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)

Forty-four patients with Ph positive leukemia (36 developing blast crisis after chronic phase and eight presenting in acute leukemia) were classified into subgroups on the basis of reactivity of blasts with an anti-serum made against non-T,non-B acute lymphoid leukemia (ALL+), levels of terminal transferase enzyme (TdT+) and morphology. Positivity with anti-ALL serum was the most sensitive and reliable marker, and TdT was an important aid. The presence of "lymphoid" blasts in blast crisis of CML was related to the response to chemotherapy incorporating Vincristine and Prednisolone (VP). Patients with ALL+ blasts frequently (14 of 15 cases) responded to therapy while 21 of 25 patients who had no ALL+ blasts failed to respond. The clinical course of the ALL+ patients was variable: eight patients remitted with return to the appearances of the chronic phase; four patients demonstrated elimination of the Ph1 positive clone with hypoplasia and this was followed by normal (Ph1 negative) marrow regeneration in two. Subsequent relapse was of either the ALL+ "lymphoid" or the ALL-myeloid type. A regimen incorporating VP should be the treatment of choice in "lymphoid" blast crisis of CML.
Cancer 1979 Feb
PMID:Relation of "lymphoid" phenotype and response to chemotherapy incorporating vincristine-prednisolone in the acute phase of Ph1 positive leukemia. 28 75

We have radiolabelled surface glycoproteins of different types of leukemic cell. The labelled proteins were separated by polyacrylamide slab gel electrophoresis and visualized by fluorography. Surface glycoprotein patterns discriminatory for acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) were found. We conclude that the analysis of the surface glycoprotein profile provides a useful method for the classification of leukemic cells according to cell type and stage of differentiation.
Int J Cancer 1979 Mar 15
PMID:Cell surface glycoprotein analysis: a diagnostic tool in human leukemias. 28 25

A 10-year-old boy, who had been in an uninterrupted remission of acute lymphocytic leukemia (ALL) for six years, developed polycythemia vera (PV). One and a half months after detection of PV, he was found to have active leukemia. Both the polycythemia and leukemia receded with anti-leukemia therapy. Three possible explanations for the development of PV in a child with ALL are discussed: 1) PV was a part of his original ALL and recurred whtn patient relapsed. The PV phase was detected only during relapse because the patient was under close observation. 2) PV was a second neoplasm independent of ALL. 3) PV was part of a second leukemia which was different from the original leukemia; this new ALL was derived from a pluripotential cell line involving both erythroid and lymphoid elements. A precedent for this explanation has been observed in chronic myelogenous leukemia.
Cancer 1979 May
PMID:Polycythemia vera in a child with acute lymphocytic leukemia. 28 32

The incidence of circulating granulocyte-macrophage colony-forming cells (CFU-c) was determined in 60 patients in different stages of chronic myelocytic leukemia (CML). Like others, we found uniformly increased circulating CFU-c during the uncontrolled chronic stage, decreasing to values indistinguishable from those of healthy controls during remission. Unlike some investigators who described grossly deficient colony formation during the blastic stage of CML, we found normal to greatly increased colony formation in the accelerated-resistant and blastic stages. The fact that laboratories using somewhat different culture techniques obtain similar results with specimens from the chronic stage of CML but divergent results with specimens from terminal stage disease suggests that CFU-c from blastic disease have more fastidious growth requirements than do those from chronic stage disease or from normal subjects. In contrast to the correlation between CFU-c and disease status in the chronic stage of CML, CFU-c incidence in the accelerated-resistant and blastic stages of the disease did not correlate with white blood cell count, percentage of immature cells, clinical status, or survival. There was no correlation between the percentage of myeloblasts and promyelocytes in circulating blood and the incidence of CFU-c in any stage of CML, which suggests that no direct relationship exists between clonogenic units and the number of identifiable proliferating cells.
Cancer Res 1979 Jul
PMID:Circulating colony-forming cells in different stages of chronic myelocytic leukemia. 28 38

Four patients with multiple myeloma in whom a Ph1 chromosome was found were described; 1 patient had a (9;22) translocation, 2 had no evidence of a translocation, and 1 had a complex translocation (3;8;22). Ph1 chromosomes with standard (9;22) or with unusual translocations were recently found in various myeloproliferative disorders (other than chronic myelogenous leukemia) and in acute lymphoblastic leukemia. These findings point to the genesis of a Ph1 chromosome in diseases other than chronic myelogenous leukemia and other myeloproliferative disorders.
J Natl Cancer Inst 1979 Jul
PMID:Philadelphia chromosome in human multiple myeloma. 28 21

In a 3 1/2 year cytogenetic study of 107 leukemia patients diagnosed in childhood and adloescence, 8 presented with chronic myelogenous leukemia (CML). Seven of the 8 had chromosomal abnormalities. Six had the Ph1 chromosome; 5 had the usual 9;22 translocation. Two patients had involvement with chromosome 15; one had a 9;15 translocation in Ph1 positive cells during remission while a second had a 1;15 translocation during blastic crisis. The 2 patients who did not have a Ph1 chromosome survived 13 and 30 months, respectively, considerably less time than the 4+ year survival in most of those with Ph1 positive CML.
Cancer 1979 Jul
PMID:Cytogenetic studies of chronic myelocytic leukemia in children and adolescents. 28 50

The rapid appearance of acute respiratory distress during the course of 25 hyperleukocytic leukemias was associated with the rapid increase of the leukocytosis. The regression of the tachypnea was spectacular when treating hyperleukocytosis by exchange transfusion and chemotherapy. Blood gas studies, although blurred to some extent by in vitro blast consumption of oxygen, showed a hypoxemia with a hypo-or normocapnia. The symptoms seem to be related to the leukostasis by the mechanical obstruction of the pulmonary capillaries. This leukostasis was shown to be responsible for a septal and alveolar oedema. The high frequency of this syndrome during the course of AGL and of acute phase of CGL seems to be linked to the low deformability of the myeloblasts. In CGL at its chronic phase, CLL or even in ALL, the absence of this syndrome could be explained by the greater deformability of the circulating cells. The hyperleukocytic AGL patients which do not have this syndrome are all characterized by a stable or slowly increasing leukocytosis. Thus, this syndrome seems to characterized by hyperleukocytic granulocytic leukemias with a rapid blood leukocyte doubling rate. Treatment in such cases is an emergency.
Cancer 1979 Jul
PMID:Respiratory distress of hyperleukocytic granulocytic leukemias. 28 51

Vinblastine (6 mg/m2) was given to 15 patients in the terminal phase of Ph1 chromosome-positive chronic myelocytic leukemia and to one patient with chronic myelomonocytic leukemia. In each of these patients, there was prompt reduction in leukocyte counts (median, 80% decrease). Effects on platelet counts and hematocrit levels were inconsistent. Nine patients had decreases in the percentage of circulating blast cells. Reduction in splenomegaly and relief of bone pain were recorded in patients with these manifestations. Serious leukopenia was induced in only one patient, and was of brief duration. Additional doses of vinblastine at intervals of greater than or equal to 3 weeks were given to eight patients who had shown improvement in the differential cell count, as an adjunct to maintenance schedules of combination chemotherapy. Good results were obtained initially, but the quality and duration of responses decreased after two to six injections.
Cancer Treat Rep 1979 Aug
PMID:Use of vinblastine in the terminal phase of chronic myelocytic leukemia. 28 41

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

A 47-year-old white male developed massive hepatosplenomegaly, a pleural effusion, leucocytosis, and a left parasternal mass following a relatively symptom-free persistent hypereosinophilia for about 5 years. Bone marrow aspiration and biopsy and peripheral blood differential showed eosinophilia and a shift to the left with immature cells. A high serum B12 vitamin level and low LAP activity were found. Biopsy of the soft tissue mass revealed a granulocytic sarcoma (chloroma) with a hyperdiploid karyotype (49,XY, + 10, + 15, + 19,3q-), whereas the bone marrow cells had a normal male karyotype. The patient responded temporarily to chemotherapy but eventually developed CNS leukemia and went on to terminate in a frank blastic phase. This case illustrates hypereosinophilia and a myeloproliferative syndrome characterized by a somewhat indolent chronic course evolving into "eosinophilic leukemia" and granulocytic sarcoma, CNS involvement by leukemic cells and, finally, blastic transformation. It is possible that this case represents a variant of Ph1-negative CML to which the term "chronic eosinophilic leukemia" could be justifiably applied.
Cancer 1979 Oct
PMID:Chromosomes and causation of human cancer and leukemia. XXXIV. A case of "hypereosinophilic syndrome" with unusual cytogenetic findings in a chloroma, terminating in blastic transformation and CNS leukemia. 29 66


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