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)

Bone marrow transplantation, used in the treatment of cancer, aplastic anemia, and metabolic diseases, involves the use of potentially neurotoxic agents to suppress immunity and eradicate malignancy. Fifty-seven patients with a median age of 11 years (age range, 6 months to 24 years) underwent bone marrow transplantation at the Children's Hospital of Philadelphia. Fifty-nine percent developed neurological abnormalities. Twenty-six patients (46%) had central nervous system (CNS) dysfunction, including infection (8), cerebrovascular accident (5), CNS leukemia (7), metabolic encephalopathy (5), and paraparesis with CNS toxoplasmosis (1). Neuropsychological dysfunction was present in 4 of 5 long-term survivors who were tested. Fourteen of 19 patients (74%) on whom postmortem examination was performed were found to have CNS abnormalities, including cerebral atrophy (10), focal cerebral injury (6), leukemia (5), and infection (3). Fourteen patients (24%) had peripheral nervous system dysfunction. CNS dysfunction was more common in patients with lymphoreticular malignancies. Cerebrovascular accidents (in patients with lymphoreticular malignancies) and infections (in our general population and in patients with lymphoreticular malignancies) occurred more often in our patients than in patients with similar illnesses who did not undergo bone marrow transplantation. The combination of prior treatment and preparative therapy for bone marrow transplantation predisposes patients to neurological and neuropsychological sequelae.
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PMID:Neurological complications of bone marrow transplantation in childhood. 639 64

Hemorrhagic infarction of the basal ganglia was observed in 2 young adult patients with acute leukemia who presented with progressive hemiparesis combined with severe mental alterations. In case 1 (AML) lethal infarction due to thrombosis of both internal cerebral veins occurred during induction therapy for relapsed leukemia; in case 2 (cALL) a devastating stroke probably due to deep cerebral venous thrombosis happened during the third remission. Neither of them had hyperleukocytosis, signs of infection, disseminated intravascular coagulation or CNS leukemia. We discuss long-term glucocorticoid therapy (case 1) and combined prophylactic CNS treatment (case 2) as possible risk factors for cerebrovascular thrombosis in acute leukemia.
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PMID:Hemorrhagic infarction of the basal ganglia. An unusual complication of acute leukemia. 664 5

The temporal bones of a 2-year-old child who had drowned were examined histopathologically. The abnormalities were limited to the submucosa and lumen of the tympanomastoid space. Abnormalities included severe edema, vascular congestion, and focal ecchymosis without inflammation in the submucosa and hemorrhage into the tympanomastoid air space. To determine the incidence of tympanomastoid hemorrhage in autopsy material, 258 temporal bones were reviewed, and 11 were found to have free blood in the tympanomastoid space. When specimens from victims of skull fractures, cerebrovascular accidents, and leukemia were excluded from the 11, the only specimen remaining was found to be that from a drowning victim. Tympanomastoid hemorrhage in the absence of otitis media, head trauma, cerebrovascular accident, or a bleeding diathesis appears to be strong supporting evidence for death by drowning.
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PMID:Temporal bone pathology in drowning. 710 54

In a population based register of stroke (n = 536) compiled in Perth, Western Australia during an 18 month period in 1989-90, 60 cases (11%) of primary intracerebral haemorrhage were identified among 56 persons (52% men). The mean age of these patients was 68 (range 23-93) and 46 (77%) events were first ever strokes. The crude annual incidence was 35 per 100,000, with a peak in the eighth decade, and a male predominance. Deep and lobar haemorrhages each accounted for almost one third of all cases. The clinical presentations included sudden coma (12%), headache (8%), seizures (8%), and pure sensory-motor stroke (3%). Primary intracerebral haemorrhage was the first presentation of leukaemia in two cases (both fatal) and it followed an alcoholic binge in four cases. 55% had a history of hypertension. 16 (27%) patients, half of whom had a history of hypertension, were taking antiplatelet agents, and one patient was taking warfarin. There were only two confirmed cases of amyloid angiopathy. The overall 28 day case fatality was 35%, but this varied from 100% for haemorrhages in the brainstem to 22% for those in the basal ganglionic or thalamic region. Other predictors of early death were intraventricular extension of blood, volume of haematoma, mass effect, and coma and severe paresis at onset. Although based on small numbers, these data confirm the heterogeneous nature of primary intracerebral haemorrhage, but they also suggest a different clinical spectrum of this type of stroke in the community compared with the experience of specialist neurological units.
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PMID:Spectrum of primary intracerebral haemorrhage in Perth, Western Australia, 1989-90: incidence and outcome. 805 17

Cerebrovascular disorders often complicate the clinical course of a variety of solid tumors and hematologic/lymphoreticular malignancies. In rare instances, cerebrovascular disease is the presenting sign of cancer. Cerebral hemorrhages are more common in leukemia, and infarctions are more common in lymphoma and solid tumors. The usual causes of stroke are the direct effects of tumor in the brain or adjacent structures, coagulation disorders, infection, or toxicity of antineoplastic therapy. The type of systemic cancer, the extent of systemic and central nervous system metastasis, and the type of antineoplastic treatment are the most important clues in determining the etiology of cerebrovascular disease in cancer patients. Neuroimaging studies often assist in diagnosis and disease localization. Coagulation function tests are most useful in identifying coagulopathies associated with hemorrhage.
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PMID:Cerebrovascular complications in cancer patients. 807 80

The occurrence of cancer and neurological disorders in first- and second-degree relatives of children in the United States and Canada diagnosed with brain tumor before age six was investigated. A pair-matched case-control study with 155 astrocytoma and 166 primitive neuroectodermal tumor (PNET) cases was performed. Cases were identified through the Childrens Cancer Group. Controls were selected by random-digit dialing and matched to cases on age, race, and telephone area code and exchange. Childhood cancers were more common in PNET relatives compared with the general population (standardized incidence ratio [SIR] = 2.5, 95 percent confidence interval [CI] 1.1-4.8, P = 0.02) and with control relatives (odds ratio [OR] = 3.0, CI = 0.5-30, P = 0.29). For astrocytoma, nonsignificant excesses of brain tumor, leukemia/lymphoma, and childhood cancer occurred among case relatives compared with control relatives, but not compared with the general population. Astrocytoma cases were significantly more likely than controls to have a relative with seizures (OR = 2.5, CI = 1.2-4.9, P = 0.009), especially childhood seizures (OR = 3.4, CI = 1.2-12, P = 0.02), epilepsy (OR = 3.0, CI = 0.9-13, P = 0.08), and febrile convulsions (OR = 4.5, CI = 0.9-43, P = 0.07). A family history of stroke was not a risk factor for either type of brain tumor. These results suggest that some childhood brain tumors may result from a genetic susceptibility and that some risk factors may affect childhood astrocytoma and PNET differently.
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PMID:Family history of cancer and seizures in young children with brain tumors: a report from the Childrens Cancer Group (United States and Canada). 821 78

The mechanisms of endothelial cell damage that lead to cerebral hemorrhage are not completely understood. In this study, a cloned murine retrovirus, TR1.3, that uniformly induced stroke in neonatal BALB/c mice is described. Restriction digest mapping suggests that TR1.3 is part of the Friend murine leukemia virus (FMuLV) family. However, unlike mice exposed to other FMuLVs, mice infected with TR1.3 virus developed tremors and seizures within 8 to 18 days postinoculation. This was uniformly followed by paralysis and death within 1 to 2 days. Postmortem examination of TR1.3-inoculated mice revealed edematous brain tissue with large areas of intracerebral hemorrhage. Histologic analysis revealed prominent small vessel pathology including syncytium formation of endothelial cells. Immunohistochemical analysis of frozen brain sections using double fluorescence staining demonstrated that TR1.3 virus specifically infected small vessel endothelial cells. Although infection of vessel endothelial cells was detected in several organs, only brain endothelial cells displayed viral infection associated with hemorrhage. The primary determinant of TR1.3-induced neuropathogenicity was found to reside within a 3.0-kb fragment containing the 3' end of the pol gene, the env gene, and the U3 region of the long terminal repeat. The restricted tropism and acute pathogenicity of this cloned murine retrovirus provide a model for studying virus-induced stroke and for elucidating the mechanisms involved in syncytium formation by retroviruses in vivo.
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PMID:Intracerebral hemorrhages and syncytium formation induced by endothelial cell infection with a murine leukemia virus. 839 66

The detailed mortality and morbidity statistics on smoking tend to conceal the overall impact of the habit on health. About 3 million people die each year from smoking in economically developed countries, half of them before the age of 70. Cancers of eight sites are recognized as being caused by smoking--lung cancer almost entirely and the others (upper respiratory, bladder, pancreas, oesophagus, stomach, kidney, leukaemia) to a substantial extent. Six other potentially fatal diseases are also judged to be caused by smoking: respiratory heart disease, chronic obstructive lung disease, stroke, pneumonia, aortic aneurysm and ischaemic heart disease, the most common cause of death in economically developed countries. Non-fatal diseases, such as peripheral vascular disease, cataracts, hip fracture, and periodontal disease, which cause appreciable disability, cost and inconvenience are also caused by smoking. In pregnancy, smoking increases the risk of limb reduction defects, spontaneous abortion, ectopic pregnancy, and low birth weight. While there are some diseases for which smoking shows a protective effect, the 'benefits' of these are negligible in relation to the illness and premature mortality caused by smoking. About 20% of all deaths in developed countries are caused by smoking; an enormous human cost which can be completely avoided.
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PMID:Cigarette smoking: an epidemiological overview. 874 92

Large granular lymphocyte leukemia (LGLL) is defined as clonal proliferation of LGLs in peripheral blood. The following studies were conducted to address some issues in chronic LGLL. (1) Chronic LGLL is characterized by the indolent course, and the diagnosis of leukemia is difficult in such patients as those without distinct organomegaly and/or any evidence of monoclonality. We performed immunohistological studies in a patient with persistent NK lymphocytosis. No organomegaly had been seen in the patient during a three-year-observation, who died from cerebrovascular accident. The autopsy findings revealed multi-organ infiltration including spleen, liver, bone marrow, lymph nodes and lung. These findings suggest that the cells of chronic LGLL have infiltrative capacity characteristic of malignant cells. (2) Lymphocytosis in chronic LGLL is usually stable for a long period. We found that both T- and NK-LGLL cells strongly expressed CD95, an apoptosis related protein. Anit-CD95 did not induce apoptosis, but suppressed proliferation induced by IL-2 or anti-CD3. These results suggest that CD95-CD95 ligand system is involved in the slow cell growth characteristic of chronic LGLL. (3) CD4+CD8+ double positive (DP) cases are rarely seen in LGLL, and the physiologic counterpart of the leukemic cells has not been determined yet. We found that the DP-LGLL had alpha alpha type in the CD8 subunit and did not express RAG-1, these findings being characteristic of peripheral T cells. We also found that they expressed IL-4 mRNA and secreted IL-4 on activation. These results strongly suggest that DP-T-LGLL represents an expansion of a rare subset of peripheral DP-T cells, possibly derived from IL-4 activated CD4 single positive T cells.
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PMID:[Large granular lymphocyte leukemia]. 893 81

Many long term sequelae result from previous treatment for malignancy in childhood. However, little information exists on cardiopulmonary response and energy expenditure during exercise and their possible associations with excess body fat. Measurements of body composition and exercise capacity both at low intensity and maximal aerobic capacity were made on 56 long term survivors of childhood malignancy (35 survivors of acute lymphoblastic leukaemia (ALL) and 21 survivors of other malignancies) and 32 siblings acting as controls. Female survivors of ALL had significantly greater mean (SD) body fat than survivors of other malignancies and siblings (32.5 (6.4)% v 24.3 (4.4)% and 26.3 (8.5)% respectively, p < 0.005). Energy expenditure at low intensity exercise was reduced in survivors of ALL, and negatively correlated with body fat after controlling for weight (partial r range -0.21 to -0.47, p < 0.05). Stroke volume, measured indirectly, was reduced and heart rate raised in ALL survivors at sub-maximal exercise levels. Peak oxygen consumption was significantly reduced in girls and boys treated for ALL compared with siblings (30.5 v 41.3 ml/kg/min for girls, p < 0.05 and 39.9 v 47.6 ml/kg/min for boys, p < 0.05 respectively). Reduced exercise capacity may account in part for the excess adiposity observed in long term survivors of ALL.
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PMID:Relationship between cardiopulmonary response to exercise and adiposity in survivors of childhood malignancy. 916 19


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