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)

Among 22 neonates treated at the Children's Cancer Research Center of Philadelphia, 11 had neuroblastoma, which in two cases was widely metastatic. There were three infants with teratoma, three with sarcoma, three with leukemia, one with Wilms' tumor, and one with parotid carcinoma. Nine of eleven patients (82%) are long-term survivors following complete surgical excision of tumor, whereas only one of eight (13%) has survived following incomplete surgical excision. All three neonates with leukemia died. The overall two-year actuarial survival is 45% (10/22). The problems associated with treating neonates with chemotherapy, radiation therapy, or both are especially difficult because of the immaturity of the organs and structures. Surgical excision alone has been the treatment of choice for solid tumors. Chemotherapy or radiation therapy, when indicated, require careful monitoring for both acute toxicities and potential long-term morbidities.
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PMID:Cancer in neonates: the experience at the Children's Hospital of Philadelphia. 711 Aug 16

The incidence of childhood cancer in Queensland has been studied using the data of the population-based Queensland Childhood Malignancy Registry. During the 7-year period 1973-1979, 454 cases were registered, giving an annual age-specific incidence of 11.34/10(5) for the age group 0-14 years inclusive. There was a male/female ratio of 1.36. The commonest group of diseases was that of the leukaemias, followed by that of CNS tumours. The incidences of the various types of tumour in Queensland have been compared with those from other reported series. The incidence of leukaemia was midway between that of U.S. whites and that of Manchester, while the incidences of lymphoma and Wilms' tumour were much closer to those of the United States. Ewing's tumour was considerably commoner than osteosarcoma.
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PMID:Incidence of childhood tumours in Queensland. 731 68

Survival of some types of childhood neoplasms has improved considerably but remained poor for other types. Improvement in survival rate of common types of childhood neoplasms over the past three decades was assessed at the largest children's hospital in Japan. Using the data of the cancer registry of the hospital which recorded all the patients from 1965 to 1993, totalling 1026 cases, survival rate was analyzed for each type of neoplasm categorized by the S-classification for childhood neoplasms, a modification of the International Classification of Diseases. Survival was assessed for five 5 year periods from 1965 and a 4 year period from 1990-93. The 5 year survival rate for all neoplasms combined improved from 21.8% in the 1965-69 period to 73.3% in the 1985-89 period. Female patients' survival was better than male patients' in all periods. The improvement in survival rate was considerable for leukemia and malignant lymphoma, fairly good for neoplasms of the renal (mostly Wilms' tumor) and digestive (mostly hepatoblastoma) organs and moderate for neuroblastoma. Overall, survival rates of childhood neoplasms improved considerably. Much of this improvement was explained by a great improvement in survival rates of neoplasms of the blood which constituted the majority of patients.
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PMID:Trends in survival of childhood malignancy for the past three decades. I: Leukemia, malignant lymphoma, neuroblastoma, retinoblastoma and neoplasms of the urinary and digestive organs. The Committee for the Studies of the Treatments and the Biological Characteristics of Childhood Cancers. 757 49

This study records the disease profile and outcome of all 492 children with confirmed cancer below the age of 15 who were admitted to Tygerberg Hospital, South Africa, from 1983 to 1993. The black (48.3%), so-called coloured (30.3%) and caucasian (21.3%) children did not represent a confined geographical area. Leukaemia (22.8%), brain tumours (20.5%), lymphomas (15.2%), nephroblastomas (10%), neuroblastomas (8.5%) and retinoblastomas (5.7%) were the most common tumours. All children were treated with standard protocols and included in the Kaplan-Meier survival analyses. 14 patients were lost to follow-up. Projected survival in (acute lymphoblastic leukaemia) ALL was 63% in white children, but only 17% in black children. Survival was 65% in stage 1 and 2 Wilms' tumour, and exceeded 50% in medulloblastoma and astrocytoma. So-called African Burkitt's lymphoma occurred in all population groups. Overall, 5-year survival in Hodgkin's disease was 70%. Black and coloured children with neuroblastoma presented mainly with stage 3 and 4 disease. All 26 black and coloured children with retinoblastoma had a negative family history and advanced disease which needed enucleation.
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PMID:The Tygerberg Hospital Children's Tumour Registry 1983-1993. 757 74

The wt1 gene is located on chromosome 11p13 and encodes a zinc finger motif-containing transcription factor involved in regulation of growth and differentiation. Its expression was shown during embryonic development in various tissues as well as in a few human malignancies including acute leukemias. Using RT-PCR, we found wt1 gene expression in blast cells of the majority of 150 acute leukemia patients. Particularly, the wt1 transcript was detected in 12 of 14 (86%) pre-pre-B-ALL patients, in 33 of 41 (80%) cALL patients, in 23 of 31 (74%) T-ALL patients, and in 53 of 57 (93%) AML patients. Additionally, mononuclear cells from CML patients expressed the wt1 gene only when diagnosed with blast crisis. In contrast to acute human leukemias, mononuclear cells from reactive bone marrow (n = 4), and peripheral blood of healthy volunteers (n = 20), as well as normal peripheral CD34+ hematopoietic progenitors (n = 6) did not express the wt1 gene at detectable levels. Using the anti-WT1 MoAb 6F-H2 in an immunofluorescence assay on single cell level, we found the translated WT1 protein only in nuclei of leukemia blast cells but not in nuclei of normal CD34+ hematopoietic progenitor cells. Blast cells of 12 of 20 leukemia patients (60%) all tested positive for the wt1 gene expression by RT-PCR displayed a strong nuclear immunofluorescence. Its expression in the majority of human acute leukemias but not in normal mononuclear blood cells and normal CD34+ hematopoietic progenitors qualifies the wt1 gene transcript as a 'pan-acute leukemic' marker probably useful in monitoring minimal residual disease after chemotherapy and in detecting leukemic blast cells in purged or unpurged hematopoietic stem cell preparations intended to be used for autologous bone marrow transplantation.
Leukemia 1995 Jun
PMID:Presence of Wilms' tumor gene (wt1) transcripts and the WT1 nuclear protein in the majority of human acute leukemias. 759 70

The WT 1 gene has been isolated as a tumor suppressor gene of Wilms' tumor. Using reverse transcriptase-polymerase chain reaction (RT-PCR), relative levels of the WT 1 gene expression was examined in 87 patients with acute leukemia, 25 with chronic myelogenous leukemia (CML), and 24 with non-Hodgkin's lymphoma (NHL). Significant levels of the WT 1 gene were expressed in all leukemia patients, and for CML the levels increased as the clinical phase progressed. No point mutations were found in the WT 1 gene when samples from 15 acute leukemia patients were subjected to PCR single-strand conformation polymorphism analysis. In striking contrast to acute leukemia, the levels of WT1 gene expression for NHL were significantly low or even undetectable. The levels of WT 1 gene expression inversely correlated with the prognosis of acute leukemia. The quantification of the WT 1 gene expression made it possible to detect minimal residual disease (MRD) in acute leukemia regardless of the presence of absence of tumor-specific DNA markers. Simultaneous monitoring of MRD by RT-PCR using primers for specific DNA markers in four patients (two AML-M3 with PML/RAR-alpha, one AML-M2 with AML1/ETO, and one CML with bcr/abl) detected MRD comparable to that obtained from quantitation of WT 1 gene expression. In a patient with acute promyelocytic leukemia, the limits of leukemic cell detection by RT-PCR using either WT 1 or PML/RAR-alpha gene primers were 10(-3)-10(-4) and 10(-4) for bone marrow, and 10(-5) and 10(-4) for peripheral blood, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[WT 1 and leukemia]. 764 50

Translocations in bands 11q23.3-11q24 are associated with several human cancers, including acute lymphoid and acute myeloid leukemias (AML) and Ewing's sarcoma. We have characterized two independent deletions in this region, one derived from a patient with AML who previously had a T-cell lymphoma, and another from a Wilms' tumor patient. Cytogenetic analysis of the ML-2 cell line established from the malignant cells of the AML patient indicated that one chromosome 11 homolog had an interstitial deletion, del(11) (q23q24), and the remaining homolog was involved in a recurring translocation, t(6;11) (q27;q23). According to karyotype analysis on the Wilms' tumor patient (EH), one chromosome 11 was normal and the other carried an interstitial deletion at 11q23.3-11q25. Somatic cell hybrids segregating the EH deletion (EHR4) and the ML-2 deletion (MLR4) have been isolated. The EH deletion is distal to the MLL probe recently associated with 11q23.3 leukemia breakpoints (Ziemin-van der Poel et al.: Proc Natl Acad Sci USA 88:10735-10739, 1991). The ML-2 deletion could involve the MLL gene at a point distal to other breakpoints within MLL. Both deletions include the Ewing's sarcoma breakpoint at 11q24.1. By Southern blot analysis we identified three anonymous DNA markers (D11S272, D11S273, and D11S219) and the ETS/oncogene, which map within each deleted region. These markers are conserved based on zoo blot analysis, and they are valuable for physical mapping and genetic characterization of a region that may code for gene products associated with growth control and tumor suppression in a variety of cancers.
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PMID:Characterization of two 11q23.3-11q24 deletions and mapping of associated anonymous DNA markers. 768 55

Urine and serum samples of rats bearing three different experimental tumours (hepatocellular carcinoma, myelomonocytic leukemia and mesoblastic nephroma) were investigated for mutagenicity with the Ames Salmonella test. Enhancement of mutagenic activity in TA98 and TA100 was observed only in the case of urine samples obtained from animals bearing nephromas. Mutagenicity increased with increasing time after implantation of tumours. There was no coincidence between urinary and serum mutagenicity under the experimental conditions employed. Further studies are needed to determine the origins, and chemical and genotoxic characteristics of urinary mutagens. In addition, the question as to whether any mutagenic substances can be detected in fractions of plasma/serum should also be experimentally addressed.
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PMID:Urinary and serum mutagenicity studies with rats bearing experimental tumours. 773

Survival from cancer in childhood and adolescence was studied in a population-based series of 8312 cases in children aged 0-19 years notified to the Danish Cancer Registry during 1943-87. During the first period (1943-72), 5-year survival rates from all malignant neoplasms increased from 23% (1943-52) to 33% (1963-72). The greatest improvement was seen during the period 1973-87 when 5-year survival rates reached 64% (1983-87). Between 1973-77 and 1983-87, 5-year survival rates increased from 32% to 62% for leukaemia, from 40% to 70% for acute lymphoblastic leukaemia, from 35% to 54% for non-Hodgkin's lymphoma, from 50% to 66% for central nervous system neoplasms and from 25% to 49% for bone tumours. An improvement in 5-year survival rates from Wilms' tumour was seen between 1960 (19%) and 1980 (81%). Up to 1972, the 5-year survival rate from germ-cell neoplasms was approximately 40%; among patients diagnosed in 1983-87, 76% survived for 5-years. Annual lethality decreased by 2.5% for all malignant neoplasms in 1943-72 and by 4.4% in 1972-87. Lethality was similar for boys and girls during the period 1943-72, but was significantly lower for girls subsequently. A marked effect of age at diagnosis was seen in the early registration period, where lethality rate for the age group 0-9 years was substantially higher compared with that in the age group 10-19 years. This inequality persisted only for children less than 2 years of age at the time of diagnosis in the later period.
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PMID:Trends in survival after childhood cancer in Denmark, 1943-87: a population-based study. 778 Feb 56

The Wilms' tumor gene (wt-1) is expressed in the developing fetal kidney, gonads and in Wilms' tumors. Recently, the expression of wt-1 in leukemia-derived cell lines and cases of acute leukemias (AL) was reported. The present study was designed to investigate the potential of wt-1 as genetic marker for acute myelocytic leukemias (AML). Blast cells from 52 patients with AML, 14 patients in complete remission (CR) and four leukemic cell lines were examined for expression of wt-1 mRNA. Peripheral blood mononuclear cells (PBMNC) and bone marrow (BM) from 13 healthy persons were used as negative controls. RNA of the wt-1 gene was expressed in 41/52 (79%) patients with previously untreated AML. The majority of the 14 patients studied in CR lost wt-1 expression. In three out of the four patients in CR reappearance of wt-1 expression preceded relapse of the disease. In three of the four tested cell lines wt-1 specific transcription was demonstrated. No correlation to FAB classification, immunophenotype or response to treatment was found. Our experiments indicate wt-1 expression in the majority of AML, but not in bone marrow or PBMNC of healthy controls. Therefore, wt-1 expression may be associated with the presence of malignant blast cells and the analysis of wt-1 gene expression via PCR may be a sensitive method for the detection of leukemic blast cells.
Leukemia 1994 Dec
PMID:The expression of the Wilms' tumor gene in acute myelocytic leukemias as a possible marker for leukemic blast cells. 780 2


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