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)

A retrospective review of HLA antibody testing and transfusion records of 100 cancer patients who required extensive platelet support revealed that 27 of 100 patients exhibited positive HLA antibody tests; only 13 remained positive on repetitive examination, while 88% of aplastic anemia patients so tested were positive. Sixty-five patients with leukemia, 16 with Ewing's sarcoma, and 19 with recurrent undifferentiated lymphoma were studied. Each patient received at least 10 U of platelets (mean of 72). HLA antibodies were detected in 31% (20/65) of the leukemias, 12% (2/16) of the Ewing's, and 26% (5/19) of the lymphoma patients. Fourteen of the 27 patients who developed antibodies became antibody negative again within 2 mo and remained so. There were no significant differences in quantity of platelet transfusions between antibody-negative patients and alloimmunized patients. A smaller group (n = 8) of aplastic anemia patients followed at the NCl exhibited a frequency of alloimmunization of 88% (7/8) after a mean of 44 U of platelets were transfused. Granulocyte transfusions given therapeutically for granulocytopenia and documented infection did not appear to influence HLA antibody formation. These data indicate that significant immunosuppression occurs in intensively treated cancer patients, as measured by their ability to from antibodies to HLA antigens expressed on the surface of transfused platelets.
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PMID:Suppression of transfusion-related alloimmunization in intensively treated cancer patients. 723 86

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

Fli-1, an ets related gene, was found to be rearranged in 75% of erythroleukemias induced by Friend murine leukemia virus. We have shown previously that the Fli-1 gene codes for a sequence specific transcriptional activator which contains two autonomous transcriptional activation domains, one at the amino terminal region and the other at the carboxy terminal region. Recently human Fli-1 gene was shown to be involved in Ewing's sarcoma and related subtypes of primitive neuroectodermal tumors which share t(11;22) (q24;q12) chromosome translocation. In these tumors the carboxyl terminal region of Fli-1 was found to be fused with the amino terminal region of a putative RNA binding protein, EWS. Because part of the amino terminal transcriptional activation domain of Fli-1 was replaced with the amino terminal domain of the EWS (NTD-EWS) which shares homology with RNA polymerase II, it was speculated that NTD-EWS may interfere with RNA pol II function. Alternatively, NTD-EWS could also contribute to the transcriptional activation function of EWS/Fli-1 chimeric protein by providing either a modulatory/regulatory domain or a novel transcriptional activation domain. Here we show that EWS/Fli-1 chimeric protein functions as a transcriptional activator. Deletion analysis reveals that the EWS domain functions as a modulatory/regulatory domain for the transcriptional activation properties of the carboxy terminal transcriptional activation domain of EWS/Fli-1. We therefore propose that replacement of the amino terminal transcriptional activation domain of the Fli-1 protein with the regulatory domain of NTD-EWS results in the activation of the carboxy terminal transcriptional activation domain of Fli-1 which may be the molecular mechanism involved in these human tumors.
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PMID:EWS/Fli-1 chimeric protein is a transcriptional activator. 750 13

We report a novel human thymocyte differentiation antigen ICT-1 with a molecular weight of 49 kDa that is noncovalently associated with another 12-kDa protein. The ICT-1 antigen is expressed in 50-70% of total thymocytes, but not in resting or PHA-activated peripheral blood T-cells and bone marrow cells. The thymocytes expressing ICT-1 antigen appear after the 18th week of gestation during fetal development. Since the distribution pattern of the ICT-1 antigen within thymus partly overlaps with that of the CD1 antigens, we investigated whether ICT-1 was one of the CD1 antigen family. However, the failure of anti-ICT-1 antibody to react with mouse L cells transfected with cDNA of CD1a, -b, and -c and the different histologic distribution patterns from that of CD1d strongly suggest that the anti-ICT-1 antibody recognizes an antigen distinct from CD1. Furthermore, ICT-1 is also expressed in human neuroglial cells such as oligodendroglioma, glioblastoma multiforme, Ewing's sarcoma, and cerebellar astrocyte. Hence we believe that the ICT-1 antigen may be a novel thymus-leukemia (TL) antigen or a nonclassical MHC class I antigen.
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PMID:A novel T-cell differentiation antigen expressed in immature human thymocytes and neuroglial cells. 754 48

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

In a group of 10 patients (six with acute lymphatic leukaemia, one patient with Ewing's sarcoma, one patient with lung cancer, one patient with a myeloma and one patient with Hodgkin's lymphogranuloma) treatment with leucocytic growth factors (Neupogen Hoffman La Roche) was started only after the onset of leukopenia. Even after this mode of administration of leucocytic growth factors septic conditions in leukopenic patients were more easily controlled and it was thus possible to complete chemotherapy with planned doses in the planned time interval. In five patients with acute lymphatic leukaemia the leucocytic growth factors participated in the achievement of remission, in patients with myeloma and lymphogranuloma they contributed to marked improvement of the general condition and reduction of the time spent in hospital.
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PMID:[Leukocyte growth factors in patients with neoplasms]. 769 71

RFLP typing of members of a neurofibromatosis type 2 (NF2) family suggested that affected individuals were hemizygous at the neurofilament heavy chain (NEFH) locus, possibly as a result of a disease-associated deletion. Conventional karyotyping revealed no evidence for a deletion and all or a majority of the affected family members were heterozygous for closely linked markers which mapped proximal to the NEFH locus (D22S1 and D22S56) and for the distal marker D22S32. FISH analysis confirmed a disease-associated germinal deletion on 22q which encompassed the NEFH locus, which is known to be very closely linked to NF2, but did not extend as far as the proximal Ewing sarcoma region or the distal leukaemia factor (LIF) locus. PFGE analysis with a LIF cosmid subclone identified patient-specific NotI and MluI fragments and suggested that the deletion is about 700 kb in length. Although this large deletion could be expected to eliminate a considerable fraction, and possibly all of the NF2 gene, the resulting phenotype is the mild, so-called Gardner subtype of NF2. The deletion should provide a useful mapping resource for characterising the chromosomal region containing the NF2 locus.
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PMID:A disease-associated germline deletion maps the type 2 neurofibromatosis (NF2) gene between the Ewing sarcoma region and the leukaemia inhibitory factor locus. 810 69

High-molecular-mass alkaline phosphatase (H-Mr AP) was detected in sera from children with solid tumors without liver metastases. H-Mr AP activities were determined by a liquid chromatographic and an electrophoretic method. In 5 out of 10 cases with solid tumors--Ewing sarcoma (n = 2), neuroblastoma (n = 2), and rhabdoid tumor (n = 1)--H-Mr AP activities ranged from 3.1-40.4 U/L and 3.1-16% of total serum AP activity. In sera of patients with leukemia (n = 18) H-Mr AP was not detectable. After the treatment of the sera with papain and phosphatidylinositol-specific phospholipase C, which release membrane-associated AP from membrane particles, H-Mr AP was no longer detectable. These results indicate that H-Mr AP in the sera of patients with solid tumors may derive from increasing cell shedding of the tumor cells with elevated levels of membrane fragments in serum, which is a well known phenomenon in liver tumors. H-Mr AP was not more detectable in the serum after successful tumor treatment. These data suggest that H-Mr AP was produced by the tumors and that this parameter may be a serological marker for some solid tumors even in the presence of normal total AP serum activity.
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PMID:High-molecular-mass or macromolecular alkaline phosphatase in sera of children with solid tumors. 815 5

From 1976 to 1989 the authors treated 21 infants and children with malignant tumors of the chest wall. Fifteen were classified as Askin's tumors or Ewing's sarcoma, which we now consider as a single entity of primitive neuroectodermal origin. They are infrequent but highly aggressive tumors that involve the chest wall in children. Five patients presented with metastatic disease; despite chemotherapy and radiotherapy, all succumbed to progressive disease. Ten patients with localized disease received combined modality therapy including surgical resection (three after initial chemotherapy), radiotherapy, and chemotherapy. Surgery involved resection of the mass and up to three ribs, with prosthetic mesh reconstruction in one patient. Six of the 10 patients with localized disease are continuously disease-free 3.5 to 9 years (median, 5 years) following diagnosis. No patient had local recurrence. Of the four whose treatment failed, one died (free of disease) from complications after resection of an extensive primary tumor. In the second patient, acute monocytic leukemia developed shortly after relapse in a distant bone site. The patient died during induction for the leukemia. In the other two patients, hilar and carinal lymph node relapse occurred 68 and 80 months after initial treatment. One of the patients is considered in second remission (now 105 months later) after further chemotherapy (Adria-VAC) and radiation; the other succumbed to secondary relapse 17 months after second remission was achieved through chemotherapy, radiation, and surgery. Initial percutaneous needle biopsy of the large lesions has provided adequate material for histological, immunohistochemical, cytogenetic and ultrastructural diagnosis, and permitted initial chemotherapy before proceeding to surgical resection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant small round cell tumor (Ewing's-PNET) of the chest wall in children. 817 88

A highly informative dinucleotide repeat polymorphism has been identified at the D11S614 locus on chromosome 11q23. Ten different alleles have been observed at this locus, and the heterozygosity frequency is approximately 85%. Physical localization of this marker in a panel of somatic cell hybrids containing chromosome 11 translocations showed that it maps to 11q23.3, within the interval between the recurrent t(4;11) leukaemia breakpoint and the t(11;22) Ewing's sarcoma breakpoint. This physical mapping data is consistent with the genetic mapping which indicates tight linkage to other markers in the q23.3 region including PBGD, CD3D and D11S29. Regional localization of highly informative markers such as D11S614 will facilitate integration of the genetic and physical maps.
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PMID:Identification and regional localization of a highly polymorphic dinucleotide repeat D11S614 to the interval in 11q23.3 flanked by recurrent translocation breakpoints. 817 90


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