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)

The chromosomes of a cell line (NALM-1) derived from the leukocytes of a patient with chronic myelocytic leukemia (CML) were examined with several banding techniques. The modal chromosome number was 46 and the cells contained a Philadelphia chromosome (Ph1), due to the standard translocation of the missing segment of the long arm of chromosome No. 22 onto the distal end of the long arm of chromosome No. 9, i.e., t(9;22) (q34;q11). The Ph1-positive modal cells of the NALM-1 line also had two common marker chromosomes, an extra X-chromosome, and missing chromosomes in groups No. 7, 9, and 15. Immunologic examination of the NALM-1 cells revealed them to have non-T-non-B (null) surface characteristics. An antigen specific for cells of acute leukemia and a human la-like antigen were detected. These facts suggested that the NALM-1 cell line originated from CML cells and maintained the cytogenetic and Immunologic characteristics of such cells.
J Natl Cancer Inst 1977 Sep
PMID:Cytogenetic study of a new Ph1-positive cell line (NALM-1). 30 41

The following rare Ph1-positive chromosome constitutions, based on the cytogenetic findings in three cases with acute leukemia, are presented. 1) A hypodiploid karyotype, primarily 43, -X, -7, -8,9p+ and a Ph1, in a patient with acute lymphoblastic leukemia (ALL) in relapse, followed by a complete remission and a normal chromosomal picture and then by the appearance of cells with a 46,XX,Ph1 karyotype. The Ph1 was due to a standard translocation between chromosomes no. 9 and no. 22. 2) The first demonstration of an unusual Ph1-translocation between chromosomes no. 19 and no. 22 in a condition other than chronic myelocytic leukemia (CML), i.e., acute myeloblastic leukemia (AML). 3) The presence of a Ph1 in acute erythroleukemia (EL) due to a translocation between chromosomes no. 4 and no. 22, this apparently being the first description of such a translocation in any disease. The cytogenetic findings, particularly those in the Ph1-positive case of ALL, were evaluated in relation to the cytologic and immunologic features, clinical courses and implications, and the interrelationship between the three conditions (AML, blastic phase of CML and ALL), which have to be considered in cases of Ph1-positive acute leukemia.
Cancer 1977 Sep
PMID:Chromosomes and causation of human cancer and leukemia. XXV. Significance of the Ph1 (including unusual translocations) in various acute leukemias. 33 21

A man received a cadaver renal allograft for end-stage renal failure. After 35 months of immunosuppressive therapy with azathioprine and prednisone, he developed septicemia and a high leukocyte count. In spite of successful treatment of the infection, the leukocyte count continued to rise and a diagnosis of Philadelphia chromosome positive chronic granulocytic leukemia was made. An increased incidence of malignant disease, especially lymphoreticular malignancy, is well described in immunosuppressed patients with allografts. However, the association of chronic granulocytic leukemia and immunosuppressive therapy previously has not been reported. An additional etiological factor in this patient may have been the extensive diagnostic radiological investigations undertaken in childhood. The recent addition of allopurinol to the immunosuppressive therapy has normalized the platelet and leukocyte counts, probably by potentiating mercaptopurine.
Arch Intern Med 1978 Sep
PMID:Chronic granulocytic leukemia in a patient with a renal allograft. 35 95

Regeneration of T-cell activities in vivo or in vitro from mouse bone marrow precursors differentiating in the presence of an allogeneic thymus was investigated. The data indicated that T-depleted bone marrow cells fail to affect long-term reconstitution of allogeneic recipients unless a pool of rapidly maturing T-precursor cells is also removed (post-thymic pool). Animals reconstituted with pre-thymic bone marrow stem cells become stable chimaeras in which cells capable of generating an in vitro CML response to host antigens, as well as cells capable of suppressing that response, could be demonstrated. Similar data (CML directed against the H-2 antigens of the 'host' thymus feeder layer and cells capable of inhibiting that response) were obtained when pre-thymic bone marrow cells were grown in vitro on allogeneic thymus feeder cells. When cytotoxic T-lymphocyte precursor (CTLp) and helper (CTLh) cells were separately investigated, a restriction in their co-operation for an anti-host response was observed when precursor cells differentiated in an allogeneic environment. Only CTLp and CTLh differentiating in the presence of the same allogeneic thymus source (whether in vivo or in vitro) could co-operate to generate CTL directed to H-2 antigens of that thymus source.
Immunology 1979 Sep
PMID:Differentiation of functionally active mouse T lymphocytes from functionally inactive bone marrow precursors. IV. Recovery of T-cell function from bone marrow precursors in a histo-incompatible environment. 38 77

A patient with chronic granulocytic leukemia developed overwhelming histoplasmosis. During massive fungemia, 59% of peripheral blood neutrophils contained yeast forms. Disseminated intravascular coagulation occurred. Histoplasma capsulatum was isolated not only from the patient's tissues and urine, but also from a serum sample submitted to a reference laboratory for serological testing. The microorganism was demonstrated by specific immunofluorescent staining of peripheral blood films. We suggest that histoplasmosis deserves a definite place on the roster of "opportunistic fungi".
Sabouraudia 1979 Sep
PMID:Overwhelming opportunistic histoplasmosis. 39 63

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.
Southeast Asian J Trop Med Public Health 1977 Sep
PMID:Vitamin B12 and vitamin B12 binding proteins in liver diseases. 60 23

Splenic lymphoblasts or normal spleen cells were treated with varying concentrations of TNBS in order to assess whether cell membrane H-2 molecules were derivatized with TNP. Cells treated with high concentrations of TNBS had their cell membrane H-2 molecules derivatized and functioned antigenically as inhibitors in a cold target TNP-CML competition assay. In contrast, cells derivatized with lower concentrations of TNBS had a significant proportion of their membrane proteins derivatized with TNP but did not have their H-2 molecules derivatized. These latter cells were unable to block anti-TNP cytotoxic effector cells in the competition assay. When cells were treated with 3H-TNBS, it was observed that TNP couples to cell membrane H-2, Ia and Ig molecules, and an estimate of the number of TNP molecules bound per cell at varying concentrations of TNBS was determined. The data obtained are consistent with there being a requirement for TNP to directly derivatize H-2 molecules on the cell membrane in order to create antigenic determinants that can be recognized by cytotoxic anti-TNP effector cells. As an alternative, there may be a requirement for the presence of a high density of TNP molecules per cell rather than direct H-2 derivatization by TNP in order to account for activity.
J Immunol 1978 Sep
PMID:Relationship between trinitrophenol and H-2 antigens on trinitrophenyl-modified spleen cells. III. Quantitative aspects of trinitrophenol binding on cells treated with trinitrobenzene sulfonic acid. 69 Apr 47

The utility of the enzymatic radiochemical assay of histamine in diagnosing diseases with known abnormalities in histamine production was investigated. Whole blood histamine levels were abnormal only in patients with basophilia, i.e. chronic myelocytic leukemia or polycythemia vera. Histamine was not detectable (less than 1 ng/ml) in normal plasma but was detected in plasma of some patients witheither mastocytosis or chronic myelocytic leukemia. These patients also had symptoms which could be attributed to histamine release as, for example, hyperchlorhydria and hypotension. Urinary histamine excretion was also abnormally high in these diseases compared to normal subjects (range less than 5-42 microgram/24 h, n = 31). Patients with systemic mastocytosis had higher urine values (greater than 150 microgram/24 h) than those with cutaneous mastocytosis (39-88 microgram/24 h), and the urinary histamine excretion appeared to be an index of the severity of the diseases. Studies with L-histidine loading suggest that the kidney is one possible source of urinary histamine.
Clin Chim Acta 1977 Sep 01
PMID:Blood and urine histamine levels in normal and pathological states as measured by a radiochemical assay. 89 Sep 80

Polyriboinosinic-polyribocytidylic acid (poly I - poly C), an interferon inducer, was administered in multiple doses of 0.3-75 mg/m2 to 26 patients with a variety of solid tumors, 9 with acute leukemia, and 2 with chronic myelogenous leukemia in blast crisis. Forty-four separate drug trials were comprised of various schedules and routes of administration. Toxic reactions included fever (in 66% of the trials), transient elevation of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase (25%), minimal laboratory evidence of coagulation abnormalities (59%), and hypersensitivity (5%). These toxic manifestations did not relate to dose level or magnitude of interferon induction. Poly I - poly C administered iv induced low serum concentrations of interferon in 24/38 trials (63%), but the correlation between drug dose and peak interferon titer was not linear. Poly I - poly C administered iv or im was not effective as an inducer of interferon in the cerebrospinal fluid. Similarly, poly I - poly C administered im or by inhalation did not produce detectable serum levels of interferon. No patients experienced an objective tumor response to the administration of poly I - poly C, and most (76%) had progression of their disease while receiving the drug.
J Natl Cancer Inst 1976 Sep
PMID:A phase I-II trial of multiple-dose polyriboinosic-polyribocytidylic acid in patieonts with leukemia or solid tumors. 97 71

Foam cells in the spleen, bone marrow, liver and lymph nodes were examined on the 73 reliably recorded and sampled leukemia autopsy cases encountered at Kobe University from 1958 to 1972. Although the substances stored in the foam cells were biochemically unknown, the foam cells in leukemia could be morphologically classified into two types: The one was identified with the Gaucher type, but the other was not identified with the sea-blue type and might be considered as to be the transitional type described in another report. Foam cells could be found in the spleen of 6 out of 12 cases of chronic myeloid leukemia, one out of 2 cases of chronic lymphatic leukemia, one out of 7 cases of leukemic lymphosarcoma, one out of 9 cases of acute lymphatic leukemia, and none in 3 cases of monocytic leukemia. In acute myeloid leukemia, the incidence of foam cells in the spleen was 47.5% in 40 cases, and acquired lipidoses were more frequently seen in cases under 19 years of age, in male cases, in cases with an enlarged spleen over 400 g, and in cases of over 4 months' duration.
Acta Pathol Jpn 1976 Sep
PMID:Secondary lipidosis in leukemia. 99 40


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