Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of cancer resembles that of many other diseases in that multiple factors may be required. Because of this, the role or viruses in the etiology of human cancers is especially difficult to assess. When animal tumor systems were used as models, the roles of various predisposing characteristics in virus oncogenesis were elucidated. Extrapolation of these findings to the human diseases suggests the importance of genetics, age, hormones, immune competence, and stress in determining susceptibility to tumor development in individuals infected with an oncogenic virus. The importance of cofactors in induction of those human tumors most strongly associated with virus infection, including Burkitt's lymphoma, nasopharyngeal carcinoma, cerviccal carcinoma, acute myelogenous leukemia, and breast cancer, is reviewed. Understanding of the role of these cofactors in virus carcinogenesis may lead to disease prevention through elimination of one or more of the cofactors.
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PMID:The viral etiology of cancer: a realistic approach. 19 10

Since initial studies identifying the important role of vitamin A and its derivatives (retinoids) in maintaining the integrity of epithelial tissues, these compounds have served as paradigms for experimental studies exploring the pharmacologic modification of carcinogenesis. Retinoids have clearly been shown to inhibit chemically induced mammary and urothelial carcinogenesis in experimental animals. Prohibitive toxicity of the parent compound, vitamin A, led to a systematic search for synthetic derivatives with an improved therapeutic index. More than 1500 such compounds have been synthesized, many retaining chemopreventive potential, but with less toxicity. Although several anecdotal reports confirming therapeutic benefits of cis-retinoic acid in patients with acute promyelocytic leukemia and myelodysplastic syndromes appeared in the late 1970s and early 1980s, the remarkable studies of Huang and his colleagues in China in 1988 reporting complete remissions in patients with this uncommon variety of acute myelogenous leukemia with the transisomer of retinoic acid (all-trans-retinoic acid) led to a resurgence of interest in the retinoids as differentiating agents for the prevention and therapy of cancer. Furthermore, molecular studies showing DNA rearrangements of the alpha nuclear receptor for retinoic acid located on chromosome 17 in patients with acute promyelocytic leukemia, a disease invariably associated with a translocation between chromosomes 15 and 17, provided a direct connection between an altered nuclear receptor and the development of a human malignancy. The retinoids also may have important beneficial effects in prevention of recurrent malignancies once the primary tumor has been treated, such as in squamous cell carcinoma of the head and neck. Because retinoids appear to be less effective in inducing differentiation in nonpromyelocytic leukemia cells, investigators have conducted a number of studies to exploit potential synergism between retinoids and other differentiating agents or biologic effectors. Differentiation therapy and chemoprevention are attractive alternative approaches to intensive cytotoxic chemotherapy. It is now clear that retinoids represent one class of compounds with which it may be possible to reverse the progression of malignant disease and prevent carcinogenesis.
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PMID:Retinoids in cancer treatment. 144 94

Simultaneous tumors are rarely encountered during the course of acute leukemias. We report on a case of seminoma of the testis that occurred during the evolution of acute myelogenous leukemia. To our knowledge, this simultaneous association has not previously been described, but a causal relationship was not apparent in the present case. The likelihood of a common carcinogenesis existed, but direct exposure to carcinogens could not be established. Although the results of a physical examination and echography were normal at the time of diagnosis, we cannot exclude the presence of microscopic cancer of the testis. Since the dissemination pattern of seminoma is usually slower than that observed in this case and the disease remains limited to the lymph nodes for long periods following dissemination, the rapid development of the present case might have been attributable to the immunosuppression and the scrotal sepsis that occurred during the induction therapy. Immunosuppression might have stimulated the progression of a primary microscopic seminoma and the development of metastasis, whereas the scrotal sepsis and inflammation might have favored the occurrence of metastasis through bypass of the lymphatic barrier.
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PMID:Simultaneous occurrence of acute myelogenous leukemia and seminoma of the testis. 162 74

The frequency of chromosome aberrations in the peripheral blood of patients successfully treated for Hodgkin's disease (HD) and non-Hodgkin's lymphoma is compared with that seen in age-matched haematologically normal subjects. Findings are considered in relation to risk factors associated with the development of secondary myelodysplastic syndrome (MDS) or acute myeloid leukaemia (AML). Overall aberration frequencies were not significantly increased in patients compared with normal subjects. However, there were differences in aberration type. The frequency of exchanges was significantly higher among patients (P less than 0.01) and the frequency of gaps lower (P less than 0.0005). The mean frequency of exchanges was also greater in patients receiving multiple compared to single courses of therapy (P less than 0.0005) and in patients receiving radiotherapy or combined modality therapy compared to chemotherapy alone (P less than 0.005 and P less than 0.0005). Four patients had aberration frequencies greater than 2 SD above the patient mean. One of these was also found to have a mutation of the ras oncogene. None of the patients has yet developed secondary MDS/AML.
Carcinogenesis 1992 Jul
PMID:Chromosome aberrations following cytotoxic therapy in patients in complete remission from lymphoma. 163 73

Flow cytometry (FCM) is a useful method for clinical research of oncogene products since it can analyze proteins quantitatively which are located at cell surfaces or inside of cells. Oncogene products are now under study by FCM not only as tumor markers but also as functioning proteins in carcinogenesis. The examples of oncogene products analyzed by FCM are ras, myc, p53, myb and fos; those of cell-proliferation-related proteins are Ki-67, PCNA and DNA polymerase alpha. In some diseases the relationship between these proteins and disease classification, stage, pathophysiology, or prognosis have been clarified. Using dual color FCM of H-ras p21 and DNA, we analyzed the expression of H-ras p21 in human multiple myeloma and leukemias and found that H-ras p21 levels in multiple myeloma strongly correlated to the prognosis of patients (p = 0.03). When AML cells were stimulated by adding G-CSF, it was found that many cells proliferated but some were dying. The percentage of dying cells was small in one AML case whose myeloblasts showed increased expression of H-ras p21 by G-CSF stimulation. Together with other papers reviewed, it is conceivable that H-ras p21 expression is related to cell proliferation and inhibition of cell autolysis. Thus FCM is useful in the classification of the role of oncogene products in carcinogenesis in clinical cases.
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PMID:[Application of flow cytometry to the study of hematologic disorders: analysis of oncogene products]. 214 49

The clonal malignancies of acute myeloid leukemia and the myelodysplastic syndromes are associated with numerous chromosomal and oncogenic abnormalities. Activation of oncogenes has been demonstrated, although there is little evidence that this alone causes malignant transformation of diploid cells as a consequence. Patterns of abnormalities can be seen as the patient progresses from myelodysplastic syndrome to acute myeloid leukemia, but no unique or invariant findings have been described. Chromosomal changes, with the exception of some translocations, are neither disease nor lineage specific. At this time the data provide good support for the multistep view of carcinogenesis, and there is indirect or circumstantial evidence for the presence of tumor suppressor genes on 5q and 7q. The continued study of these clonal hematological disorders will provide considerable insight into mechanisms of tumorigenesis and possibly may lead to new modes of therapy, for example, through altering the microenvironment, interfering with deranged signal transmission, or introducing antioncogenes.
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PMID:Oncogene involvement in myelodysplasia and acute myeloid leukemia. 224 55

The role of oncogenes in carcinogenesis is intensively studied. Certain oncogenes are often found in some kinds of tumors. In acute myeloid leukemia (AML), of all oncogenes presently known, only those belonging to the ras group are activated in a larger number of cases. In single cases myc, myb, sis, and ets oncogenes have been found. It is possible that a disorder in regulation of myc and myb protooncogenes exists in AML.
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PMID:[Oncogenes in acute myeloid leukemia]. 269 10

While the carcinogenicity of asbestos has been established in malignant mesotheliomas and lung cancers, and has recently been suspected in several other types of cancer, asbestos has not been implicated in the pathogenesis of acute leukemias. This article includes two cases of acute myelocytic leukemia in individuals with a long history of exposure to asbestos. Significant numbers of asbestos bodies were detected in specimens of their lungs and bone marrow. In addition, the kind of asbestos in both organs was crocidolite, which is implicated in carcinogenesis. No asbestos bodies were detected in the bone marrow specimens from a control group consisting of ten patients with lung cancer with similar occupational histories. The role of asbestos exposure in the development of leukemia requires further study.
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PMID:Acute myelocytic leukemia after exposure to asbestos. 284 Jan 93

The levels of adenosine diphosphate ribosyl transferase (ADPRT) have been quantified in Ficoll-Isopaque isolated marrow cells from 36 patients with acute myeloid leukemia (AML). The in vitro growth pattern in agar at diagnosis was also determined, and in 16 patients the in vitro drug sensitivity of the clonogenic cells (CFU-GM) to cytosine arabinoside and daunorubicin was measured. The ADPRT activities of the various marrow cell preparations correlated to the morphological diagnoses, in vitro growth patterns, in vitro drug sensitivities to cytosine arabinoside, and to the prognoses of the AML patients. Hence, ADPRT may be a useful marker for the pathophysiology associated to AML.
Carcinogenesis 1985 Jul
PMID:Adenosine diphosphate ribosyl transferase in marrow cells of patients with acute myeloid leukemia is related to differentiation and drug sensitivity. 299 Jul 54

Within a very short time the application of molecular biology to cancer research has resulted in an essential change and extension of our knowledge of transformation processes and tumor development. For the first time these mechanisms can be understood in a causal manner and causal cancer therapy seems to be possible in the near future. In this manuscript an attempt is made to give a brief survey of the influence of oncogenes on carcinogenesis. An account is given of the origin of viral oncogenes, viral mechanisms of cell transformation and activation of cellular oncogenes. Additionally, kinetics and targets of tumor proteins are discussed. The complexity and diversity of genetic regulation of growth and differentiation is discussed in some well known diseases such as chronic myeloid leukemia, Burkitt lymphoma, retinoblastoma and acute myeloid leukemia.
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PMID:[Oncogenes]. 303 83


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