Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the phenotypes of blast cells of 53 patients with acute leukemia by a modified streptavidin-biotin alkaline phosphatase (SAB-AP) labeling technique, using a panel of monoclonal antibodies [MoAb; anti-CD11b, CD13, CD14, CD33, CD34, CD41, CD3, CD7, CD10, CD19, anti-HLA-DR, and anti-myeloperoxidase (MPO)]. The selection of an optimal fixative solution for each antigen from five options of various combinations of formalin, acetone, methanol, and/or ethanol, successfully conserved cell morphology and improved specific reaction compared with the conventional methods which used a single fixative for multiple antigens. We compared the SAB-AP results with those obtained by flow cytometry (FCM) for surface markers in each case. High concordance rates for both positive and negative results were observed for each marker. However, positive reaction for some markers (anti-CD13, CD14, CD33, and CD34) were often noted only in the cytoplasm by the SAB-AP method, indicating that combination of these two methods is essential for the precise immunophenotyping of poorly differentiated leukemia cells.
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PMID:Usefulness of immunocytochemistry for phenotypical analysis of acute leukemia; improved fixation procedure and comparative study with flow cytometry. 771 39

Two adult patients with acute leukemia developed marked jaundice during Pseudomonas aeruginosa bacteremia. The progressive increase in serum conjugated bilirubin levels was disproportionate to the gradual decrease in serum alkaline phosphatase and transaminase activity to or below low normal. The production of coagulation factors decreased. Autopsy revealed periportal cholestasis with minimal liver-cell damage. These findings suggested decreased metabolic activity of liver cells associated with bacteremia, probably leading to impaired bilirubin excretion. Both patients died despite appropriate antibiotic therapy. Isolated hyperbilirubinemia, thus, seemed to be an ominous prognostic sign in severe infection.
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PMID:Jaundice associated with Pseudomonas aeruginosa bacteremia complicating acute leukemia. 772 72

The expression of the Ig-linked mb-1 polypeptide was analyzed by immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase technique) using a specific monoclonal antibody in 165 cases of acute leukemia, with 88 being lymphoblastic (ALL) and 77 myeloid (AML). The purpose of the study was to investigate the specificity of this reagent for B-lineage cases and its reactivity on leukemias that coexpress myeloid and B-cell antigens (biphenotypic). The majority (89%) of 72 B-cell precursor ALL patients were positive. Of these, mb-1 was expressed in all 9 patients with early-B-ALL (CD10-, c mu-), in all 11 patients with pre-B-ALL (c mu+) and in the single case of B-ALL (smIgM+). Forty-three of 51 patients with common-ALL (CD10+, c mu+) were also positive. All 16 T-lineage ALL patients and 72 (93.5%) of the AML patients examined were mb-1 negative. Four of the 5 mb-1-positive AML patients were considered biphenotypic and expressed other B-cell antigens such as CD10, CD19, and/or cCD22 and all showed rearrangement of the Ig heavy chain genes. Within the AML cases, mb-1 and cCD22 were more useful than other B-cell antigens in detecting biphenotypic cases, and mb-1 showed the highest correlation with the clonal rearrangement of Ig heavy chain genes. These results indicate that mb-1 is a sensitive and specific reagent for B-lineage blasts that will aid in the classification of B-cell precursor ALL and in the identification of biphenotypic leukemia presenting as AML.
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PMID:mb-1: a new marker for B-lineage lymphoblastic leukemia. 833 49

Trisomy 13, as a sole karyotypic abnormality in acute leukemia, has been reported in several cases. However, in chronic myelogenous leukemia (CML), only two cases with this abnormality were reported so far. We describe herein a 68-year-old case with Philadelphia chromosome-negative CML and trisomy 13. Leukocytosis was pointed out during the treatment for other diseases. After 7 months, abrupt increase in leukocyte count (108,000/microliters) and splenomegaly developed. Decreased neutrophil alkaline phosphatase activity and morphological features fulfilled the diagnostic terms for CML. However, the karyotypic analysis revealed trisomy 13 instead of Philadelphia chromosome, and the BCR gene rearrangement was not detected. In cases with acute leukemia accompanied by trisomy 13, malignant transformation of an immature hematopoietic precursor cell has been suggested by the expression of antigens characteristic of both the myeloid and lymphoid lineage. In a few cases with myelodysplastic syndrome, a multipotent stem cell disorder, trisomy 13 has also been reported. From these standpoints, there might be a possibility that trisomy 13 as a sole abnormality in hematologic disorders would be related to tumorigenesis in the levels of multipotent stem cells.
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PMID:[Philadelphia chromosome-negative chronic myelogenous leukemia with trisomy 13]. 869 71

The diagnostic value of immunophenotyping (IP) as a first-line diagnostic method in diseases that infiltrate the childhood bone marrow (BM) or mimic infiltrated BM was examined. Two hundred and fifty unselected BM samples from 250 children suspected to have a malignancy infiltrating their BM were evaluated by means of IP and conventional morophological-cytochemical (MC) studies. We applied the alkaline phosphatase anti-alkaline phosphatase method for IP using a panel of monoclonal antibodies (Mabs) against leukocyte-associated antigens, neuroectodermal antigens, and intermediate filament antigens. Four cases of neuroblastoma, two cases of Ewing sarcoma, and one case of rhabdomyosarcoma were diagnosed by IP but not by MC studies. In nine cases of acute leukemia bone marrow blasts could not be ascribed to a specific lineage on the basis of blast morphology or histochemistry. Eight samples without morphological evidence of malignant infiltration revealed an increased percentage of immature B cell precursors (CD10+, TdT+) suggesting acute lymphoblastic leukemia. None of these children has developed malignant lymphoproliferative disease. Our data suggest that the immunological evaluation of BM in childhood is highly capable of discriminating between different malignant populations but it does not recognize malignancy and therefore supplements but cannot replace conventional methods for diagnosis.
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PMID:Differential diagnosis based on immunological-phenotyping in suspected malignant bone marrow involvement in childhood. 902 11

Inhibitory effects of 1,25(OH)2D3 and D3 on growth of four neoplastically derived cells were observed in human acute leukemia cell culture CEM-C-1 and CEM-C-7, human cervical carcinoma cell lines C-4-1 and human epithelioid carcinoma cells of cervix HeLa S3K. Concurrently, in dexamethasone-responsive cells C-4-1 and HeLa S3K there was a 1,25(OH)2D3 and D3 induced elevation of alkaline phosphatase with 1,25(OH)2D3 showing the greater effects. It is supposed that vitamins D3-induced alkaline phosphatase activity in malignant cells, which is proposed to be a possible marker of cell differentiation, can be associated with the membrane effects of these vitamins.
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PMID:Effect of vitamin D3 and 1,25(OH)2D3 on growth of neoplastically derived cell lines and their alkaline phosphatase activity. 958 17

The effect of alpha-tocopherol and its derivatives on viability and growth of attached cells culture: human epithelioid carcinoma of cervix HeLa-S3K and human cervical carcinoma cell line C-4-1 according to protein content and level of alkaline phosphatase, as well to unattached cells: human acute leukemia cell cultures CEM-C-1 and CEM-C-7 according to the amount of viable cells in suspension has been studied. It has been shown that alpha-tocopherol acetate and tocopherol maintain the viability of cells, while the derivatives of tocopherol with shorted side chain considerably inhibit growth of researched cultures, alpha-tocopherol with lacking side chain being most active among them.
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PMID:[Effect of alpha-tocopherol and its derivatives on the viability of cultured malignant cells]. 984 59

Detection of unusual or aberrant cell immunophenotype with flow cytometry is the basis for the immunologic recognition of minimal residual disease (MRD) in patients with acute leukemia (AL). In this study, we have shown that the double immunocytochemical alkaline phosphatase antialkaline phosphatase (APAAP) staining technique also makes possible the detection of leukemic cells with unusual (leukemic) combinations of antigens (ULCA) both at diagnosis and during follow-up of patients with ULCA+ AL. The applicability of double APAAP was analyzed on bone marrow (BM) samples obtained from 12 patients (8 with AML, 3 with ALL, and 1 with undifferentiated acute leukemia [AUL]) randomly chosen from a larger group of 22 ULCA+ patients treated at our center in a 3-year period (22% observed ULCA+ AL frequency). The percentages of ULCA+ BM cells before chemotherapy were in the range of 5%-60%, which dropped to 0%-7% in 10 patients who achieved remission (range 0%-7%, p < 0.01). However, these cells could also be found 60 days after the initiation of therapy, ranging from 0%-2% of all nucleated cells. In 2 of 10 patients who achieved remission, 2% ULCA+ BM cells were found on days 35 and 60 after initiation of chemotherapy, and this finding was followed by relapse on days 110 and 270. However, the other 8 patients remained in remission despite positive finding of ULCA+ BM cells ranging from 0.2%-2% on at least one occasion. In 2 patients with AML FAB-M3 and cytomorphologic remission, the finding of ULCA+ cells by double APAAP correlated with the molecular finding of PML/RARalpha junction. These results indicate that double APAAP staining can identify leukemic cells in samples with a cytomorphologic pattern consistent with remission, but its applicability in detection of MRD awaits additional studies on a larger number of patients with ULCA+ AL.
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PMID:Double immunoenzymatic APAAP staining for the detection of leukemia-associated immunophenotypes. 1064 71

A 28-year-old Japanese woman with suspected essential thrombocythemia (ET) had marked thrombocytosis, mild leukocytosis with normal neutrophil alkaline phosphatase activity, and no anemia. She was monitored without being given any medication. Eleven years later, complete blood counts showed no remarkable changes but some non-lobulated mononuclear megakaryocytes were found in the bone marrow. Cytogenetic analysis revealed deletion of the long arm of chromosome 5 (5q-). Subsequently, hemoglobin and platelet counts decreased gradually, splenomegaly appeared and progressed, after which myelofibrosis developed. Acute leukemia developed 16 years after the first documentation of thrombocytosis. 5q- syndrome is known to be a myelodysplastic syndrome (MDS) with unique clinical features and cases with this syndrome presenting with thrombocytosis of more than 1,000 x 10(9)/L but without anemia are rare. Furthermore, it is noteworthy that in this patient transition to acute leukemia occurred following development of myelofibrosis and marked splenomegaly, which are generally observed in blastic crises resulting from chronic myeloproliferative disorders (CMPD). The patient showed features indicative of CMPD rather than of MDS in spite of presenting with 5q- chromosomal abnormality. This case supports the concept of "mixed myelodysplastic and myeloproliferative syndromes" and suggests the possibility of the appearance of CMPD-like manifestations in 5q- syndrome.
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PMID:5q- syndrome presenting chronic myeloproliferative disorders-like manifestation: a case report. 1081 92

The chromosome aberration t(7;11)(p15;p15) is uncommon but recurrent in leukemia. We experienced a case of acute leukemia with t(7;11)(p15;p15), the hematological appearance of which mimicked myeloid crisis in chronic myeloid leukemia (CML). This case showed splenomegaly, a decreased neutrophil alkaline phosphatase (NAP) score, increased vitamin B12 value, and cells at all stages of neutrophilic maturation in both bone marrow and peripheral blood. We initially had difficulty differentiating acute myeloid leukemia (AML) M2 with marked myeloid differentiation from myeloid crisis of Philadelphia chromosome (Ph)-negative CML. Immature myeloid cells in the peripheral blood disappeared and cytogenetic analysis indicated that marrow cells changed to the normal karyotype after remission induction therapy. Therefore, this case was thought not to be myeloid crisis but AML M2 subtype. The NUP98/HOXA9 fusion transcript was detected by reverse transcription-polymerase chain reaction (RT-PCR) at exon A but not exon B of NUP98.
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PMID:A case of acute myeloid leukemia with t(7;11)(p15;p15) mimicking myeloid crisis of chronic myelogenous leukemia. 1213 1


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