemistry, and molecular mechanisms. (bvsalud.org)
  • Molecular Cell , 82 (1), 190-208. (axonmedchem.com)
  • Molecular cell, 82(1), 106-122. (axonmedchem.com)
  • Here we describe the phenotypic and molecular characteristics of the B cell leukemia/lymphoma in the Tg mice. (biomedcentral.com)
  • Our studies integrate molecular genetics, genomics, biochemistry and cell biology to address fundamental questions in virus replication and virus-cell interactions. (wisc.edu)
  • OBJECTIVE: The etiology and pathogenesis of Langerhans cell histiocytosis (LCH) remain poorly understood. (thedoctorsdoctor.com)
  • The somatic mutation occurs initially in a single cell, which continues to grow and divide, producing a group of cells with the same mutation (a clonal population). (medlineplus.gov)
  • And, AML occurs as the result of mutations in hematopoietic stem/progenitor cells. (cancer-research-network.com)
  • This study aimed to explore the significance of nutritional status in extranodal NK/T-cell lymphoma (ENKTL). (bvsalud.org)
  • The transformed B cell population consists of CD19 + pre-BCR + CD127 + CD43 + CD93 + precursor B cells and are clonal. (biomedcentral.com)
  • Patients can be expected to develop complications secondary to decreased production of functional white blood cells (infection), decreased numbers of red blood cells (anemia), and decreased numbers of platelets (bleeding). (medscape.com)
  • This process theoretically provides a line of T cells with greater tumor specificity than those obtained from the blood. (msdmanuals.com)
  • HN - 2008 BX - Granulosa Cells, Cumulus MH - Coronary Sinus UI - D054326 MN - A07.231.908.194.500 MS - A short vein that collects about two thirds of the venous blood from the MYOCARDIUM and drains into the RIGHT ATRIUM. (bvsalud.org)
  • Its morphology adjustments from a complicated network in procyclic cells to an individual tube-like framework in the blood stream form (12). (irjs.info)
  • At present, a European lab offers a blood test which filters and isolates circulating tumor cells (a.k.a. micrometastatic cells) from a patient's blood, genetically fingerprints them, then pharmacogenetically tests the cells for the effectiveness of various medical therapies. (dunphynunley.com)
  • This test filters circulating tumor cells from a patient's blood sample and gives a numerical probability of metastasis for colon, breast, prostate and ovarian adenocarcinomas. (dunphynunley.com)
  • Obese and diabetic topics have raised plasma degrees of nonesterified essential fatty acids (NEFAs) and hyperglycemia, that are believed to trigger reduced insulin synthesis and impaired blood sugar responsiveness in pancreatic -cells, termed glucolipotoxicity [2] also, [3]. (cgp60474.com)
  • Detection of elevated ER tension marker appearance including ATF3, Bip and CHOP in mouse islets subjected to raised lipids and high blood sugar and in -cells of type 2 diabetics supports the participation of ER tension in the pathogenesis of Type 2 diabetes [12]C[14]. (cgp60474.com)
  • First, compared with control blood cells, the methylomes of ALL cells shared 9,406 predominantly hypermethylated CpG sites, independent of cytogenetic background. (biomedcentral.com)
  • for 5 min and resuspended in CelLytic M Cell Lysis Reagent (Sigma-Aldrich) containing Halt Protease Inhibitor Cocktail and Halt Phosphatase Inhibitor Cocktail (Thermo Scientific, Waltham, MA) and 5 mM EDTA at 4 C. Proteins concentrations were established with Bio-Rad Proteins Assay Reagent (Hercules, CA) and examples had been diluted with 1/3 quantity 4X SDS test buffer and warmed at 95 C for 5 min. (antiviralbiologic.com)
  • In passive cellular immunotherapy, specific effector cells are directly infused and are not induced within the patient. (msdmanuals.com)
  • In passive cellular immunotherapy, specific effector cells. (msdmanuals.com)
  • The ISR (Fig. 1 ) is a complex signaling pathway that regulates cellular responses to stress stimuli and enables either adaptation or the instigation of cell death mechanisms [ 2 ]. (biomedcentral.com)
  • Because age-related cellular senescence and type 2 diabetes (T2D) have been recognised as risk factors for CRC development, the recent finding that type 2 diabetic patients present an elevated circulating volume of senescent cells raises the question whether type 2 diabetes facilitates the process of CRC tumorigenesis by inducing premature cell senescence. (frontiersin.org)
  • In contrast to TCR T cells, CAR T cells recognize only relatively large proteins on the surface of tumor cells. (msdmanuals.com)
  • By altering membrane transport in the early secretory pathway, TFG fusion proteins may modulate cargo export, potentially enhancing the secretion of growth factors that help to sustain a rich tumor microenvironment. (wisc.edu)
  • ATF4 activates the transcription of C/EBP homologous proteins (CHOP), considered to mediate palmitate-induced -cell loss of life [10], [11]. (cgp60474.com)