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 phenomenon of premature chromosome condensation (PCC) was used to compare the bone marrow proliferation characteristics of 163 patients with various forms of leukemia prior to the initiation of new therapy. The proliferative potential index (PPI, or fraction of G1 cells in late G1 phase) and the fraction of cells in S phase was determined and compared to the type of disease and the bone marrow blast infiltrate for each patient. Previously untreated patients with acute leukemia exhibited an average PPI value three times that of normal bone marrow (37.5% for acute myeloblastic leukemia [AML], acute monomyeloblastic leukemia [AMML], or acute promyelocytic leukemia [APML] and 42% for acute lymphocytic leukemia [ALL] or acute undifferentiated leukemia [AUL]). Untreated chronic myelogenous leukemia (CML) patients showed intermediate PPI values (25.2%), whereas CML patients with controlled disease exhibited nearly normal PPI values (14.6%). On the other hand, blastic-phase CML patients exhibited PPI values closer to that observed in patients with acute leukemia (35.4%). Seven patients with chronic lymphocytic leukemia (CLL) exhibited even higher PPI values. No correlations were observed between PPI values, fraction of cells in S phase, and marrow blast infiltrate. For untreated acute disease patients, PPI values were prognostic for response only at low and high PPI values. These results suggest that the PCC-determined proliferative potential is a biologic reflection of the degree of malignancy within the bone marrow.
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PMID:Premature chromosome condensation studies in human leukemia. I. Pretreatment characteristics. 29 41

Vindesine was administered to 18 patients with acute leukemia who had failed conventional chemotherapy. Each course of therapy consisted of an iv bolus infusion at a dose of 1-2 mg/m2 given daily x 5-10 days. Of 13 patients with acute lymphoblastic leukemia, two had partial remissions which lasted 2 and 3 months and five had minor responses. One of three patients with acute nonlymphoblastic leukemia and one of two patients with blastic crisis of chronic myelogenous leukemia each had a minor response. The data suggest that vindesine has activity in the treatment of acute leukemia.
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PMID:Phase II trial of vindesine in patients with acute leukemia. 29 7

As prognosis has improved over the last several years, an increasing incidence of meningeal involvement has been recognized in adult patients with acute leukemias and malignant lymphomas. In 210 patients evaluated retrospectively, the incidence of meningeal disease was 33% for patients with acute lymphocytic leukemia (ALL), 20% for patients with acute myelogenous leukemia (AML), 22% for patients with non-Hodgkin's lymphomas with an unfavorable histology (NHL), 3% for patients with chronic myelogenous leukemia (CML), and 1% for patients with chronic lymphocytic leukemia (CLL). In most patients, meningeal involvement appeared several months after diagnosis of acute leukemia, often preceding systemic relapse if bone marrow remission had been achieved before. Prophylactic treatment of the CNS was begun in eight patients with ALL or AML after bone marrow remission was achieved. Of these patients, three with ALL and one with AML were free of disease up to 2 years after diagnosis. Methods, benefits, and risks of prophylactic treatment of the CNS for adult patients are discussed in detail.
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PMID:Meningeal involvement in leukemias and malignant lymphomas of adults: incidence, course of disease, and treatment for prevention. 29 27

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.
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PMID:Cytogenetic study of a new Ph1-positive cell line (NALM-1). 30 41

Fifty-six untreated patients with acute leukemia (38 acute myelogenous leukemia, 16 acute lymphoblastic leukemia, and 2 blast crisis of chronic granulocytic leukemia) were randomized on admission to one of three groups--one to receive oral anticandidal prophylaxis through the period of remission induction chemotherapy with nystatin, another to receive natamycin, and the third to receive no anticandidal prophylaxis. Neither of the first two groups show any advantage over the last and it is concluded that provided gut sterilization regimes are not employed, prophylactic oral anticandidal treatment is of no value in these patients and should be reserved until there is clinical evidence of infection.
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PMID:Oral anticandidal prophylaxis in patients undergoing chemotherapy for acut- leukemia. 31 10

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.
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PMID:Chromosomes and causation of human cancer and leukemia. XXV. Significance of the Ph1 (including unusual translocations) in various acute leukemias. 33 21

Current therapies of chronic myeloid leukemia (CML) do not prevent the progression of the disease towards blastic metamorphosis, and have not resulted in a remarkable prolongation of survival. Splenectomy was proposed with the aim of removing a part of the tumor without cytotoxics and of removing a potentially privileged pool of malignant blast cells. Acute leukemia-like chemotherapy was proposed with the aim of eradicating or better controlling the highly malignant subclones that emerge during the chronic phase. A preliminary analysis of 2 clinical trials these therapeutic measures, suggests that splenectomy does not modify the rate of blastic transformation, during the first 2 to 3 years from diagnosis. Also the rate of blastic transformation is similar for patients receiving hydroxyurea at first, and arabinosyl cytosine (ARA-C), vincristine (VCR) and prednisone (P) thereafter, as for patients receiving from the clinical onset of CML a more intensive chemotherapy with ARA-C, thioguanine (TG) and daunomycin (DAUNO), but not VCR + P.
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PMID:Therapy of chronic myeloid leukemia (CML): interim report on protocols CML/73 and CML/74. 36 86

Piperazinedione was administered to 79 patients with solid tumors on an intermittent schedule with single doses of 1.5-36 mg/m2. Courses were usually repeated at 4-week intervals. Twenty-five patients with leukemia were treated at doses of 18-36 mg/m2 (occasionally for 2 successive days) every 1-4 weeks. Of 48 evaluable patients with malignant melanoma, three (6%) achieved partial remission and nine (20%) had stable disease. Eight of 17 (47%) patients with adenocarcinomas and one of two (50%) patients with lymphomas also had stable disease. Six of 14 (43%) patients with acute myelogenous leukemia showed hematologic improvement, as did one of 11 (9%) patients with blast cell crisis of chronic myelogenous leukemia. The principal toxic effect was myelosuppression, which occurred in 69% of the patients with solid tumors. Profound bone marrow aplasia occurred in 19% of the patients, resulting in six deaths (8%). Risk factors for marrow aplasia included extensive prior therapy, prior nitrosoureas, cumulative toxicity from piperazinedione, and abnormal liver function tests. The recommended doses for further studies are 9 mg/m2 for patients with risk factors for marrow aplasia, 12 mg/m2 for patients with prior therapy, 15 mg/m2 for previously untreated patients, and 24-36 mg/m2 for patients with acute leukemia.
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PMID:Phase I-II study of piperazinedione in adults with solid tumors and acute leukemia. 38 Aug 2

Total hemolytic complement (CH50) and eight antigenic fractions of the complement system were determined in 30 patients with hematological neoplasias, distributed into the following groups: six cases of non-Hodgkin's lymphomas (NHL), seven cases of chronic lymphocytic leukemia (CLL), five cases of Hodgkin's disease (HD), seven cases of acute leukemia (AL), three cases of chronic myeloid leukemia (CML) and two cases of multiple myeloma (MM). CH50 was titred accordingly to a modification of the Kabat and Mayer method, C1q, C1s, C3, C4, C5, INHC1, C3A and properdin were determined with specific antisera by Manani and Laurell's techniques. The results obtained showed significant increase in CH50 above normal values in patients with HD, AL, and CML, especially the former, even in early stages. C1s was found to be increased in CML and AL, as well as C3 in CML. C4 is increased in CML and HD. C5 follows a course similar to C4, being also increased CLL and MM. C9 is increased in all groups, except NHL. A significant increase in C3A was found in NHL, HD and AL. There were no significant variations in C1s, INHC1 and properdin in any of the former groups. No correlation was found between clinical course and complement increase. The role of complement in neoplastic disease is discussed.
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PMID:Complement in hematological neoplasias. 47 24

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.
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PMID:A phase I-II trial of multiple-dose polyriboinosic-polyribocytidylic acid in patieonts with leukemia or solid tumors. 97 71


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