Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most recent progress in the treatment of leukemia and choice of therapies for obtaining "cure" from leukemia are discussed. Chemotherapy can now provide about 40% long term survival in acute myeloblastic leukemia (AML) and about 20% disease-free survival in acute lymphoblastic leukemia (ALL) of adults. Bone marrow transplantation (BMT) should be applied for the patients at risk in those leukemias (Cytogenetic abnormalities for AML and prognostic factors in ALL). In CML patients, BMT offers the only cure. Update result of interferon (IFN) therapy for CML is still a matter of controversy. Ex vivo treatment of autologous cells with IFN or drugs may be beneficial for CML patients without HLA identical donor.
 ...
PMID:[Recent advances in the chemotherapy of leukemias]. 138 49

We analyzed the structural alteration of the p53 gene, by Southern blotting with conventional and/or pulsed-field gel electrophoresis, in patients with Philadelphia chromosome-positive leukemia (chronic myelogenous leukemia; CML, 34 cases and acute leukemia; AL, 5 cases). We found an alteration of the p53 gene in one of 5 AL patients. Loss of heterozygosity was detected in two CML patients with i(17q) chromosome, but we could find no other alterations in the remaining CML patients.
 ...
PMID:Alterations of the p53 gene in Philadelphia chromosome-positive leukemia including chronic myelogenous leukemia and acute leukemia. 139 1

Based on the incidence survey of leukemia and aplastic anemia (AA) from 1986 to 1988, Case control studies (1257 new leukemia cases and 339 new AA cases) were carried out according to the type of leukemia and AA in order to better understand the epidemiologic characteristics of the diseases. Controls were matched randomly (age, sex and ethnic group) from the same population. The data were analyzed with the conditional Logistic multi-regression model and calculated on an IBM-PC/XT. The risk factors of M2a were found to be X-rays, antipyretics, benzene, pesticides and bimolane; that of M3 was chloramphenicol; that of M5 was X-rays; and that of other ANLLs was phenylbutazone. The risk factors of ALL were chloramphenicol, phenylbutazone and family members with cancer; those of CML were X-rays and hepatitis; those of CLL were chloramphenicol and benzene; those of AAA were antipyretics and hepatitis; and that of CAA ws X-rays.
 ...
PMID:[Risk factors analysis of leukemia and aplastic anemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 139 36

The expression of C-myc proto-oncogene were studied at the levels of protein in bone marrow cells obtained from patients with AML and CML. It was found that the expression of C-myc in florid AML and during blast phase of CML were much higher than that in remission of AML and in chronic phase of CML. In 7 cases of AML diagnosed for the first time, 2 cases with high C-myc expression had no remission after 3-6 months, while 5 with rare C-myc expression had remission after 3-6 months. This results suggest that the expression of C-myc proto-oncogene are possibly sensitive indicator of the prognosis of leukemia.
 ...
PMID:[The expression of C-myc oncogene in leukemia and its relationship to clinical symptoms]. 139 24

Tremendous advances in our understanding of acute leukemia have been made through the development of new technologies and close collaboration between immunologists, molecular biologists, and clinical oncologists. These technological advances have included the development of monoclonal antibodies (MoAb) reactive with surface antigens on leukemic cells which can help confirm the lineage and diagnosis of acute leukemia. More importantly, MoAb in conjunction with morphology and cytochemical stains have led to the identification of FAB-MO and the more common recognition of FAB-M7. MoAbs have also helped define prognostic groups, e.g., T-cell leukemia, mature B-cell leukemia, and rare groups such as CD7+ AML. However, the greatest advances in our understanding of acute leukemia has occurred with the application of genetic techniques. Disregulation of genes responsible for normal growth and differentiation initiates the molecular events that lead to the transformation and proliferation of cells recognized clinically as leukemia. Non-random cytogenetic abnormalities apparently contribute to this gene disregulation and specific abnormalities are associated with clinically important subgroups. In acute lymphoblastic leukemia (ALL), the t(9;22), t(1;19), and t(4;11) appear to have a poor prognosis. In acute myeloblastic leukemia (AML), -7/7q-;-5/5q-, 11q23 abnormalities have poor outcomes while t(15;17) and in some series t(9;11), t(8;21), and inv(16) have a good response to therapy. Molecular studies of somatic cell (immunoglobulin and T-cell receptor) gene rearrangements have assisted in the diagnosis and classification of ALL. The application of the polymerase chain reaction technique to specific gene rearrangements has provided a useful approach to minimal residual disease. Specific gene activation (N-myc, evi-1) or fusion genes such as the alpha retinoic acid receptor (alpha RAR) and pml have been identified as the specific cause of some cases of leukemia. The cloning of specific chromosomal breakpoints identified in leukemia (as has been done for CML) will result in specific probes which can be used to make the diagnosis rapidly at the molecular level. Because of the tremendous number of recent developments, this paper will focus only on major developments that will soon have a clinical impact.
Leukemia 1992 Nov
PMID:Pathology and immunology of acute leukemia. 143 16

The human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The origin and spread of human leukemia. 143 86

An attempt to prevent the blast crisis in chronic myeloid leukemia by the use of pulsed doses of (cytarabine cytosine arabinoside) and lomustine was attempted as a cooperative group study by Cancer and Leukemia Group B. The basis for this study was to delay the development of blast crisis by pulsing dose of drugs known to be effective against emerging "blast" cells. The experimental arm which consisted of cytarabine and lomustine did not produce overall results superior to conventional treatment with busulfan. This was related to the non-hematologic effects of the combination which produced significant gastrointestinal toxicity leading to relatively early discontinuation of the combination. Nevertheless, the trial design allowed relatively prompt discontinuation of experimental arm and cross-over to conventional treatment with either hydrea or busulfan. No evidence existed that the use of new drug combinations in CML prejudiced the patient's chance to response to conventional chemotherapy. Thus, a role model for future trials in this disease was developed. With the development of the interferons and other experimental forms of therapy this conceptual development may be of significance.
 ...
PMID:Attempted prevention of blast crisis in chronic myeloid leukemia by the use of pulsed doses of cytarabine and lomustine. A Cancer and Leukemia Group B study. 147 33

Ph1-positive leukemias consist of acute leukemia (Ph1 AL) and CML. Cytogenetically, Ph1 AL is often associated with +6, -7, +8, +21, or +Ph1. CML is predominantly accompanied by +Ph1, +8, i (17q), +19 in myeloid crisis and +Ph1, +8, +21 in lymphoid crisis. Thus, i(17q) seems specific for myeloid crisis of CML. Ph1 constricts ABL/BCR within M-BCR in CML and in one half of the adult Ph1 AL. BCR breaks upstream to M-BCR in the other half of adult AL and in most of childhood AL. However, the breakpoint does not affect clinical and hematological features in AL. Consequently, there seems to be two types of Ph1 leukemia; one is AL representing m-BCR rearrangement and the other is CML and Ph1 AL showing M-BCR rearrangement.
 ...
PMID:[Ph1-positive leukemia: cytogenetic outline and prognosis]. 151 45

Genetic polymorphism of transferrin (Tf) was investigated in Han nationality population in Guangzhou area using isoelectric focusing technique. In addition, three diseases (Leukaemia, Heptocarcinoma, Systemic-lupus-erythematosis, SLE) were also typed for Tf and compared with that in normal population. The increased TfC1 gene frequency in acute myelocytic leukaemia (AML) patients was found (chi 2 = 4.16, P less than 0.05). The increased frequency of TfC1C1 was also observed (P less than 0.05). Relative Incident(RI) was 1.9 But TfC1 gene and TfC1C1 phenotype frequencies did not increase in ALL, CML and primary heptocarcinoma patients. It suggests that TfC1 may relative to AML in this area. Besides, the increased TfC1 gene frequency was observed in SLE patients (chi 2 x 6.15, P less than 0.025). RI of TfC1C2 was 2.3. It suggests that Tfc2 may relate to SLE in this area.
 ...
PMID:[Studies of the relationship between transferrin genetic polymorphism and diseases]. 152 51

A nationwide cooperative incidence survey of leukemia was carried out by the Institute of Hematology, CAMS, from 1986 to 1988. The cooperative survey network covered 46 investigating areas, involving 22 provinces, municipalities and autonomous regions. More than 60 million person-years were supervised and 1670 new cases identified. The annual incidence rate of leukemia was 2.76/10(5) and the 95% confidence interval of population rate ranged from 2.63/10(5) to 2.89/10(5). The incidence rates in oil fields and polluted areas were significantly higher than those in other areas. The incidence rate of ANLL was 1.62/10(5); ALL, 0.69/10(5); CML, 0.36/10(5); CLL, 0.05/10(5); and special types, 0.03/10(5). The incidence rate and constituent ratio of CLL were significantly lower than those in Europe and America. A peak of ALL incidence rate before age 10 was seen; this rate then declined with increasing age until 30. However, the incidence rates of other leukemia rose with age reaching peaks at old age (50-70). The leukemia rate in males was significantly higher than that in females, both in youth (10-29), caused by ALL, and at old age (greater than or equal to 60), mainly caused by ANLL. The incidence rates of ANLL subtypes (including M2b) are also reported.
 ...
PMID:[Incidence survey of leukemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 153 78


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>