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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerical and structural chromosome aberrations are frequently found in neoplastic cells. As demonstrated by the new chromosome banding techniques these aberrations are not random, but tend to show a specific occurrence. A model example is the leukemias where many cytogenetical investigations have been done to date. In leukemia chromosome analysis serves the following purposes: to identify a neoplastic process, to confirm and strengthen the hematological diagnosis, for the early diagnosis of transformation from a chronic leukemia into its blastic phase and for following up the clonal evolution of a leukemic cell line. In the discussion of chromosomes and neoplasms it must be mentioned that individuals demonstrating chromosomal instability and some trisomic patients show a greater tendency toward the development of a malignancy. Malignancy is primarily a cellular phenomenon caused by a disturbance in cellular regulation, whose fine events are not known. Therefore the exact role of the chromosomes in neoplastic processes cannot be stated. From experimental investigations it appears that the affected chromosomes carry cell growth regulating factors and also that a specific aberration is the result of the action of a specific agent.
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PMID:Editorial: Chromosomes and human neoplasms. Achievements using new staining techniques. 6 Feb 37

Association with family history of cancer of each site was examined for each type of childhood malignancies using data of National Childhood Malignancy Registry in Japan as materials (n = 16,555). 2,926 cases were with cancer family history. Family history of same type of malignancy was found significantly in excess for leukemia, a malignant lymphoma, brain tumor, neuroblastoma and retinoblastoma. When observed by cell type, association with family history of leukemia was most striking in acute myeloid leukemia. Median age at first diagnosis of retinoblastoma was 11 months earlier when family history of retinoblastoma existed. Family history of leukemia and history of exposure to prenatal radiation exposure was found to enhance relative risk for childhood leukemia when combined, suggesting existence of genetic environment interaction. Mode of interaction was interpreted as multiplicative.
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PMID:[Interaction of cancer family history and environmental factors in the risk of cancer--with special reference to childhood malignancies]. 303 33

Thirty patients with lymphoma (12), leukemia (two), myeloma (one), or metastatic solid tumors (15) were explored for 31 episodes of spontaneous intestinal perforation during an 11-year period at Memorial Sloan-Kettering Cancer Center. Twenty-three patients (76.6%) were receiving corticosteroids alone or in combination with chemotherapy and seven patients (23.4%) were receiving chemotherapy alone at the time of perforation. Fourteen perforations (45%) occurred in the small intestine and 17 perforations (55%) occurred in the colon. Malignancy was histologically demonstrated at the site of perforation in 16 patients (52%). Twenty major postoperative complications occurred in 15 patients (50%) and the operative mortality rate was 53%. Factors such as age, sex, duration or type of symptoms, site of perforation, malignancy at the site of perforation, peripheral leukocyte count, and serum albumin and total protein levels were not significantly related to patient survival. Early diagnosis and aggressive surgical intervention is essential to improve survival following intestinal perforation in this high-risk population.
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PMID:Emergency laparotomy for spontaneous intestinal and colonic perforations in cancer patients receiving corticosteroids and chemotherapy. 333 95

The mortality experience of 5,406 men (cohort I) employed at one aluminum smelter on Jan. 1, 1950, and 485 men employed at a second plant (cohort II) on Jan. 1, 1951, is reported. For each man, the total number of years of exposure to tars, the number of years since first exposure to tars, and an index of exposure to tars expressed in tar-years were calculated. More than 99% of the men in the first cohort and 98% of the men in the second cohort were traced. Of the 1,539 men in cohort I who were deceased as of December 31, 1977, death certificates were obtained for 1,432 (93%). Of the 92 men in cohort II who were deceased as of December 31, 1977, death certificates were obtained for 80 (87%). The results showed that men in cohort I died of the following causes at approximately the same rate as or less frequently than men of similar age in the Province of Quebec: tuberculosis; circulatory disease; hypertensive heart disease; trauma; leukemia and aleukemia; and malignant neoplasms of the pancreas, genital organs, brain, intestine, and rectum and other abdominal areas. There were no deaths from pneumoconiosis or Alzheimer's disease. Although the observed and expected numbers of deaths in some of the cause-of-death categories were small, men in cohort I died of the following causes more frequently than did men of similar age in the Province of Quebec: respiratory disease; pneumonia and bronchitis; malignant neoplasms (all sites); malignant neoplasms of the stomach and esophagus, bladder, and lung; other malignant neoplasms; Hodgkin's disease; and other hypertensive disease. Mortality from malignant neoplasms of the bladder and lung was meaningfully related to numbers of tar-years and of years of exposure. Exposure-response relationships were less clear for malignant neoplasms of the esophagus and stomach and for other malignancies. Mortality from respiratory disease for men with 21 or more tar-years of exposure was approximately twice that of persons never exposed to tars. The apparent excess of other hypertensive disease was restricted to men never exposed to tars. Malignant neoplasm of the lung was the only cause of death in cohort II that was in excess of that expected at Quebec provincial rates.
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PMID:Mortality of aluminum reduction plant workers, 1950 through 1977. 406 80

Malignancy in patients with constitutional chromosome abnormality is of interest not only because it permits insights into the relationship between the chromosome abnormality and cancer, but also because it provides opportunities to address such questions as the clonality and evolution of tumors. We report Ph1-positive chronic myelogenous leukemia (CML) in a 50-year-old mosaic (45,X/46,XX) Turner syndrome patient whose leukemia was restricted to the monosomic cell line. Our extensive cytogenetic studies of this patient demonstrated that non-leukemic normal cells persisted in the marrow and were able to proliferate during a period of temporary suppression of the leukemic clone following aggressive treatment.
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PMID:Chronic myelogenous leukemia in the monosomic cell line of a fertile Turner syndrome mosaic (45,X/46,XX). 695 Aug 10

The incidence of childhood cancer in Queensland has been studied using the data of the population-based Queensland Childhood Malignancy Registry. During the 7-year period 1973-1979, 454 cases were registered, giving an annual age-specific incidence of 11.34/10(5) for the age group 0-14 years inclusive. There was a male/female ratio of 1.36. The commonest group of diseases was that of the leukaemias, followed by that of CNS tumours. The incidences of the various types of tumour in Queensland have been compared with those from other reported series. The incidence of leukaemia was midway between that of U.S. whites and that of Manchester, while the incidences of lymphoma and Wilms' tumour were much closer to those of the United States. Ewing's tumour was considerably commoner than osteosarcoma.
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PMID:Incidence of childhood tumours in Queensland. 731 68

Malignancy may be associated with impairment of the immune system. In children with acute leukemia, an impaired immunoglobulin M (IgM) antibody response to poliovirus was documented previously. It was of interest, therefore, to determine the immunoclass of antibodies produced against the O antigens of bacteria causing bacteremia in patients with leukemia and other malignancies. For control purposes, parallel studies were carried out in patients without maligancies but with infections caused by gram-negative bacteria. The patients with malignancies were adults, and those without malignancies were children. The serum specimens were selected from patients mounting an antibody response. IgG and IgM antibodies were identified by mercaptoethanol reduction and chromatography. Antibody titers against the O antigens of enteric bacteria were determined by the hemagglutination procedure. Antibodies of both IgM and IgG immunoclasses were produced by all but 1 of 16 patients with leukemia and by all but 1 of 12 subjects with other malignancies. Thus, a specific IgM immune deficiency in adult patients with leukemia or other malignancies complicated by bacteremia was not present; however, the magnitude of the antibody response of the patient with leukemia was less than that of the subjets with other maligancies, with the median antibody titers of the former being 320 and those of the latter being 2,560.
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PMID:Immunoglobulin G and immunoglobulin M antibody responses of patients with malignancies to the O antigens of bacteria causing bacteremia. 741 2

Hematopoiesis gives rise to blood cells of different lineages throughout normal life. Abnormalities in this developmental program lead to blood cell diseases including leukemia. The establishment of a cell culture system for the clonal development of hematopoietic cells made it possible to discover proteins that regulate cell viability, multiplication and differentiation of different hematopoietic cell lineages, and the molecular basis of normal and abnormal blood cell development. These regulators include cytokines now called colony-stimulating factors (CSFs) and interleukins (ILs). There is a network of cytokine interactions, which has positive regulators such as CSFs and ILs and negative regulators such as transforming growth factor beta and tumor necrosis factor (TNF). This multigene cytokine network provides flexibility depending on which part of the network is activated and allows amplification of response to a particular stimulus. Malignancy can be suppressed in certain types of leukemic cells by inducing differentiation with cytokines that regulate normal hematopoiesis or with other compounds that use alternative differentiation pathways. This created the basis for the clinical use of differentiation therapy. The suppression of malignancy by inducing differentiation can bypass genetic abnormalities that give rise to malignancy. Different CSFs and ILs suppress programmed cell death (apoptosis) and induce cell multiplication and differentiation, and these processes of development are separately regulated. The same cytokines suppress apoptosis in normal and leukemic cells, including apoptosis induced by irradiation and cytotoxic cancer chemotherapeutic compounds. An excess of cytokines can increase leukemic cell resistance to cytotoxic therapy. The tumor suppressor gene wild-type p53 induces apoptosis that can also be suppressed by cytokines. The oncogene mutant p53 suppresses apoptosis. Hematopoietic cytokines such as granulocyte CSF are now used clinically to correct defects in hematopoiesis, including repair of chemotherapy-associated suppression of normal hematopoiesis in cancer patients, stimulation of normal granulocyte development in patients with infantile congenital agranulocytosis, and increase of hematopoietic precursors for blood cell transplantation. Treatments that decrease the level of apoptosis-suppressing cytokines and downregulate expression of mutant p53 and other apoptosis suppressing genes in cancer cells could improve cytotoxic cancer therapy. The basic studies on hematopoiesis and leukemia have thus provided new approaches to therapy.
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PMID:The control of hematopoiesis and leukemia: from basic biology to the clinic. 864 73

Underlying diseases, complications, clinical findings, and laboratory findings were evaluated in 158 cases of septicaemia admitted to Jikei University Hospital from 1975 to 1994, in order to conjectured factors that prescribe for the prognosis. 50% of the patients had underlying diseases. Malignancy including leukaemia (31 cases, 39.2%) was the most common underlying disease, followed by low birth weight infant (17 cases, 21.5%), aplastic anemia (9 case, 11.4%), and congenital heart disease (7 cases, 8.9%). The death rate for patients with underlying disease (27.8%) was significantly greater than the mortality for normal patients with septicaemia (8.9%) (p < 0.05). Meningitis (24.7%) was the most common complication, followed by DIC (19.6%), shock (15.2%), and pneumonia (10.8%). The mortality rate of septicaemia complicated by shock was 66.7% (p < 0.01), and that complicated by DIC was 45.2% (p < 0.01). The mortality rate for patients with the clinical findings of respiratory distress, cough, abdominal distention, cyanosis, splenomegaly, or peripheral coldness was more than 40% and significantly greater (p < 0.01). Mortality rate in patients with granulocyte counts of < 4.000/mm3, platelet counts of < 5 x 10(4)/ mm3, total protein of < 5.0 g/dl, or ESR of < 20 mm/hr were significantly greater (p < 0.01) than those in patients with normal laboratory findings. Coincidence rate of blood and stool cultures was 57.9% for E. coli, and 28.6% for Klebsiella sp., and that of blood and throat cultures was more than 30% for Pseudomonas sp., Haemophilus influenzae, and Staphylococcus aureus. In the study of antimicrobial susceptibility for microorganisms isolated, the number of drug resistant S. aureus had increased in the last 10 years.
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PMID:[Study on septicaemia in infants and children in the past 20 years. Part 2. An analysis of factors that prescribe for the prognosis]. 889 May 45

Malignancy occurs in 2-4% of children infected with human immunodeficiency virus (HIV). The most commonly reported type is non-Hodgkin's lymphoma. We describe the first reported case of chronic myelogenous leukemia (CML) in a child infected with HIV. The initial diagnosis was consistent with Philadelphia chromosome positive acute lymphocyte leukemia. However, on review of the patient's history and the persistence of the Philadelphia chromosome, the diagnosis of CML was made. CML needs to be added to the list of malignancies seen in patients with HIV.
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PMID:Pediatric HIV infection and chronic myelogenous leukemia. 1136 94


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