Search results for "Lymph"

showing 10 items of 4590 documents

Mechanisms of Autocrine and Paracrine Growth Control in Acute Myelogenous Leukemia

1990

Blast cells of a high proportion of patients with acute myelogenous leukemia (AML) proliferate in response to exogenous hematopoetic growth factors, both in vitro [9, 14, 26, 36, 48, 65] and in vivo [20]. Whereas leukemic colony-forming cells (L-CFCs) from most patients share their growth factor dependence with normal committed myeloid progenitor cells (CFU-GMs), some AML samples autonomously form colonies in agar and are therefore believed to bypass growth factor requirements [17, 42, 72]. Autocrine growth factor production has been identified as one mechanism used by AML blasts to supply various growth-promoting molecules. Moreover nontransformed accessory bone marrow cells have been show…

business.industryGrowth factormedicine.medical_treatmentmedicine.diseaseColony-stimulating factorMyelogenousLeukemiaParacrine signallingmedicine.anatomical_structureCytokinehemic and lymphatic diseasesImmunologymedicineCancer researchBone marrowAutocrine signallingbusiness
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Glofitamab (Glofit) in Combination with Polatuzumab Vedotin (Pola): Phase Ib/II Preliminary Data Support Manageable Safety and Encouraging Efficacy i…

2021

Abstract Background: Glofit is a novel, CD20xCD3 T-cell-engaging bispecific antibody that provides monovalent binding to CD3 on T cells and bivalent binding to CD20 on B cells. As monotherapy, Glofit has shown promising response rates with manageable safety in R/R B-cell non-Hodgkin lymphoma (B-NHL) patients (pts; [Carlo-Stella et al. EHA 2021]). Because of their distinct and complementary mechanism of action, there is a rationale for combining Glofit with the anti-CD79b-targeted antibody-drug conjugate, Pola. NP39488 (NCT03533283) is a Phase Ib/II, open-label, multicenter, dose-escalation (DE) and expansion study evaluating Glofit + Pola or atezolizumab in R/R B-NHL pts (Hutchings et al. A…

business.industryImmunologyRelapsed refractoryCancer researchMedicineCell BiologyHematologybusinessmedicine.diseaseBiochemistryDiffuse large B-cell lymphomaPolatuzumab vedotin
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Immune pathogenesis of hepatitis A

1992

In an effort to elucidate the mechanism of liver damage resulting from Hepatitis A virus (HAV) infection, we have studied infected skin fibroblasts and autologous lymphocytes from HAV patients. We report here that HLA-restricted virus-specific T cells play an essential role in HAV-related hepatocellular injury.

business.industryMechanism (biology)virusesfungivirus diseasesHepatitis AAutologous lymphocytebiochemical phenomena metabolism and nutritionmedicine.diseaseVirologydigestive system diseasesHepatitis a virusImmune pathogenesismedicineLiver damageHepatocellular injurybusiness
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Obstructive Malformations of the Internal Jugular Vein

2021

Obstructive malformations of the internal jugular veins represent a relatively new clinical problem, which as of yet has not been fully understood. In normal subjects, the internal jugular vein is valveless, except for a single valve, situated just above the junction of this vein with the brachiocephalic vein. Usually, normal jugular valves exhibit a two-leaflet structure. Stenotic lesions of these veins were described for the first time in 2009 in a group of multiple sclerosis patients. The most common obstructive malformation of the internal jugular vein is a stenotic valve. There are several morphological types of such aberrant valves, comprising annular stenoses, valves with fused, reve…

business.industryMultiple sclerosisCentral nervous systemAnatomymedicine.diseaseChronic cerebrospinal venous insufficiencymedicine.anatomical_structurecardiovascular systemMedicineGlymphatic systemClinical significancecardiovascular diseasesbusinessVeinInternal jugular veinBrachiocephalic vein
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Acute Myeloid Leukemia in Adults

2018

AML is a malignancy of hematopoietic immature precursors (myeloblasts) that accumulate in the BM at the expense of their normal counterparts.

business.industryMyeloid leukemiaMalignancymedicine.disease03 medical and health sciencesHaematopoiesis0302 clinical medicineText mininghemic and lymphatic diseases030220 oncology & carcinogenesisCancer researchmedicinebusinessneoplasms030215 immunology
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Preemptive Transfer of GMP-Grade CD8-Depleted Donor Lymphocytes after T-Cell Depleted Reduced-Intensity Transplantation.

2005

Abstract The combination of fludarabin (150mg/m2) / melphalan (140mg/m2) based reduced-intensity allo-transplantation (RIT) with in vivo T-cell depletion (TCD) by the anti-CD52 antibody alemtuzumab (100mg) has demonstrated efficient engraftment and reduced graft-versus-host disease (GVHD) (Kottaridis et al., Blood 2000). However, the slow lymphocyte recovery following this protocol is associated with reduced anti-infectious and antitumor immunity. In an attempt to improve immune-reconstitution after TCD / RIT, we investigated the early preemptive use of CD8-depleted donor lymphocyte infusions (DLIs). For CD8 depletion of donor leukaphereses, a new depletion protocol using clinical grade CD8…

business.industryT cellLymphocyteImmunologyCell BiologyHematologyLeukapheresismedicine.diseaseDonor LymphocytesBiochemistryTransplantationAnimal datamedicine.anatomical_structureGraft-versus-host diseaseImmunologymedicineAlemtuzumabbusinessmedicine.drugBlood
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Graft-Versus-Host Disease or Infection: Rapid Detection of HLA Mismatch-Reactive T Cells Ex Vivo Can Facilitate Diagnosis and Guide Therapy after All…

2007

Abstract Diagnosis of graft-versus-host disease (GVHD) is mainly based on clinical features and on tissue biopsies. However, clinicians and pathologists are well aware of cases, in which GVHD cannot be distinguished from infections arising from severe immunodeficiency after allogeneic stem-cell transplantation (SCT). This may pose a deep therapeutic dilemma of whether to modify immunosuppressive treatment or to use donor lymphocyte infusion (DLI) for promoting anti-microbial immunity. We observed a 68-year-old patient with myelodysplastic syndrome who developed acute GVHD grade II of skin and gut at d+16 after T-cell depleted reduced-intensity SCT (Fig. 1). GVHD was confirmed by histology a…

business.industryT cellmedicine.medical_treatmentImmunologyImmunosuppressionCell BiologyHematologyHuman leukocyte antigenmedicine.diseaseBiochemistryHLA MismatchDonor lymphocyte infusionTransplantationGraft-versus-host diseasemedicine.anatomical_structureImmunologymedicinebusinessImmunodeficiencyBlood
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T-Cell Vaccination in Patients with Nickel Allergic Contact Dermatitis

1995

business.industryT-LymphocytesT-cell vaccinationCell BiologyDermatologymedicine.diseaseImmunotherapy AdoptiveBiochemistryNickelDermatitis Allergic ContactImmunologyHumansMedicineIn patientbusinessMolecular BiologyAllergic contact dermatitisJournal of Investigative Dermatology
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Wild-type JAK2 secondary acute erythroleukemia developing after JAK2-V617F-mutated primary myelofibrosis.

2009

A 54-year-old female patient developed acute erythroleukemia after an 8-year course of primary myelofibrosis. The latter harbors the JAK2-V617F mutation and was treated with hydroxyurea and anagrelide. A bone marrow trephine biopsy disclosed 2 morphologically distinct areas of chronic primary myelofibrosis and acute erythroleukemia. Microdissection and a separate molecular pathological analysis was performed. Although the activating JAK2-V617F mutation was not maintained in blasts of acute erythroleukemia, it was detectable in the chronic phase of primary myelofibrosis, indicating that this mutation did not play a role in the leukemic transformation of erythroid cells.

business.industryWild typeHematologyGeneral MedicineAnagrelideJanus Kinase 2Middle Agedmedicine.diseaseCell Transformation NeoplasticFatal OutcomePrimary Myelofibrosishemic and lymphatic diseasesMutation (genetic algorithm)Female patientCancer researchMedicineAcute erythroleukemiaHumansFemaleLeukemia Erythroblastic AcutebusinessMyelofibrosisJAK2 V617Fmedicine.drugActa haematologica
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Hepatosplenic γδ T-cell lymphoma: complete response induced by treatment with pentostatin

2002

business.industrymedicineCancer researchPentostatinT-cell lymphomaHematologybusinessmedicine.diseaseComplete responsemedicine.drugBritish Journal of Haematology
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