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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lipid composition of leukocytes maintained in long-term culture was examined in order to clarify the role of immaturity in previously observed differences between normal mature leukocytes and leukemic cells. Cell cultures derived from three types of leukocytes were examined: normal lymphocytes, Burkitt lymphoma, and chronic myelocytic leukemia. Lipid extracts were analyzed for total lipid weight, phospholipids, neutral lipids, and glycolipids. Distribution of individual phospholipids was determined by quantitative two-dimensional thin-layer chromatography. The main phospholipids were phosphatidylcholine (51-54%) and phosphatidylethanolamine (24-25%), with smaller amounts of phosphatidylinositol, phosphatidylserine, sphingomyelin, and cardiolipin. All three types of cultured cells showed a remarkable similarity in total phospholipid content (17-18 x 10(-15) moles/cell) as well as in phospholipid distribution. More variation was seen in neutral lipid content. Glycolipid was abundant (17-23% of total lipid weight) and was present mostly as ceramide dihexoside. Compared with normal lymphocytes or polymorphonuclear leukocytes, the cultured cells showed increased phosphatidylcholine, decreased sphingomyelin, and decreased cholesterol content, similar to the changes found in leukemic leukocytes. These findings suggest that the altered lipid patterns found in leukemic leukocytes are a reflection of cell immaturity rather than a characteristic peculiar to the leukemic state.
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PMID:Lipid patterns in human leukocytes maintained in long-term culture. 432 7

We have cloned a human V lambda cDNA sequence from an Ig lambda-producing human Burkitt lymphoma cell line (BL2) by taking advantage of a cloned constant region gene as a primer for cDNA synthesis instead of an oligo(dT) primer. The amino acid sequence deduced from the nucleotide sequence of V lambda clones is highly related to that of the NEW V lambda protein of subgroup I. Southern blot hybridization of human DNAs with the V lambda I probe showed at least 12 hybridizing V lambda fragments. These fragments are amplified in K562 cells which derive from a case of chronic myelogenous leukemia and contain an amplified c-abl oncogene and amplified C lambda sequences.
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PMID:Molecular cloning of a human immunoglobulin lambda chain variable sequence. 609 99

Recent improvement in the methods of chromosome analysis has allowed recognition of consistent chromosome alterations in several human cancers, especially leukemias and lymphomas. At the same time, newly discovered human cellular oncogenes have been mapped to individual chromosomes, with precise band assignment. Some of the assignments are coincident with the breakpoints of translocations observed in particular tumors. In fact, a relocation of the corresponding oncogenes has been observed in the cells of some of these tumors. Two notable examples are that of the t(9;22) translocation of chronic myelogenous leukemia (CML), causing the transfer of the oncogene c-abl from chromosome 9 to chromosome 22, and that of the t(8;14) translocation of Burkitt lymphoma, causing the transfer of the oncogene c-myc from chromosome 8 to chromosome 14. These findings can be taken as indicative of a critical role of chromosome alterations in the origin of cancer, through the activation of one or more cellular oncogenes, although there is no firm evidence that such an activation actually occurs. In addition, some concern exists over the validity of accepting in vitro transformation of a cell line by oncogenes as a model of carcinogenesis in man. For these reasons the question on the significance of chromosome alterations in leukemias and lymphomas should not be considered entirely settled yet. Useful models, whose study may lead to the clarification of this important point, are represented by premalignant conditions, such as the myeloproliferative disorders, where chromosome abnormalities are present before the development of a bona fide neoplasm, and by the aneuploidy syndromes, in which there exists an association between a constitutional chromosome anomaly and an increased risk of cancer.
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PMID:Some questions on the significance of chromosome alterations in leukemias and lymphomas: a review. 638 40

In situ chromosomal hybridization of a probe for part of the lambda light chain constant region (C lambda) has demonstrated that the 22q11 breakpoints of chronic myelogenous leukemia (CML) t(9;22) and Burkitt lymphoma t(8;22) are not identical. For CML, the breakpoint is distal to the IGLC genes, whereas for Burkitt lymphoma it is proximal. The study provides direct evidence for regional assignment of the IGLC gene cluster to 22q11.
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PMID:In situ hybridization and translocation breakpoint mapping. I. Nonidentical 22q11 breakpoints for the t(9;22) of CML and the t(8;22) of Burkitt lymphoma. 646 87

Nonrandom chromosome changes have been identified in a number of malignant human tumors. The leukemias are among the best studied malignant cells and they provide the largest body of relevant cytogenetic data. In chronic myeloid leukemia, a reasonably consistent translocation [t(9;22) (q34;q11)] is observed in 93 percent of all Ph1 positive patients. In the other patients, translocations are either two-way, involving No. 22 with some other chromosome or complex translocations involving Nos. 9 and 22 and another chromosome. In acute nonlymphocytic leukemia, two translocations are each specifically associated with leukemic cells arrested at two different stages of maturation. One of these, t(8;21)(q22;q22), is found mainly in patients with acute myeloblastic leukemia with maturation (AML-M2). The other, t(15;17)(q22?;q21?), is seen only in patients with acute promyelocytic leukemia (APL-M3). Various translocations have been observed in B-cell acute lymphoblastic leukemia or in Burkitt lymphoma. The most common is t(8;14)(q24;q32), but variants of this, namely t(2;8)(p13?;q24) and t(8;22)(q24;q11), have also been observed; in all of these, the consistent change involves 8q24. The various immunoglobulin loci are located on chromosomes 2, 14, and 22 in the same chromosome band affected by the translocations in B-cell leukemia. These translocations may occur randomly. If a specific translocation provides a particular cell type with a growth advantage, then selection could act to cause the proliferation of this aneuploid cell line vis-a-vis cells with a normal karyotype. In this view, the chromosome change could be the fundamental event leading to the leukemic transformation of an otherwise normal cell. The challenge for the future is to define the genes located at the sites of consistent translocations in myeloid leukemias and to determine the alterations in gene function that are associated with the translocation.
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PMID:Chromosome abnormalities in leukemia and lymphoma. 660 85

Flow karyotype analysis was performed to assess the feasibility of fluorescence-activated sorting of Burkitt lymphoma (BL)-associated translocation chromosomes. The typical 14q+ chromosome in the t(8;14) and the two "variant translocations", the 2q+ in the t(2;8) and the small 22q- in the t(8;22), could be identified as single peaks within the flow karyotypes of metaphase chromosomes isolated from several different BL-lines for each translocation. The translocation chromosomes could be separated with a high degree of purity and in quantities suitable for biochemical analysis. The same analytical and preparative technique was also successfully applied to the identification and sorting of the Philadelphia (Ph1) chromosome in a 9;22 translocation-carrying CML-derived line and a familial (11;22) translocation.
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PMID:Flow karyotype analysis and fluorescence-activated sorting of Burkitt-lymphoma-associated translocation chromosomes. 687 39

Glucocorticoid (GC) receptor and terminal deoxynucleotidyl transferase (TdT) activities were studied in leukemia cells to investigate their diagnostic and therapeutic implications. Among cell lines with T-cell character, higher GC-receptor and TdT activities were found in T-ALL (HPB-ALL and ALL-Ichikawa) than in cells from adult pleomorphic T-cell leukemia (HPB-MLT). HPB-Null with pre-B cell-character exhibited moderate GC receptor but low TdT activity; Raji cells and CCRF-SB, derived from B-cell Burkitt lymphoma and B-ALL, respectively, manifested low GC receptor and no TdT activity. The highest GC receptor activity was demonstrated in null-cell ALL, followed, in order, by juvenile T-ALL, adult pleomorphic T-cell leukemia, and AML. Other kinds of lymphoid and monocytic leukemias exhibited low GC receptor and no TdT activity. Although low GC receptor and negative TdT were demonstrated in cells from seven out of nine patients under CML blastic crisis, the last patient had cells with positive TdT and GC receptor activity.
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PMID:Glucocorticoid receptors and terminal deoxynucleotidyl transferase activities in leukemic cells. 697 4

Specific consistent chromosome translocations are regularly observed in certain human leukemias and lymphomas. For the myeloid leukemias, the constant recombinants are: the long arm of 9 to chromosome 22 in chronic myeloid leukemia, the long arm of 21 to chromosome 8 in acute myeloblastic leukemia, and the long arm of 17 to chromosome 15 in acute promyelocytic leukemia. Three related translocations are seen in Burkitt lymphoma and B cell acute lymphocytic leukemia; in each one, chromosome 8 is involved with chromosome 2, 14, or 22. Analysis of a complex translocation affecting chromosomes 8 and 14 indicates that the translocation of chromosome 8 to chromosome 14 is the critical constant rearrangement. The analysis of the DNA at the translocation sites of these chromosomes, rather than the reciprocal of each translocation, appears to be the most productive focus for initial study. The various immunoglobulin loci are located in chromosomes 2, 14, and 22, the chromosomes regularly involved in translocations in Burkitt lymphoma and B cell acute lymphocytic leukemia.
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PMID:Identification of the constant chromosome regions involved in human hematologic malignant disease. 707 37

Several new 4-diazopyrazole derivatives were synthesized by reaction of 1-(R-substituted)phenyl-3-methyl-5-benzamidopyrazoles with a sevenfold excess of nitrous acid in acetic media. The compounds were tested at 20 microM concentration for their antineoplastic activity in vitro against Raji (human Burkitt lymphoma), K562 (human chronic myelogenous leukemia) and U937 (human histiocytic lymphoma) cell lines. They showed a percent of growth inhibition in the range 23.4-100%.
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PMID:Synthesis and antineoplastic activity of new 4-diazopyrazole derivatives. 950 64

Applications of nucleic acid testing in most areas of the clinical laboratory have increased rapidly. The advantages of nucleic acid testing include enhanced specificity and sensitivity, ease of sample procurement, and more rapid turnaround time compared to conventional laboratory testing methods. However, the cost of testing is usually higher due to the need for additional laboratory space, specialized equipment, safety apparel, and the need for highly trained personnel. Most nucleic acid techniques currently used in a clinical setting can be categorized as either hybridization or amplification assays. Hybridization assays, including blotting techniques and microarrays, involve the complementary binding of an oligonucleotide probe of known DNA sequence with nucleic acid derived from the patient sample. To amplify small amounts of nucleic acid, assays such as the polymerase chain reaction and branched chain DNA employ either signal amplification or exponential amplification of target nucleic acid. Clinical applications of nucleic acid testing involve the detection of genetic diseases, e.g., sickle cell anemia and Huntington disease; and identification of infectious agents, e.g., HCV and HIV; or malignancies, e.g., chronic myelogenous leukemia and Burkitt lymphoma. Quantitative molecular assays also play important roles in predicting prognosis and monitoring responsiveness to therapy.
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PMID:The new millennium laboratory: molecular diagnostics goes clinical. 1176 Aug 24


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