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 clinical and pathological findings in 46 patients with cryptococcosis at Memorial Sloan-Kettering Cancer Center from 1956 to 1972 are reported. The striking predilection for cryptococcal infection in patients with leukemias and lymphomas is again confirmed. Of 41 patients with neoplastic disease, those with chronic lymphatic leukemia (CLL), Hodgkin's Disease, chronic myelogenous leukemia (CML), myeloma and lymphosarcoma had the highest incidence of cryptococcosis. In all cases, neoplastic disease was widespread when infection occurred. All of these patients had leukopenia and absolute lymphopenia at the time of infection. Thirty-nine were on steroids. Thirty-one patients with neoplastic disease had disseminated infection. Review of pathology revealed a spectrum of inflammatory lesions. Histiocytic-lymphocytic infiltrates occurred in the central nervous system in 10 patients. In six cases, reaction was granulomatous. There were single instances of suppurative and fibrotic reactions. Mortality from infection was high in patients with neoplastic disease. Twenty-four of 28 deaths occurred within 60 days as a result of infection. Within one year, 10 more patients died, nine of cryptococcosis. Only three survived more than one year, and all patients died within 600 days. Twenty-nine patients with neoplastic disease received amphotericin B. Only nine survived more than 60 days.
Cancer 1977 May
PMID:Cryptococcosis in a cancer hospital: clinical and pathological correlates in forty-six patients. 32 54

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

Chronic granulocytic leukemia developed four years after renal transplantation in a patient, who had been treated with immunosuppressive agents since then. The low incidence of leukemia in comparison with malignant lymphoma in renal transplant recipients and some pathogenetic mechanisms are discussed.
Cancer 1978 Jan
PMID:Chronic granulocytic leukemia in a renal transplant recipient. 34 89

The use of immunosuppressive therapy has markedly increased over the past several years, and concomitant with its use has been an increased frequency of associated neoplasia. The patient presented is a 22-year-old white male who, following two renal transplants and prolonged immunosuppressive therapy with azathioprine and methylprednisolone, developed chronic granulocytic leukemia. Chromosome karyotyping demonstrated the somewhat unusual development of a Philadelphia chromosome with translocation to the No. 7 of the C group. A review of transplantation centers revealed that five cases of chronic granulocytic leukemia have occurred in a population of 25,000 renal transplant patients, a 5-fold increased incidence over the general population. Possible etiologies that may be responsible for the development of chronic granulocytic leukemia in patients on immunosuppressive therapy are discussed. It is our hope that by the introduction of these reports of chronic granulocytic leukemia into the medical literature, the need for caution in the use of immunosuppressive drugs in nonmalignant disease will again be emphasized.
Cancer 1978 Jun
PMID:Chronic granulocytic leukemia following successful renal transplantation. 35 Mar 75

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.
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PMID:Chronic granulocytic leukemia in a patient with a renal allograft. 35 95

Five cases of Ph1-positive AML were studied. In all cases a Ph1-chromosome was shown with banding techniques to be due to a translocation between chromosomes No. 9 and No. 22. Cases 1 and 4 were found to have more than one Ph1 with evidence of only on Ph1-translocation accompanying other chromosome abnormalities. Two cases represented an unusual pattern of appearance and disappearance of the Ph1-positive clone during their clinical courses: Case No. 2 was originally Ph1-positive (46,XY,Ph1) but two months before his expiration the Ph1-positive clone was completely replaced by a newly developed Ph1-negative clone with an abnormal chromosome No. 21 (46,XY,21q+), whereas case No. 3, primarily Ph1-negative, developed a Ph1-positive clone among the previously karyotypically normal cells one month before death. The Ph1-positive AML cases presented have been discussed in relation to: 1) the genesis and significance of the Ph1-positive clone, 2) differentiation from the blastic phase of CML and 31 the general experience with Ph1-positive acute non-lymphocytic leukemia (ANLL), the world literature of which have been tabulated.
Cancer 1979 Jun
PMID:Chromosomes and causation of human cancer and leukemia. XXXII. Unusual features of Ph1-positive acute myeloblastic leukemia (AML), including a review of the literature. 37 56

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.
Cancer Treat Rep 1979 Jun
PMID:Phase I-II study of piperazinedione in adults with solid tumors and acute leukemia. 38 Aug 2

Splenectomies have been performed on 58 patients with chronic myelogenous leukemia (CML) during the last 16 years. For the 27 patients operated upon during the first 12 years, the operative mortality was 26%. Four patients also had to be re-explored for bleeding and three required drainage of subphrenic abscesses. There has been no operative mortality in the 31 patients operated using a standardized procedure during the last four years but two had to be re-explored for bleeding and one required drainage of a subphrenic abscess. The operative risks for leukemic patients are infection, perhaps related to granulocyte abnormalities and hemorrhage in patients with thrombocytopenia or qualitative platelet abnormalities. When the splenectomy in patients with CML is timed with the patient's chemotherapy cycle, the use of local antibiotics and platelet concentrates should permit a safe operation. Survival rates were not comprised even when the patients had their splenectomy during CML-blast crisis.
Cancer 1977 Feb
PMID:Chronic myelogenous leukemia: management of splenectomy in a high-risk population. 40 88

Because of recent developments in the study of vitamin B12-binding proteins, the levels of the three serum binders were compared in serum and plasma samples from subjects with various disorders. The results allow the following conclusions: (1) As previously reported, transcobalamin (TC) III and to a lesser extent TC I are artifactually elevated in serum. The appear to be released in vitro during the clotting process, presumably from granulocytes. (2) Blood cells of patients with polycythemia vera release exceedingly large amounts of TC I and TC III in vitro. (3) The above findings support, but do not prove, at least a partial granulocytic source of TC I. Nevertheless, factors other than granulocytes influence TC I levels, as disorders characterized by increased TC I (most prominently chronic myelogenous leukemia but also several cases of cancer) manifest relatively little cellular release of TC I in vitro. (4) Despite the serum artifact, the serum abnormalities described in various conditions were seen in plasma also, even though the actual values of themselves were lower in plasma. The chief exception was TC III, which was elevated in plasma only in polycythemia vera (and in a few cases of leukocytosis). (5) EDTA-NaF anticoagulant is not suitable, as it causes plasma dilution, thus explaining previous reports of TC II level differences between serum and plasma. EDTA is therefore a preferable anticoagulant for vitamin B12-binding protein studies, although it too may not be ideal.
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PMID:Vitamin B12-binding proteins in serum and plasma in various disorders. Effect of anticoagulants. 41 9

Thirteen leukemic patients with disease refractory to conventional chemotherapy were treated with 1.0 to 7.5 g/m2 of Cytosine Arabinoside (Ara-C) over 29 drug cycles. Drug infusions were spaced at 12-hour intervals; a maximum of four doses was administered over 36 hours. After single dose tolerance had been established, three or four dose cycles were given at 2- to 30-day intervals. There were three partial remissions (PR) and one complete remission (CR) in a treatment group of four patients with AML, five with ALL, two with lymphoma converted to leukemic phase, one CML in blast crisis, and one promyelocytic leukemia. Five of the patients were septic and considered terminally ill at the time of treatment. All other patients had evidence of drug responsiveness. The nadir of the white count occurred from 3 to 12 days after treatment, with subsequent recovery of the peripheral granulocyte count between days 12 and 28. Toxicity included nausea and vomiting (GI symptoms) in twelve patients, central nervous system (CNS) disturbances in eight patients, one episode of inappropriate antidiuretic hormone syndromes (SIADH), one of hyperuricemia, and fever in eleven patients. There was no evidence of hepatic or renal dysfunction. These high doses of Ara-C appear useful for treatment of patients with refractory leukemia. Hospitalization is brief and toxicity acceptable.
Cancer 1979 Oct
PMID:High dose cytosine arabinoside (HDARAC) in refractory acute leukemia. 49 9


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