Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac involvement by metastatic neoplasms is relatively uncommon and usually occurs with widely disseminated disease. Ninety-five cases with cardiac metastases from autopsies performed over a 14-year period (1974-1987) at Loyola University Medical Center are reviewed. During this period, 3314 autopsies were performed with an average annual autopsy rate of 35%. In 806 (24.3%), a malignant disease was found, and in 95 (11.8%), there was cardiac involvement by tumor. The most common malignancies encountered in order of decreasing frequency were lung, lymphoma, breast, leukemia, stomach, melanoma, liver, and colon. Although the percentage of cardiac metastasis compares favorably with previous reports in the literature, an identical rate was present during both halves of the 14-year period studied. Improved diagnostic capabilities and treatment protocols in recent years have apparently not significantly affected the incidence, distribution, or patterns of metastatic spread to the heart.
Am J Cardiovasc Pathol 1990
PMID:Neoplasms metastatic to the heart: review of 3314 consecutive autopsies. 209 26

Informed consent for blood transfusion has become a necessity in light of the known risks associated with this service. All transfusion services should institute written informed consent that clearly defines the patient's options, including the use of homologous blood, autologous blood, and directed donations. The risk of transfusion with an infectious blood product is dependent on the number of donors per recipient and the prevalence of undetected, contaminated blood in the tested blood supply. The chance that an adverse transfusion will occur can be calculated by use of these variables. Comparative risks can be explained to patients, thereby providing an understanding of the transfusion risk of human immunodeficiency virus, the human T-cell leukemia virus, and the agent of non-A, non-B hepatitis (hepatitis C).
J Thorac Cardiovasc Surg 1990 Jul
PMID:Informed consent, risk, and blood transfusion. 199 54

Receptor-mediated activation of guanine nucleotide binding proteins (G-proteins) is profoundly modified by both mono- and divalent cations. Several divalent cations increase the affinity of many G-protein-coupled receptors for agonists at concentrations in the millimolar range. Micromolar concentrations of Mg2+ are required for receptor-mediated activation of G-proteins. Using the formyl peptide receptor of human leukemia (HL 60) as a model system, we have recently been able to demonstrate that two independent metal binding sites are present on the receptor-G-protein complex to mediate these two effects. We propose that the site that binds divalent cations in the millimolar range is contained in an extracellular domain of the receptor, whereas the site for micromolar Mg2+ is located on the G-protein. Sodium ions decrease the agonist affinity of many G-protein-coupled receptors and modify the interaction of G-proteins with guanine nucleotides. We suggest that sodium ions elicit these effects by interacting with a unique binding site present in an intracellular domain of either the receptor or some associated protein that is different from the G-protein.
J Cardiovasc Pharmacol 1988
PMID:Regulation of G-protein-mediated signal transfer by ions. 246 73

The extremely rare case of ruptured abdominal aortic aneurysm of inflammatory nature in patient with discovered acute myelomonoblastic leukemia is presented. The difficult problems arising from these, frequently terminal diseases, are discussed.
J Cardiovasc Surg (Torino)
PMID:Ruptured inflammatory abdominal aortic aneurysm due to acute myelomonoblastic leukemia. 346 15

Human thioredoxin, which was previously recognized as adult T-cell leukemia-derived factor, has many physiologic activities, one of which is a radical scavenger effect. Its ability to reduce reperfusion injury was assessed in vivo in a canine lung transplantation model. In 19 dogs, left lung allotransplantation was performed after 100 minutes of warm ischemia. The function of the transplanted lung was assessed after clamping of the contralateral pulmonary artery. In the human thioredoxin group (n = 6), human thioredoxin 30 mg/kg was given to the recipients during reperfusion. In the N-acetylcysteine group (n = 5), N-acetylcysteine 150 mg/kg, known as a radical scavenger, was given in the same manner. In both groups, arterial oxygen tension was significantly higher than in the control group (n = 8). In the human thioredoxin group, peak inspiratory pressure was significantly lower than in the control group. Macroscopic and microscopic examinations showed an almost normal appearance of the lung tissues in the human thioredoxin and N-acetylcysteine groups, in contrast to the abnormal findings in the control group. Thus it would appear that human thioredoxin has a protective effect on transplanted lungs, as does N-acetylcysteine, and that its action may be a radical scavenger effect.
J Thorac Cardiovasc Surg 1994 Nov
PMID:Inhibition of reperfusion injury by human thioredoxin (adult T-cell leukemia-derived factor) in canine lung transplantation. 796 75

Adult T-cell leukemia-derived factor (ADF), identified in the supernatant of adult T-cell leukemia (ATL) cell culture, is a human homologue of thioredoxin and consists of 104 amino acids; it has two redox-active half-cysteine residues in an exposed active center. Human thioredoxin has many biological activities, including growth promotion, cell activation, and a catalase-like radical scavenging activity. We examined the protective effect of human thioredoxin (h-thioredoxin) against reperfusion-induced arrhythmias in an isolated rat heart model with 10-min regional ischemia followed by 30-min reperfusion. Male Wistar rats were assigned to six groups: a control, a superoxide dismutase (SOD 8 x 10(4) IU/L), and a catalase group (1 x 10(6) IU/L), and three groups treated with h-thioredoxin [approximately .01 microM (TRX-I group), approximately 0.1 microM (TRX-II group), and approximately 1 microM (TRX-III group)]. In the early reperfusion period, h-thioredoxin reduced the incidence of ventricular fibrillation (VF) to 8% in the TRX-II group (p < 0.01) from the control value of 75%. SOD and catalase reduced the incidence of VF to 43 and 33%, respectively (NS). During the entire reperfusion period, the incidence of VF in the SOD group was 79%, as compared to 83% in the control group. In the catalase and TRX-II groups, the incidence of VF was significantly reduced to 42 and 25%, respectively. These findings indicate that SOD failed to protect against the reperfusion-induced arrhythmias. h-Thioredoxin exerted a protective effect against these arrhythmias; a concentration of approximately 0.1 micro was the most effective.
J Cardiovasc Pharmacol 1996 May
PMID:Protection against reperfusion-induced arrhythmias by human thioredoxin. 885 44

The treatment of malignant mesothelioma (MM) has been challenging. Many series from larger single institutions comprise small numbers of selected patients. Positive studies tend to be published, whereas publication of negative studies is delayed, appears in obscure journals, or does not occur at all. Because of the pleural distribution of the tumor, reliable determination of response is problematic. Finally, the natural history of MM is generally short, but can be quite variable. Nevertheless, doxorubicin, cisplatin, and ifosfamide and perhaps other agents as well have modest activity. Larger phase II studies are now being done by cooperative groups accruing patients from community hospitals as well as from tertiary care centers. In the Cancer and Leukemia Group B study, the response rate in patients with measurable disease was 24% for cisplatin and either mitomycin C and doxorubicin, the highest response rates reported for a cooperative group study. Survival was slightly better for the doxorubicin combination. Studies of new drugs and biologics as well as of novel methods of drug delivery are underway.
Semin Thorac Cardiovasc Surg 1997 Oct
PMID:Chemotherapy for malignant mesothelioma. 935 53

A 54-year-old woman undergoing chemotherapy for acute myeloid leukemia developed invasive pulmonary mucormycosis in the right upper lobe at the neutropenic nadir. Amphotericin B therapy became ineffective after an abscess formed in the affected lung, and insufficient infection control compelled us to interrupt chemotherapy. The lesion was suspected of invading the anterior chest wall. After right upper lobectomy combined with the anterior chest wall resection, the chest wall defect was reconstructed using autologous free rib grafts. Successful control of the fungal infection by resection enabled us to restart chemotherapy with concomitant use of Amphotericin B. In selected cases of leukemia-associated pulmonary mucormycosis refractory to Amphotericin B therapy, aggressive surgical intervention may facilitate anti-leukemia chemotherapy and prolong survival.
Jpn J Thorac Cardiovasc Surg 2003 Apr
PMID:Pulmonary resection with chest wall removal and reconstruction for invasive pulmonary mucormycosis during antileukemia chemotherapy. 1272 89

The extrinsic hypercoagulation often resulting from sepsis could contribute to disseminated intravascular coagulation and cardiovascular complications. The effective prevention and intervention remained largely complex and unclear. In a cell model of human leukemia THP-1 monocytes following bacterial endotoxin (LPS) exposure, we show the novel anticoagulant ability of polyamino acid (polyAA) to suppress the extrinsic hypercoagulation. LPS-induced monocytic tissue factor (mTF) procoagulation was readily offset by poly-L-lysine (PLK), poly-L-arginine (PLR), or poly-L-ornithine (POR) included in single-stage clotting assays. IC50 was estimated at 0.35, 0.30, or 0.58 microM for PLR, POR, or PLK, respectively, whereas, poly-L-asparatic acid (PLD) remained ineffective. In a separate approach, inclusion of cationic polyAA in human plasma significantly prolonged prothrombin time, confirming the depressed extrinsic coagulation. In chromogenic assays dissecting the extrinsic pathway, we further determined the inhibitory site(s). PLK, PLR, or POR significantly inhibited LPS-induced FVII activation, which was consistent with the diminished FVIIa formation shown on Western blotting analysis. In contrast, polyAA did not show any additional effect on either FVIIa/FXa amidolytic activities or mTF/FVIIa-catalyzed FX activation. Nor did polyAA show any effect on FVII activation directly catalyzed by FXa. Taken together, PLK, PLR, or POR preferentially inhibited mTF-dependent FVII activation, accounting for their novel anticoagulant activities. PolyAA might present the specific antagonists to arrest the extrinsic hypercoagulation following inflammation.
J Cardiovasc Pharmacol 2003 Oct
PMID:Novel anticoagulant activity of polyamino acid offsets bacterial endotoxin-induced extrinsic hypercoagulation: downregulation of monocytic tissue factor-dependent FVII activation. 1450 32

The past 3 years have been characterized by a number of impressive advances as well as setbacks in gene therapy for genetic disease. Children with X-linked severe combined immunodeficiency disorder (SCID-X1) have shown almost complete reconstitution of their immune system after receiving retrovirally transduced autologous CD34+ hematopoietic stem cells (HSCs). However, two of 11 treated patients subsequently developed a leukemia-like disease probablydue to the undesired activation of an oncogene. Gene transfer to HSCs resulted in substantial correction of immune function and multi-lineage engraftment in two patients with adenosine deaminase (ADA)-SCID. Several Phase I clinical trials for treatment of hemophilia A and B have been initiated or completed. Partial correction of hemophilia A, albeit transient, has been reported by ex vivo gene transfer to autologous fibroblasts. Intramuscular injection of adeno-associated viral (AAV) vector to patients with severe hemophilia B resulted in evidence of Factor IX gene transfer to skeletal muscle and a separate trial based on hepatic infusion of AAV vector is ongoing. Sustained therapeutic levels of coagulation factor expression have been achieved in preclinical models using retroviral, lentiviral, AAV and high capacity adenoviral vectors. Efficient lentiviral gene transfer to HSC in murine models of beta-thalassemia and sickle cell disease demonstrated sustained phenotypic correction.
Expert Rev Cardiovasc Ther 2003 Jul
PMID:Update on gene therapy for hereditary hematological disorders. 1503 Feb 82


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