Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of simian papovavirus 40 (SV40) T-antigen following in vitro infection was studied in skin fibroblasts from patients with Down syndrome (DS) and their parents to determine whether the increased susceptibility to SV40 infection reflected the cytogenetic defect or the leukemia risk associated with this syndrome. As a group, fibroblasts from patients with DS showed elevated T-antigen expression 72 hrs after infection compared to that of a healthy control population. However, among 24 patients tested, the cell lines of only 11 showed statistically significant increases in T-antigen expression. A cell line from a patient with concurrent DS and acute myelogenous leukemia had a normal value. T-antigen expression did not correlate with the percentage of cells trisomic for chromosome 21 in 18 cell lines examined or with the number of copies of this chromosome in disomic and trisomic cell strains cloned from three mosaic patients.Collectively, cell lines from parents of trisomy 21 patients also showed increased susceptibility to SV40 infection; however, in five families tested, a consistent pattern of genetic transmission of elevated T-antigen expression from parent to offspring was not observed. Q-banding of cell lines in one family showed that elevated T-antigen expression is not a marker of parental nondisjunction. Variation in susceptibility to human interferon, an antiviral agent, did not account for variation in T-antigen levels among these cell lines. Thus, the abnormalities of T-antigen expression in DS appear independent of the hyperdiploid state and are not a sensitive indicator of cancer risk.
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PMID:SV40 T-antigen expression in cultured fibroblasts from patients with Down syndrome and their parents. 22 51

In the Tri-State Leukemia Survey, the history of diseases in 605 adult male leukemia cases 15 years and older and in 668 adult male population controls was examined. These diseases occurred at least 1 year before leukemia was diagnosed. The data were based on respondents' answers that the disease was diagnosed by a physician; the respondent was either the subject or his spouse. Of 30 diseases studied, 7 showed an excess among the patients with leukemia: infectious hepatitis, eczema, psoriasis, diabetes, arthritis and rheumatism, heart disease, and ankylosing spondylitis. Mumps had a lower reported occurrence among the cases, whereas pneumonia was less frequent in acute lymphatic cases than in population controls. Three diseases occurred significantly less in controls than in persons with specific histologic types of leukemia. Our data revealed a more frequent history of herpes zoster (shingles) in chronic lymphatic leukemia, more hives in acute chronic myeloid cases, and meningitis in acute myeloid leukemia. When we only considered the patients' responses, more of them admitted having had acne than did our controls. The remaining diseases--childhood viral diseases, infectious mononucleosis, smallpox, typhoid fever, dysentery, scarlet fever, tuberculosis, asthma, hay fever, and goiter did not occur more frequently in cases than in controls. The findings were consistent with evidence from previous laboratory and clinical studies. The increased occurrence of infectious hepatitis in our case series is consistent with the findings of other studies showing an increased frequency of Australia antigen in patients with hepatitis, leukemia, and Down's syndrome.
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PMID:Epidemiology of diseases in adult males with leukemia. 99 1

We recently began a cytogenetic and molecular study of nondisjunction in leukemic Down syndrome individuals to determine whether the mechanism by which the extra chromosome 21 originates predisposes the individual to leukemia. In the present report, we summarize our observations on 18 patients with trisomy 21 and acute or transient leukemia, including 11 patients with acute lymphocytic leukemia, three with acute myeloid leukemia, one with B-cell lymphoma, one with acute megakaryoblastic leukemia, and two with transient leukemia. Results of DNA marker studies of the parental origin of the extra chromosome 21 indicated that 16 of the 18 cases (89%) were maternally derived, a percentage similar to that seen among nonleukemic Down syndrome patients. We noted that most leukemic Down syndrome patients had one locus or more in which parental heterozygosity was maintained in the trisomic individual, indicating a meiotic rather than a mitotic origin for the trisomy.
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PMID:Characterization and molecular analysis of nondisjunction in 18 cases of trisomy 21 and leukemia. 138 63

The treatment of acute myeloid leukemia (AML) in children with Down's syndrome (DS) has engendered considerable controversy. Because of the concerns for toxicity and increased rate of infections, treatment approaches varied considerably in the past with mixed results. However, experience on the recently completed Pediatric Oncology Group (POG) 8498 AML study suggests that DS children with AML constitute a distinct subgroup that responds well to therapy. Twelve of 285 children on POG 8498 (protocol for newly diagnosed AML) had DS. Children with DS and AML were predominantly male (9 of 12) and were quite younger at diagnosis (< 24 months in 10). The white blood cell count was less than 50 x 10(3)/microL in all 12 and French-American-British types M6 and M7 were frequent (5 of 12). An abnormal cytogenetic marker, in addition to constitutional trisomy 21, was present in 9 of 12 and involved chromosome 8 in 4 of 9. All cases studied (n = 5) were positive for myeloid cell surface markers (CD33, CD13, or CD11b) and, interestingly, were also positive for the CD7 antigen. Chemotherapy included daunorubicin, cytarabine (Ara-C), and 6-thioguanine for remission induction and featured high-dose Ara-C (3 g/m2 per dose) with or without L-asparaginase early in remission. Compared with children without DS, children with DS had a superior event-free survival (EFS at 4 years 100% v 28% +/- 6.2%; P = .003). The EFS remained superior even when compared with non-DS children less than 2 years of age with a white blood cell count less than 10 x 100,000/microL (100% v 48% +/- 17.3%; P = .01).
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PMID:Acute myeloid leukemia (AML) in Down's syndrome is highly responsive to chemotherapy: experience on Pediatric Oncology Group AML Study 8498. 849 50

A 13-year-old boy with Down syndrome (DS) had a brainstem glioma confirmed at autopsy, 10 years after receiving prophylactic cranial irradiation for acute myeloblastic leukemia. There is no clear association of brain tumors with DS; despite a reported link between leukemia and glioma, a causal association with radiation therapy is more likely.
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PMID:Brainstem glioma after radiation therapy for acute myeloblastic leukemia in a child with Down syndrome. Possible pathogenetic mechanisms. 138 83

We report two cases of acute myeloid leukemia with deletion of the long arm of chromosome 9 [del(9q)] and trisomy 21. del(9q) and +21 do not often occur as a sole karyotypic abnormality in acute myeloid leukemia (AML). Their concomitant presence is rare; the significance of the findings in leukemia is discussed.
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PMID:Concomitant presence of trisomy 21 and del(9q) in acute myeloid leukemia. 145 56

Generally, malignant hematologic disorders have been believed to be of monoclonal origin. However, cytogenetically unrelated clones have been reported in some disorders including one case of acute leukemia (AL), one of acute lymphoblastic leukemia (ALL), one of acute myeloblastic leukemia (AMMoL), and five of myelodysplastic syndromes (MDS). The most frequent chromosome abnormality was trisomy 8 (75%), followed by trisomy 21 (37.5%, including tetrasomy 21) and trisomy 11 (25%). Two patients showed both trisomy 8 and 11, one also had trisomy 21 (triclonal). One patient showed two cytogenetically distinctive clones in which one was 47,XY,+8, related to myeloid cells, and the other had a del(6q) and del(9p), suggesting lymphoid cells. One patient we report and 5 from the literature had two unrelated clones with trisomy 8 and deletion of the long arm of chromosome 5 (5q-); all had MDS. Review of our records showed that 11 patients with both trisomy 8 and 5q- in the same abnormal karyotype (not biclonal) had AL, i.e., 10 of acute nonlymphocytic leukemia (ANNL) and one of chronic myelogenous leukemia (CML) in blastic crisis. These findings suggest that cytogenetically unrelated clones may indicate hematopoietic biclonality.
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PMID:Cytogenetic biclonality in malignant hematologic disorders. 152 Dec 30

During a 6-year period we received bone marrow (BM) and peripheral blood (PB) samples from 178 patients with acute myeloid leukemia (AML). All patient BM, and occasionally, PB samples were characterized according to FAB criteria, and by immunophenotyping (IP) and cytogenetics (CG). This report summarizes the findings in the 125 patients who were older than 15 years. Their mean and median ages were 39.4 and 37.0 years. There were 8 (6.4%) M1, 27 (21.6%) M2, 15 (12.0%) M3, 49 (39.2%) M4, 14 (11.2%) M5A, 9 (7.2%) M5B and 2 (1.6%) M6. IP showed that HLA-DR was most strongly and frequently expressed by M1 blasts (53.5%, 86%) and least strongly and frequently expressed by M3 blasts (4.5%, 0%). HLA-DR was also relatively strongly expressed by M4, M5A, M5B (21.5%, 43%; 34.9%, 69%; and 19.2%, 56%, respectively). CD11b was uniformly weakly expressed by all FAB subgroups. CD13 was most strongly and frequently expressed by M4 (20%, 43%), and was relatively weakly and infrequently expressed by the other FAB subtypes (9.5%, 9.2%, 16.4%, 8.4%, 16.3%). CD14 was moderately expressed by M4 (15.2%, 25%) and M5B (14.0%, 22%) and M1 (7.0%, 40%). CD33 was most strongly expressed by M3 blasts (26.3% and 61%), and was most weakly expressed by M5B (10.6% and 22%). Fourteen (11.2%) patients had blasts that showed lymphoid antigens (5 T, 5 B, 5 CALLA) in addition to myeloid characteristics. Fifty-four (51.9%) of 104 patients tested had one or more karyotypic abnormalities, the most frequent of which was 8+. Only the t(15:17) was specific, and was seen in M3. Four patients with anomalous IP had trisomy 21, one of whom also had 11q-. We conclude that Saudi Arabian AML shows FAB patterns similar to patients in the West, and that M3 patients have a characteristic IP and cytogenetic pattern. Apart from this the MIC classification failed to reveal characteristic modes.
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PMID:Morphologic immunophenotypic and cytogenetic patterns of adult acute myeloid leukemia in Saudi Arabia. 154 71

Two cases of acute myeloblastic leukemia (AML M2) associated with a deletion of chromosome 6q are described. One was a 38-year-old man with constitutional inversion of chromosome 9, and another was a 57-year-old female atomic-bomb survivor. The karyotype of these patients were 46,XY,del(6)(q12q14),inv(9)(p11q13), and 47,XX,6q-,+min, respectively. In both cases c-myb protooncogene, which is located in chromosome 6q, was neither deleted nor rearranged, and c-myb messenger RNA level was not elevated. These results suggest that c-myb is not involved in the leukemogenesis of AML with 6q- as well as lymphoid malignancies with 6q-. Out of 23 AML cases with 6q- reviewed, 6 cases had erythroleukemia, and 4 developed in Down syndrome patients.
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PMID:Deletion of chromosome 6q in two cases of acute myeloblastic leukemia and a review of the literature. 155 Oct 86

This is a review of preleukaemic states in children. In a prospective series of 109 children with AML the overt disease was preceded by MDS in 22 cases. Ten of these patients had Down's syndrome. Advanced FAB groups were represented in the series. An important subgroup is the bone marrow monosomy 7 syndrome. Cytogenetic anomalies are common in MDS, and multiple and complicated abnormalities develop in nearly all patients with progressing disease. Some children die before transformation to overt ANLL. Transformation usually occurs, few children survive. With cytostatic treatment the risk of irreversible aplasia is great. The choice of schedule should therefore be carefully considered. Bone marrow transplantation has proved beneficial in a number of cases, but these are still quite few. The dysfunction of the bone marrow preceding ALL is due to transient aplastic anaemia--spontaneous remission--overt ALL, often FAB type L1, immunophenotype CALLA. The ALL reacts to the same treatment as de novo ALL of the same type and the prognosis is the same.
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PMID:Bone marrow dysfunctions preceding acute leukemia in children: a clinical study. 173 77


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