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)

A number of clinically significant human diseases are associated with rearrangements of chromosome #22. These include the t(9;22) of chronic myelogenous leukemia (CML), the t(8;22) of Burkitt's lymphoma (BL), the t(11;22)(q23;q11) constitutional rearrangement and the t(11;22) of Ewing's sarcoma (ES) and neuroepithelioma (NE). All of these translocations have breakpoints in 22q11. Using a molecular cytogenetic approach and various cloned portions of the lambda light chain gene as probe, we have assigned a linear order within 22q11 to these breakpoints. Using chromosomal in situ hybridization we have determined that the 22q11 breakpoint in BL2, a t(8;22) Burkitt's lymphoma is proximal to the breakpoint of the t(9;22) of CML. We have demonstrated that the 22q11 breakpoint of PA682, another t(8;22) BL cell line, interrupts the lambda light chain locus. Using a combination of variable and constant region probes and PA682 cells, we have shown that the lambda light chain locus is oriented such that V lambda is proximal to C lambda in 22q11. Our results for the constitutional t(11;22) indicate that the 22q11 breakpoint is distal to that of BL, proximal both to that of CML and ES and, in addition, it interrupts the C lambda gene cluster. Our studies of the 22q11 breakpoint of the t(11;22) of ES and NE suggest that they are the most distal of the breakpoints we studied on chromosome #22.
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PMID:Translocation breakpoint mapping: molecular and cytogenetic studies of chromosome 22. 345 63

The toxicity of high dose cytosine arabinoside (Ara-C) in 23 leukemic children aged 1.5 years to 16 years 11 months was evaluated. The group included 11 children with acute lymphoblastic leukemia (ALL), nine with acute nonlymphoblastic leukemia (ANLL), two with chronic myelocytic leukemia (CML) in blastic crisis, and one with Burkitt's lymphoma. Toxicity consisted of bone marrow suppression in all patients, with a mean nadir time of 11 days for platelets and granulocytes. All patients experienced nausea and vomiting; 12 of 23 had drug induced fever; seven of 23 conjunctivitis; five of 23 mucositis; four of 23 diarrhea, and one of 23 elevated transaminase with hyperbilirubinemia. Adverse reactions were mild and reversible in all patients. No serious neurologic toxicity was seen. The toxicity observed in four patients with prior cranial irradiation was not any different from nonirradiated patients. The only life-threatening effect was neutropenia, the consequences of which were generally well controlled with antibiotic therapy. While this agent was effective in induction of remission in AML patients resistant to standard doses of Ara-C, it had no significant effect in a very small number of patients with relapsed ALL and CML in blast crisis. Side effects of high dose Ara-C though relatively substantial are manageable enough to warrant wider scale efficacy trials of this agent in childhood leukemias and solid tumors.
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PMID:Toxicity of high dose Ara-C in children and adolescents. 359 53

We have performed in situ hybridization of a probe for the lambda IGLC constant region to metaphase spreads from two DiGeorge syndrome (DGS)-related chromosomal rearrangements with breakpoints in 22q11. In this study we have demonstrated that the breakpoints are proximal to the lambda IGLC constant region cluster. Thus, at the molecular level, DGS-related breakpoints can be distinguished from the 22q11 breakpoint of CML, but not from the 8;22 translocation of Burkitt lymphoma or from the 21;22 translocations that we have previously studied.
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PMID:In situ hybridization and translocation breakpoint mapping. III. DiGeorge syndrome with partial monosomy of chromosome 22. 393 Jan 57

The presence of intracellular cytoplasmic immunoglobulin M (IgM) in leukemic cells from patients with acute lymphocytic leukemia (ALL) and chronic lymphocytic leukemia (CLL) was investigated by flow cytometry. The objective of the study was to develop a reproducible flow cytometric method. A Burkitt's lymphoma-derived B-cell line, Daudi, and a pre-B ALL, Nalm-6, served as prototypes. Normal B cells and cells from patients with chronic myelogenous leukemia (CML) were used as negative controls. Cytoplasmic mu was expressed in 77.3 +/- 7.5% (n = 10) of Nalm-6 cells. CALLA+ ALL and CML cells lacked cytoplasmic mu. The surface-membrane immunoglobulin on the viable B cells was blocked with purified goat anti-human IgM. Subsequently, the B cells were fixed in cold absolute methanol and stained with a fluorescein-conjugated goat anti-human IgM to demonstrate cytoplasmic IgM. After the surface-membrane IgM was blocked, normal B cells had no cytoplasmic IgM (0.3-0.5% positive cells) detectable by flow cytometry. However, the peripheral blood lymphocytes from five patients with CLL and the Daudi cells contained cytoplasmic IgM, ranging from 7.8 to 76.7% and 45.7 to 89.3%, respectively. We conclude that cytoplasmic mu in Nalm-6, CLL, and Daudi cells can be easily and rapidly demonstrated by flow cytometry.
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PMID:Cytoplasmic IgM in leukemic B cells by flow cytometry. 393 80

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

A brilliant, coarsely granular nuclear antigen was detected by anti-complement immunofluorescence in the nuclei of acute myeloid leukemia myeloblasts. Designated as LANA (leukemia-associated nuclear antigen), the reactivity differs from that of the Epstein-Barr-virus-determined nuclear antigen (EBNA) in immunological specificity and morphological appearance, although it is visualized by the same method. Serum from acute myeloid leukemia patients gave positive reactions in 73% of the cases. In acute lymphatic leukemia, chronic myeloid leukemia, chronic lymphatic leukemia, and Burkitt's lymphoma the sera were positive in 35, 14, 19, and 24%, respectively. Two of five polycythemia and two of eleven myeloma sera were also positive. Among 61 healthy controls, 58 were negative, whereas three showed a diffuse nuclear staining with a different pattern. Among 24 carcinoma patients, 18 were negative, whereas six gave a nuclear staining with a different, diffuse pattern. Sera from 20 patients who had recovered from infectious mononucleosis were all negative. In addition to the blasts of acute myeloid leukemia, a similar reactivity was seen with two Epstein-Barr virus DNA and EBNA-negative African lymphoma biopsies and in a short-lived tissue culture line derived from one of them. LANA could be a fetal or tissue-specific antigen, a virally determined antigen, or a specific form of anti-nuclear reactivity.
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PMID:Human leukemia-associated anti-nuclear reactivity. 459 70

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

Cellular immune response to antigens associated with a type C retrovirus derived from Burkitt's lymphoma (BL) lymphoblastoid cells was studied in patients with hematopoietic malignancies, noncancer patients and healthy controls. Response was determined by lymphocyte blastogenesis assay measuring [3H]-thymidine incorporation, thereby enabling the calculation of stimulation indices (SI). Positive response (SI greater than 2.0) was demonstrated in patients with multiple myeloma (MM), chronic lymphocytic leukemia (CLL), chronic myelocytic leukemia (CML) and BL. No response was demonstrated in the non-cancer and healthy controls. Specific blastogenic response was obtained towards antigen extracted from three different cell lines infected with the tested type C retrovirus. No response was evident towards purified whole or purified disrupted virions or antigen extracted from murine myeloma MOPC-315 cells secreting a murine type C retrovirus or an antigen extracted from Mason-Pfizer monkey virus-infected NC-37 cells. The correlation between human hematopoietic malignancies and the in vitro lymphocyte blastogenic response to the BL-derived type C retrovirus was statistically highly significant.
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PMID:Blastogenic response of lymphocytes derived from patients with hematopoietic malignancies to antigens of a type C retrovirus isolated from a Burkitt's lymphoma cell line. 631 44

At Saitama Cancer Center a Phase II study of Vindesine was carried out in 18 patients with hematological malignancy being refractory to standard chemotherapies. Vindesine (VDS) was given weekly at a dose of 3 mg/m2 as single-agent chemotherapy. One cytoreduction effect (CE) in 5 patients with acute lympho blastic leukemia, two CEs in 2 patients with acute non-lymphocytic leukemia, one PR and one CE in 4 patients with CML/BC, three PRs in 3 patients with diffuse non-Hodgkin's lymphoma (NHL) of large cell type, one CR in 2 patients with lymphoblastic lymphoma and one PR in 2 patients with Burkitt's lymphoma were obtained. VDS was discontinued in two patients because of neurologic toxicities such as incontinence of urine, abdominal distension, and severe constipation.
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PMID:[Phase II study of Vindesine in patients with hematological malignancy]. 634 82

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


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