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

The distribution of oncornavirus DNA sequences in various tissues of normal chickens and of chickens with leukemia or kidney tumors induced by avian myeloblastosis virus (AMV) was analyzed by DNA-RNA hybridization using 35S AMV RNA as a probe. All the tissues from normal chickens which were tested contained the same average cellular concentration of endogenous oncornavirus DNA. In contrast, different tissues from lekemic chickens and from chickens bearing kidney tumors contained different concentrations of AMV homologous DNA: in some tissues there was no increase whereas other tissues acquired additional AMV-specific DNA sequences. The increase was the greatest in tissues which can become neoplastic after infection, such as myeloblasts, erythrocytes, and kidney cells. It was directly demonstrated that DNA from AMV-induced kidney tumor contains AMV sequences which are absent in DNA from normal cells. A similar finding had been previously obtained with leukemic cells (15). 3H-labeled 35S RNA from purified AMV was exhaustively hybridized with an excess of normal chicken DNA to remove all the viral RNA sequences which are complementary to DNA from uninfected cells. The 3H-labeled RNA which failed to hybridize was isolated by hydroxylapatite column chromatography which separates DNA-RNA hybrids from single-stranded RNA. The residual RNA hybridized to chicken kidney tumor DNA but did not rehybridize with normal chicken DNA.
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PMID:Acquisition of viral DNA sequences in target organs of chickens infected with avian myeloblastosis virus. 17 Apr 15

Cancer mortality among children in the United States, 1950 through 1979, as evaluated by death certificate diagnoses, revealed dramatic declines primarily in the second half of the 30-year interval. The numbers of deaths of persons younger than 15 years, 1965 through 1979, as compared with the number expected at 1950 rates, fell 50% for leukemia, 32% for non-Hodgkin's lymphoma, 80% for Hodgkin's disease, 50% for bone sarcoma, 68% for kidney cancer, and 31% for all other cancer. There were 17,411 fewer deaths from childhood cancer from 1965 through 1979 than expected at the 1950 rate. Leukemia mortality declined by 8,073 deaths and kidney tumor mortality by 2,393. In data subsequently received for 1980, the decline in rates persisted for leukemia and non-Hodgkin's lymphoma, but the rates for the other four cancer categories seem to have reached a plateau. The reduction in mortality is attributed to improved therapy.
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PMID:Decline in US childhood cancer mortality. 1950 through 1980. 636 67

The present study was undertaken to detect the spontaneous mammary tumor-associated antigen ( MTAA ), and to find the cross-reacting antigen in chemically-induced mammary tumor. The antisera against spontaneous mammary tumor were raised in the WAF1 rats of the same strain and tested for the detection of tumor-associated soluble antigen of mammary tumor induced by N-ethylnitrosourea (ENU) and N-butylnitrosourea ( BNU ). The MTAA was found in the extract of spontaneous mammary tumor by the double immunodiffusion test, while it was not found in the extract of normal and fetal tissues, hyperplastic mammary gland, spontaneous fibroadenoma, and chemically-induced mammary tumor. On the other hand, the MTAA was not detected in the other types of tumors induced by ENU or BNU , i.e. gastric cancer, intestinal tumor, brain tumor, kidney tumor, bladder tumor, hemangioma, rhabdomyosarcoma, or leukemia. The spontaneous MTAA could not be detected in the spontaneous mammary tumor of C3H mice or human breast cancer either. The MTAA was extracted effectively by 3 M KC1. Furthermore, the MTAA was found in the cytoplasm of continuous established mammary tumor cell line ( SpMT -1) by the immunofluorescence test.
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PMID:Tumor-associated antigen of spontaneous mammary tumor in rats. 642 20

A candidate tumor suppressor gene, MMAC1/PTEN, located in human chromosome band 10q23, was recently identified based on sequence alterations observed in several glioma, breast, prostate, and kidney tumor specimens or cell lines. To further investigate the mutational profile of this gene in human cancers, we examined a large set of human tumor specimens and cancer cell lines of many types for 10q23 allelic losses and MMAC1 sequence alterations. Loss of heterozygosity (LOH) at the MMAC1 locus was observed in approximately one-half of the samples examined, consistent with the high frequency of 10q allelic loss reported for many cancers. Of 124 tumor specimens exhibiting LOH that have been screened for MMAC1 alterations to date, we have detected variants in 13 (approximately 10%) of these primary tumors; the highest frequency of variants was found in glioblastoma specimens (approximately 23%). Novel alterations identified in this gene include a missense variant in a melanoma sample and a splicing variant and a nonsense mutation in pediatric glioblastomas. Of 76 tumor cell lines prescreened for probable LOH, microsequence alterations of MMAC1 were detected in 12 (approximately 16%) of the lines, including those derived from astrocytoma, leukemia, and melanoma tumors, as well as bladder, breast, lung, prostate, submaxillary gland, and testis carcinomas. In addition, in this set of tumor cell lines, we detected 11 (approximately 14%) homozygous deletions that eliminated coding portions of MMAC1, a class of abnormality not detected by our methods in primary tumors. These data support the occurrence of inactivating MMAC1 alterations in multiple human cancer types. In addition, we report the discovery of a putative pseudogene of MMAC1 localized on chromosome 9.
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PMID:MMAC1/PTEN mutations in primary tumor specimens and tumor cell lines. 939 38

The WT1 gene is a tumor-suppressor gene that was isolated as a gene responsible for Wilms' tumor, a childhood kidney neoplasm. We have previously reported that the WT1 gene is strongly expressed in leukemia cells with an increase in its expression levels at relapse and an inverse correlation between its expression levels and prognosis, thus making it a novel tumor marker for leukemic blast cells. Furthermore, WT1 antisense oligomers have been found to inhibit the growth of leukemic cells. These results strongly suggested the involvement of the WT1 gene in human leukemogenesis. The present study was performed to prove our hypothesis that the WT1 gene plays a key role in leukemogenesis and performs an oncogenic function in hematopoietic progenitor cells, rather than a tumor-suppressor gene function. 32D cl3, an interleukin-3-dependent myeloid progenitor cell line, differentiates into mature neutrophils in response to granulocyte colony-stimulating factor (G-CSF). However, when transfected wild-type WT1 gene was constitutively expressed in 32D cl3, the cells stopped differentiating and continued to proliferate in response to G-CSF. As for signal transduction mediated by G-CSF receptor (G-CSFR), Stat3alpha was constitutively activated in wild-type WT1-infected 32D cl3 in response to G-CSF, whereas, in WT1-uninfected 32D cl3, activation of Stat3alpha was only transient. However, most interesting was the fact that G-CSF stimulation resulted in constitutive activation of Stat3beta only in wild-type WT1-infected 32D cl3, but not in WT1-uninfected 32D cl3. Thus, WT1 expression constitutively activated both Stat3alpha and Stat3beta. A transient activation of Stat1 was detected in both wild-type WT1-infected and uninfected 32D cl3 after G-CSF stimulation, but no difference in its activation was found. No activation of MAP kinase was detected in both wild-type WT1-infected and uninfected 32D cl3 after G-CSF stimulation. These results demonstrated that WT1 expression competed with the differentiation-inducing signal mediated by G-CSFR and constitutively activated Stat3, resulting in the blocking of differentiation and subsequent proliferation. Therefore, the data presented here support our hypothesis that the WT1 gene plays an essential role in leukemogenesis and performs an oncogenic function in hematopoietic progenitor cells and represent the first demonstration of an important role of the WT1 gene in signal transduction in hematopoietic progenitor cells.
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PMID:Wilms' tumor gene (WT1) competes with differentiation-inducing signal in hematopoietic progenitor cells. 953 8

Human T cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T cell leukemia and HTLV-I-associated myelopathy/tropical spastic paraparesis. The HTLV-I protein Tax is well known as a transcriptional transactivator and inducer of cellular transformation. However, it is also known that extracellular Tax induces the production and release of cytokines, such as tumor necrosis factor-alpha and interleukin-6, which have adverse effects on cells of the central nervous system. The cellular process by which Tax exits the cell into the extracellular environment is currently unknown. In most cell types, Tax has been shown to localize primarily to the nucleus. However, Tax has also been found to accumulate in the cytoplasm. The results contained herein begin to characterize the process of Tax secretion from the cell. Specifically, cytoplasmic Tax was demonstrated to localize to organelles associated with the cellular secretory process including the endoplasmic reticulum and Golgi complex. Additionally, it was demonstrated that full-length Tax was secreted from both baby hamster kidney cells and a human kidney tumor cell line, suggesting that Tax enters the secretory pathway in a leaderless manner. Tax secretion was partially inhibited by brefeldin A, suggesting that Tax migrated from the endoplasmic reticulum to the Golgi complex. In addition, combined treatment of Tax-transfected BHK-21 cells with phorbol myristate acetate and ionomycin resulted in a small increase in the amount of Tax secreted, suggesting that a fraction of cytoplasmic Tax was present in the regulated secretory pathway. These studies begin to provide a link between Tax localization to the cytoplasm, the detection of Tax in the extracellular environment, its possible role as an extracellular effector molecule, and a potential role in neurodegenerative disease associated with HTLV-I infection.
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PMID:Secretion of the human T cell leukemia virus type I transactivator protein tax. 1565 97

The Wilms tumor gene was identified as a tumor suppressor gene responsible for a particular type of kidney tumor. Several years ago, it was demonstrated that it is also overexpressed in acute and chronic leukemias. Although the exact role of this gene in the hematopoietic system is still quite completely obscure, it represents a reliable marker for the detection of the presence of leukemic cells. WT1 quantitative assessment may therefore represent a useful tool for the diagnosis and follow up of leukemia patients. In this chapter, we describe the method for the quantification of WT1 transcript by real-time polymerase chain reaction.
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PMID:WT1 overexpression in acute myeloid leukemia and myelodysplastic syndromes. 1650 87

Recently, the US Food and Drug Administration proposed a ban on over-the-counter hydroquinone mainly on the basis of high absorption, reports of exogenous ochronosis in humans, and murine hepatic adenomas, renal adenomas, and leukemia with large doses over extended time periods. Systemic exposure to hydroquinone from routine topical application is no greater than that from quantities present in common foods. While murine hepatic adenomas increased, murine hepatocellular carcinomas decreased, suggesting a protective effect. Renal tumors are sex, species, and age specific and therefore do not appear relevant to humans after decades of widespread use. Murine leukemia has not been reproducible and would not be expected from small topical doses. Finally, a literature review of exogenous ochronosis and clinical studies employing hydroquinone (involving over 10,000 exposures under careful clinical supervision) reveal an incidence of exogenous ochronosis in the United States of 22 cases in more than 50 years. Therefore, the proposed ban appears to be unnecessarily extreme.
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PMID:The safety of hydroquinone: a dermatologist's response to the 2006 Federal Register. 1746 15