Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone marrow necrosis (BMN) is a rare intravitally recognized finding in acute leukaemia with an uncertain clinical significance. The clinical events in 4 patients with AML, ALL, AMoL and blastic transformation of CGL in whom bone marrow cytology and histology revealed BMN are reviewed. One patient with BMN at clinical presentation of AML entered complete, long lasting remission with marrow restoration after the standard DAT therapy. In the three remaining patients survival after BMN diagnosis was 6, 11, and 14 weeks. Clinical, haematological, histological and marrow scanning findings and their significance for early diagnosis and means to asses the extent and evaluation of BMN will be discussed. In contrast to the most earlier reports, BMN does not appear to confer a poor prognosis in all patients with blastic leukaemia.
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PMID:Bone marrow necrosis intravitally recognized in four cases of blastic leukaemia. 171 85

The usefulness of phosphotyrosine antibodies for the detection of physiologically regulated or deregulated kinases is shown in this paper. This rather rare enzymatic activity is shared by receptors for some polypeptide growth factors and by the products of class 1 oncogenes. The antibodies are able to detect proteins phosphorylated on tyrosine in fibroblasts stimulated with growth factors, such as EGF and PDGF. The major phosphorylated protein species are the receptors themselves, which undergo phosphorylation only following the addition of the exogenous factor and only transiently. Phosphotyrosine antibodies were able to detect the products of the retroviral class 1 oncogenes, which are endowed of deregulated tyrosine kinase activity. In fact, in these cases a constitutive phosphorylation of the relevant proteins was observed, which occurred continuously and independently of the presence or lack of the growth factor. A tyrosine kinase constitutively activated in human gastric carcinoma cells was detected by P-Tyr antibodies. This molecule has been characterized at molecular level and the mechanisms responsible for its enzymatic activation has been investigated. The question of whether the tyrosine kinase identified is responsible for the induction and the maintenance of the transformed phenotype in gastric carcinomas remains to be answered. It is reasonable to suggest that this might be the case by analogy with other known pathologies, such as class 1 oncogenes activated by transduction by retroviruses, abnormal expression of EGF receptors or deregulated activity of c-abl encoded proteins in CML and ALL. Thus, the search for deregulated kinases by means of phosphotyrosine antibodies seems to be useful for identifying new activated oncogenes in clinical oncology.
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PMID:Phosphotyrosine antibodies as probes for activated oncogene products endowed with tyrosine kinase activity. 172 Feb 92

A monoclonal antibody (17F11) was raised by immunization of a Balb/c mouse with leukemic blasts from a patient with acute non-lymphocytic leukemia (ANLL). This antibody recognizes most leukemic blasts of myeloid but not of lymphoid lineage and no peripheral blood cells. By screening NIH-3T3 fibroblasts transfected with the human proto-oncogene c-kit (NIH-3T3/hckit) it could be shown that 17F11 specifically recognizes the gene product P145c-kit. Immunofluorescence analysis on normal hemopoietic cells revealed that 17F11 weakly stains 1-3% of bone marrow mononuclear cells (BMMNC). By FACS sorting and colony assays it could be shown that granulocyte--macrophage progenitor cells could be enriched 10-20-fold, granulocyte progenitors 50-80-fold, and erythroid and multipotential progenitor cells 15-20-fold, in the 17F11 positive fraction. Double fluorescence analysis revealed that P145c-kit is co-expressed on 40-60% of the CD34 positive BMMNC. Finally, these data show that P145c-kit is expressed on blast cells from most patients with ANLL (26/30) and chronic myeloid leukemia in blast crisis (7/9), but is absent on blasts from patients with acute lymphoblastic leukemia expressing the T-, B-lineage, or common ALL phenotypes.
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PMID:The product of the proto-oncogene c-kit (P145c-kit) is a human bone marrow surface antigen of hemopoietic precursor cells which is expressed on a subset of acute non-lymphoblastic leukemic cells. 172 Apr 90

Diagnosis of leukemia and lymphoma has been made by morphological, cytochemical, and immunophenotypical methods. Recently molecular biological approaches have been introduced to clarify the cellular lineage of the tumor cells and to demonstrate the monoclonality. Southern blot analysis using immunoglobulin (Ig) and T cell receptor (TcR) genes revealed the presence of monoclonal components in some cases of angioimmunoblastic lymphadenopathy (AILD), in which demonstration of monoclonality was difficult by conventional methods. In preB-ALL, many cases had rearranged IgH and TcR genes simultaneously. These "dual genotype" cases were found to be of accidental involvement of TcR gene in the process of making effective IgH gene rearrangements by the precise analysis of rearranged IgH gene structures. The rearranged TcR gene which was detected in initial lymphoblastic lymphoma cells, was observed in relapsed blasts after lineage conversion to myeloid leukemia, which indicates the same clonal origin. Diagnosis and detection of minimal residual disease by the polymerase chain reaction (PCR) are now recognized as sensitive methods. PCR using oligonucleotides common to each VH and JH gene detects the rearranged IgH gene sensitively. PCR using primers located on the translocation boundary, such as bcr and abl in CML, is very useful in the diagnosis and pursuit of the disease course. PCR study also can be applied to the detection of alteration of some particular genes such as tumor suppressor genes.
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PMID:[Molecular diagnosis of leukemia and lymphoma]. 176 82

The ability to deliver high-dose chemotherapy with or without radiotherapy followed by marrow rescue has made marrow transplantation the treatment of choice for children with AML in first remission, juvenile CML, and adult-type CML in chronic phase. For patients with ALL or NHL who relapse, transplantation in second remission represents a reasonable therapeutic option. The role of marrow transplantation for patients in the advanced stages of their disease will continue to be explored to develop promising new therapies, which may improve results of transplantation earlier in the disease course. Development of transplant preparative regimens that have the same or improved therapeutic efficacy with less late effects is especially important for growing and developing children. In the meantime, all children who have received a marrow transplant must be followed for development of delayed effects, which may not appear until years after the transplant procedure. Children who are cured of their leukemia continue to occasionally visit the pediatric hematologist/oncologist, but they do so less often with increasing time after curative therapy. Thus, it is necessary for the primary care pediatrician to be familiar with the details regarding the child's previous therapy in order to anticipate and to be prepared to treat the delayed effects. Attention to school performance is of particular importance for early identification of those children who may need special educational attention. Advances in the treatment of children with leukemia continue to be made both with chemotherapy and with marrow transplantation that should result in greater numbers of children being cured.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone marrow transplantation for pediatric leukemia. 176 98

More than 50% cure can be obtained with allogeneic bone marrow transplantation (BMT) when patients are transplanted in first remission of AML and ALL or chronic phase of CML. On the other hand, considerable progress has been made recently in treating acute leukemia with chemotherapy. Recent studies of intensive chemotherapy in adults with AML report approximately 40-50% 3-year disease-free survival (DFS). Accordingly, several prospective randomized clinical trials have been conducted on the use of BMT versus intensive chemotherapy in the treatment of AML. Significant differences in DFS were found only in a few studies though the results of BMT appear to be comparable or superior to chemotherapy. Therefore, the overall advantage of BMT in first remission AML is smaller than expected. We should know not whether to transplant or to perform chemotherapy, but rather whether to transplant in first remission or to perform chemotherapy first and reserve transplantation as salvage therapy. Recently acute promyelocytic leukemia has been successfully treated with differentiation therapy using all-trans retinoic acid. Low-dose aclarubicin has also been reported to be effective as differentiation therapy in some patients with myelodysplastic syndrome and atypical AML. With the advance of molecular biology of cytokines, several of them are now available for clinical use. G-CSF, GM-CSF and M-CSF are potent stimulators for the granulocyte-macrophage production; they are very effective for accelerating hematologic recovery after chemotherapy-induced myelosuppression or BMT. Interferon-alpha (IFN-alpha) has been used in the several studies. Furthermore, Ph chromosome positivity can be reduced with long-term administration of IFN-alpha; Ph-positive clone can be undetectable in some patients. Thus, IFN-alpha will be the choice of treatment for CML even if BMT is planned.
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PMID:[New trends in the treatment of leukemia]. 177 64

In vitro amplification of genomic or cDNA sequences by polymerase chain reaction (PCR) is one of the most powerful tools in recent molecular biology. More than 10(5) copies of DNA sequence ranging from 50 bp to 7 kb can be synthesized in a couple of hours. Ever since its development, PCR has attracted much attention because this strategy would allow the detection of minimal residual disease (MRD) at a very low level. The first successful application of this ultra-sensitive technique was the detection of residual tumor cells carrying a 14;18 translocation in follicular lymphoma. The abnormal transcripts caused by 9;22 translocation in chronic myelocytic leukemia (CML) was also exploited for the amplification to detect the MRD. These techniques have successfully shown the detection of one leukemic cell in 100,000 normal cells. Besides leukemic specific sequences caused by chromosome and gene translocations, unique sequences caused by rearrangements in IgH or TCR gamma, delta chain genes have been used as clonal markers for tumor cells. By targetting these sequences for PCR amplification, almost all ALL patients can be analyzed for MRD. The successive measurement of MRD might contribute to improvement of treatments for leukemic patients.
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PMID:[The detection of minimal residual disease in leukemia by in vitro DNA amplification]. 177 67

One of the clinical features of chronic myeloid leukemia (CML) after splenectomy lies in the development of an unusual hyperthrombocytic syndrome. In the course of a long-term observation, 12 out of 14 patients subjected to splenectomy demonstrated maximum thrombocytosis ranging from 1.008 X 10(9) to 3.053 X 10(9)/l. Hemorrhagic manifestations occurred in 6 patients, no thromboses were recorded. Postsplenectomy hyperthrombocytosis is to a certain measure resistant to cytostatic therapy. Dissociation may occur--good readings of the leukogram with a high hyperthrombocytosis. According to the authors' and reported data, the postsplenectomy hyperthrombocytic syndrome in ALL patients is fraught with the danger of the occurrence of hemorrhagic manifestations and, to a less degree, of thromboses.
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PMID:[The characteristics of the postsplenectomy hyperthrombocytic syndrome in patients with chronic myeloleukemia]. 178 10

We have studied the haematologic, cytogenetic and molecular features in a patient with Ph positive ALL. The cytogenetic study showed the presence of a Ph chromosome since diagnosis. Molecular analysis showed rearrangement within the first intron of bcr gen instead of M-bcr as in CML. This an evidence of genic fusion between c-abl oncogene and bcr gene and also show the possibility of rearrangement outside M-bcr in these patients.
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PMID:[Philadelphia-positive ALL with rearrangement of the 1st intron of the BCR gene]. 181 84

Growth kinetics of bone marrow stromal layers from normal, AML, ALL and CML patients was studied. Significantly reduced time for confluency was observed in AML patients in complete remission, in CML patients in chronic phase, or CML patients after allogenic bone marrow transplantation. The functional capacity of these stromal layers did not differ: they all bound similar amounts of blast colony forming cells (BL-CFC) from normal bone marrow. The stromal layers from bone marrow transplanted patients varied in their BL-CFC binding capacity: two CML patients (10.5 and 49 months after transplantation) showed normal values, while two ALL patients (1.5 and 3 months, respectively, after transplantation) as well as one patient transplanted for CML (19.5 months after transplantation) showed significantly reduced BL-CFC binding capacity.
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PMID:Growth kinetics and blast-colony forming cell binding capacity of stromal cells in various haematological malignancies. 181 58


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