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)

Germline p53 mutations carry an increased risk of development of breast cancer, soft tissue and osteosarcomas, brain tumors, leukemia and adrenocortical carcinomas. Cerebral neoplasms are usually of astrocytic lineage and occur in 40% of affected families. This report presents clinical, neuropathological and molecular genetic data from 2 families in France with an identical p53 germline mutation in codon 248 (CGG->TGG; Arg->Trp) and a clustering of CNS tumors. The youngest patient in each family developed a malignant choroid plexus tumor while several young adults of both kindred succumbed to low-grade astrocytoma, anaplastic astrocytoma or glioblastoma. The only non-neural neoplasm was an adrenocortical carcinoma in a boy aged 4 years who developed an anaplastic choroid plexus papilloma 2 years later. Of 2 previously reported inherited choroid plexus tumors, 1 occurred in a family which also carried a germline mutation in codon 248. It remains to be shown whether this unusual pattern of CNS tumors is due to an organ-specific effect of this particular p53 mutation or whether it reflects the genetic background of the affected families.
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PMID:Astrocytomas and choroid plexus tumors in two families with identical p53 germline mutations. 982 43

Childhood cancer incidence patterns for Minnesota, obtained from the Minnesota Cancer Surveillance System, were compared with national rates as well as with historic data from eight Minnesota counties. In total, 1,140 neoplasms were diagnosed in children (ages 0 to 14) between 1988 and 1994. Leukemias were the most common diagnosis for boys (30.3%) and girls (29.6%), followed by central nervous system tumors. The average annual age-adjusted incidence rates for all cancer sites were 167.2 and 136.2 per million for boys and girls, respectively. These rates were somewhat higher than national rates. In particular, the incidence rate for astrocytoma in boys was significantly elevated. Childhood cancer incidence, particularly brain tumors, has increased in the eight-county region from 1969 to 1994. This analysis demonstrated the Minnesota's childhood cancer incidence patterns are similar to national patterns.
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PMID:Childhood cancer incidence and trends in Minnesota, 1988-1994. 986 72

Tropical spastic paraparesis/HTLV-I associated myelopathy (TSP/HAM), is characterized by infiltration of human T cell leukaemia virus type-I (HTLV-I)-infected T-cells, anti-HTLV-I cytotoxic T cells and macrophages into the patients' cerebrospinal fluid and by intrathecally formed anti-HTLV-I antibodies. This implies that the disease involves a breakdown of the blood-brain barrier. Since astrocytes play a central role in establishing this barrier, the authors investigated the hypothesis that the HTLV-I infected T cells disrupt this barrier by damaging the astrocytes. The present study revealed the HTLV-I-producing T cells conferred a severe cytopathic effect upon monolayers of astrocytoma cell line in co-cultures. Following co-cultivation, HTLV-I DNA and proteins appeared in the monolayer cells, but after reaching a peak their level gradually declined. This appearance of the viral components was proved to result from a fusion of the astrocytic cells with the virus-producing T cells, whereas their subsequent decline reflected the destruction of the resulting syncytia. This fusion could be specifically blocked by anti HTLV-I Env antibodies, indicating that it was mediated by the viral Env proteins expressed on the surface of the virus-producing cells. Similar fusion was observed between the HTLV-I-producing cells and certain other human nervous system cell lines. If such fusion of HTLV-I-infected T cells occurs also with astrocytes and other nervous system cells in TSP/HAM patients, it may account, at least partially, for the blood-brain barrier breakdown and some of the neural lesions in this syndrome.
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PMID:Rapid syncytium formation between human T-cell leukaemia virus type-I (HTLV-I)-infected T-cells and human nervous system cells: a possible implication for tropical spastic paraparesis/HTLV-I associated myelopathy. 987 96

We use here the Swedish Family-Cancer Database to analyze the time trends in childhood leukemia and brain cancer between 1960 and 1994 and the effect of parental age on childhood leukemia and brain cancer of some 1500 cases each. The database includes all persons born in Sweden after 1940 with their biological parents, over 6 million individuals, whose cancers were retrieved from the Swedish Cancer Registry from years 1958-1994. Incidence in cancer increased from 1960 to 1994; low grade astrocytoma accounted for most of the increase, whereas high grade astrocytoma has not increased in incidence. There has been a moderate increase in leukemia to about 1980. We found a parental age effect for both leukemia and brain cancer, with the former (of about 50% excess in those over 35 years) being mediated by maternal age and the latter (of about 25% excess) by paternal age. Accumulation of chromosomal aberrations and mutations during the maturation of germ cells is a likely mechanism for these findings. They can help to explain partially the secular trends of these malignancies and the excess risks in offspring of the well educated.
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PMID:Parental age as a risk factor of childhood leukemia and brain cancer in offspring. 1023 Aug 37

New oncologic treatments have improved survival in osteosarcoma and Ewing's sarcoma. However, these treatments may cause secondary malignancies after radiotherapy. This study evaluated the incidence of secondary malignancies after neoadjuvant chemotherapy. Between April 1972 and December 1990, 518 osteosarcoma and 299 Ewing's sarcoma patients entered neoadjuvant chemotherapy protocols. Follow-up records of all patients were analyzed and malignant tumors were reported. Nine patients developed another malignancy, including 5 leukemias, 1 astrocytoma, 1 liposarcoma, 1 parotid, and 1 breast carcinoma. Four leukemias were found in patients treated for osteosarcoma with chemotherapy, but not radiotherapy. Only one leukemia developed after Ewing's sarcoma treated with chemotherapy and radiotherapy. The incidence of leukemias is high, while the other tumors can be explained as unrelated cases. Incidence densities for leukemia were calculated for both groups of patients. Treated osteosarcoma patients seem to have a predisposition to develop leukemias, but whether this is chemotherapy induced needs to be investigated.
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PMID:Secondary tumors in bone sarcomas after treatment with chemotherapy. 1046 88

We describe a 7-year-old girl with therapy-related acute myeloid leukemia (AML) associated with a single and novel karyotypic abnormality. The patient had been treated with alkylating agents and etoposide for hypothalamic pilocytic astrocytoma at age 17 months, and developed mixed lineage AML. Cytogenetic analysis of the leukemic blasts showed 46,XX,der(7)t(7;11)(q22;q14) in all cells examined. Southern blot analysis revealed three copies of an unrearranged MLL gene on chromosome 11q. This is the first report of a triplicated, unrearranged MLL gene in association with a deletion of 7q anomaly and an unbalanced translocation in therapy-related leukemia.
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PMID:A novel chromosomal rearrangement associated with therapy-related acute leukemia. 1068 48

In recent years we observe the increasing number of event-free survivals of patients with acute lymphoblastic leukaemia. It is achieved with multidrug chemotherapy regiment. The important part of protocols is prophylaxis e.g. with radiation therapy of CNS. It is followed by drug toxicity and side effects of treatment (e.g. secondary CNS tumours). In our hospital we observed the case of 6-year-old girl with CNS tumour-astrocytoma. According to the regimen for ALL the radiation therapy of CNS was performed. Three months after neurosurgical operation the local recurrence was observed. The patient died of the progression of disease.
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PMID:[Astrocytoma in a 6-year-old girl after the treatment for acute lymphoblastic leukemia]. 1073 92

Survival following cancer was analysed in relation to ethnic group among children diagnosed in Britain during 1981-1996 and treated at paediatric oncology centres by members of the UK Children's Cancer Study Group. Survival was analysed for 11 diagnostic groups: acute lymphoblastic leukaemia (ALL), acute non-lymphocytic leukaemia, Hodgkin's disease, non-Hodgkin's lymphoma, astrocytoma, primitive neuroectodermal tumour, neuroblastoma, Wilms' tumour, osteosarcoma, Ewing's sarcoma and rhabdomyosarcoma. There were no significant differences in survival between White and non-White children over the study period as a whole. Among children with ALL, however, the relative risk of death allowing for period of diagnosis, age and white blood count was 1.25 for those of South Asian ethnic origin compared with Whites (P = 0.057).
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PMID:Ethnic group and survival from childhood cancer: report from the UK Children's Cancer Study Group. 1075 11

Several publications have recently suggested a relationship between cannabis use and certain types of cancer. We gathered information on the latest findings on the subject. A manual and computerized bibliographic search on cannabis and cancer was conducted. In users under 40 years of age, cannabis is suspected to increase the risk of squamous-cell carcinoma of the upper aerodigestive tract, particularly of the tongue and larynx, and possibly of lung. Other tumours being suspected are non-lymphoblastic acute leukaemia and astrocytoma. In head and neck cancer, carcinogenicity was observed for regular (i.e. more than once a day for years) cannabis smokers. Moreover, cannabis increases the risk of head and neck cancer in a dose-response manner for frequency and duration of use. Interaction was observed with cigarette smoking and alcohol use. Delta9-THC seems to have a specific carcinogenic effect different from that of the pyrolysis products. Epidemiological studies are needed as soon as possible to provide data on the European and French situation. Information on the possible risks of a regular use of cannabis should be a priority.
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PMID:[Cannabis and cancer]. 1108 27

The effects of the production of two closely related cytokines, oncostatin M (OSM) and leukaemia inhibitory factor (LIF), by astrocytoma cells were investigated using the stable cell line human U373-MG, which expressed and secreted both biologically active polypeptides. The expression of LIF by these cells caused resistance to this cytokine due to loss of the LIF receptor (LIFR), from the cell surface, suggesting its retention. In contrast, cells expressing OSM were stimulated by this cytokine, utilizing an autocrine mechanism, and possessed receptors for OSM, but not LIF, on the cell surface. In these cells the continuous up-regulation of OSM-induced gene expression was found even though the Janus kinase-signal transducer and activator of transcription ('JAK/STAT') pathway was almost exhausted due to long-term autocrine stimulation of the cells by OSM. The amount of LIFR was down-regulated in both LIF- and OSM-producing cells and this effect was not found in wild-type U373-MG cells treated with externally added cytokines. To investigate the mechanism of autocrine stimulation by OSM we constructed a stable cell line expressing a form of OSM that is retained in the endoplasmic reticulum (ER). This biologically active cytokine was not secreted, but was localized in the ER. In addition, it did not stimulate the astrocytoma cells in an autocrine manner. We conclude that expression of LIF causes resistance of astrocytoma cells to this cytokine, whereas expression of OSM leads to autocrine stimulation.
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PMID:Differential effects of oncostatin M and leukaemia inhibitory factor expression in astrocytoma cells. 1128 16


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