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)

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

Studies in the 1980s of medically irradiated populations have increased our knowledge of radiation carcinogenesis. (1) Investigations of prenatal x-ray exposures, especially in twins, provide evidence that very low doses of ionizing radiation may cause cancer in humans. (2) Fractionated doses appear as effective as single exposures of the same total dose in causing breast cancer, but seem less effective for lung cancer. (3) Excess breast cancers can occur among women exposed under age 10, indicating that the immature breast is susceptible to the carcinogenic action of radiation. (4) Moderate doses on the order of 1 Gy to the brains of children can cause tumors later in life; moderately high doses to the skin can cause cancer when followed by frequent exposure to ultraviolet light. (5) Radiotherapy for cervical cancer can increase the rate of subsequent leukemia with the best fitting dose-response functions including a negative exponential term to account for cell-killing. (6) Low-dose exposures of about 10 cGy may increase the risk of thyroid cancer. (7) Second cancers following radiotherapy for a variety of cancers occur primarily among long-term survivors. (8) Radiotherapy may not significantly increase the risk of leukemia following childhood cancer, whereas chemotherapy with alkylating agents is a major risk factor. (9) Bone cancer occurs after high-dose radiotherapy for childhood cancer, but children with retinoblastoma are not more susceptible to radiation-induced disease than children with other malignancies. (10) High-dose external beam therapy can cause thyroid cancer, whereas high-dose radioactive 131I may not. (11) Studies of cervical cancer patients indicate that the risk of radiation-induced second malignancies follows a time-response model consistent with a constant multiplication of the underlying background incidence, i.e. a relative risk model seems to hold for projecting risks forward in time.
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PMID:Carcinogenesis--a synopsis of human experience with external exposure in medicine. 304 57

The derivation of an IgG1k monoclonal antibody (HSAN 1.2) recognizing a cell membrane determinant on human neuroblastoma cells is reported. The determinant was found on all 17 cultured human neuroblastoma cells that were tested, but the density of the antigen varied widely on different cell lines. The antibody also bound to fresh and cultured Wilm's tumor cells, retinoblastoma cells, and one of two Ewing's sarcoma cell lines tested, it did not bind to mouse neuroblastoma cells, normal fibroblasts, blood, or bone marrow. Tumor cells that did not stain with HSAN 1.2 included glioma, medulloblastoma, melanoma, rhabdomyosarcoma, mesenchymoma, leukemia, and lymphoma cells. The distribution of the HSAN 1.2 antigen in normal tissues was confined to brain and newborn kidney. As few as 0.1% tumor cells in bone marrow aspirates were detectable by fluorescein-conjugated HSAN 1.2 antibody and flow cytometry. This antibody should be useful for the discrimination of neuroblastoma from other pediatric malignancies, for the detection of tumor cells in metastatic sites such as bone marrow, and for selective removal of neuroblastoma cells from marrow harvested for autologous transplantation.
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PMID:Monoclonal antibody recognizing a human neuroblastoma-associated antigen. 332 7

The Late Effects Study Group (LESG) has collected 368 cases of second malignant neoplasms (SMN) in patients having been previously treated for a first malignancy during childhood. The most frequent first neoplasm is retinoblastoma, followed by Hodgkin's disease. The second neoplasms are essentially sarcomas mostly associated with radiation therapy. Leukemias are also frequent, apparently essentially induced by alkylating agents. The incidence of SMN depends on the primary and on the treatment given, thus it varies according to the studied cohorts. In the most recently analysed material of the LESG, the 20-year incidence was 8%. Children treated for a first neoplasm have an elevated risk of developing a SMN. Genetic predisposition may increase that risk.
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PMID:Risk factors for second malignant neoplasms: report from the Late Effects Study Group. 335 54

A 12-year-old girl with acute lymphoblastic leukemia (ALL) had two types of acquired cytogenetic abnormalities in her pretreatment peripheral blood and bone marrow: hyperdiploidy due to tetrasomy 8, 10, and 21; and, in the hyperdiploid cells, a shift from heterozygosity to homozygosity for a polymorphic variant on chromosome 15. Both abnormalities disappeared after chemotherapy, when the patient entered clinical remission. It has recently been found that shifts to homozygosity occur in retinoblastoma and Wilms' tumor. Our observation extends this finding to leukemia and indicates that such shifts may have general importance in tumorigenesis.
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PMID:Somatic shift to homozygosity for a chromosomal polymorphism in a child with acute lymphoblastic leukemia. 345 27

The statewide population-based New Mexico Tumor Registry identified 473 malignant tumors among children of ages 0-14 years, during the period 1970-82. There were 235 non-Hispanic whites (50%), 189 Hispanic whites (40%), 38 American Indians (8%), and 11 other nonwhites (2%). The average annual age-adjusted incidence rates per million for non-Hispanic whites were 138.6 for males and 108.3 for females; for Hispanic whites, the rates were 108.5 for males and 80.9 for females; for American Indians, the rates were 75.5 for males and 78.0 for females. The incidence rates for all sites of cancer combined were lower for Hispanics and American Indians than for New Mexico's non-Hispanic whites and U.S. whites. Leukemia was the most common cancer in all racial-ethnic groups. In comparison with U.S. whites, American Indians were at low risk for leukemias, lymphomas, central nervous system (CNS), sympathetic nervous system (SNS), and kidney tumors and were at high risk for retinoblastoma, bone, and sex organ tumors. Hispanics were at low risk for CNS, SNS, kidney, sex organ, and liver tumors. Hispanic and non-Hispanic white males both were at increased risk for melanoma.
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PMID:Childhood cancer epidemiology in New Mexico's American Indians, Hispanic whites, and non-Hispanic whites, 1970-82. 345 38

Increasing attention is being given to the occurrence of second primary tumours among survivors of childhood cancer. Our aims are to examine the risk of a subsequent primary, particularly in relation to chemotherapy, in a well-defined cohort; and to examine interesting associations between first and second primary tumours in relation to therapy generally and chemotherapy in particular among a less well-defined group of cases developing at least two primary tumours. There is suggestive evidence from our data that chemotherapy is involved either directly or indirectly in the development of secondary leukaemia, and this confirms previous work. Our data, although based on small numbers, indicate consistent evidence of an association between cyclophosphamide and an increased risk of a second primary tumour following retinoblastoma; this may be due to cyclophosphamide, radiotherapy or an interaction between the two. Two cases of uterine cancer were observed among three patients given oestrogen replacement therapy.
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PMID:Second primary tumours among survivors of childhood cancer treated with anticancer drugs. 347 36

One hundred and sixty one children who have developed more than one primary neoplasm have been identified. Children with tumours of the central nervous system, retinoblastoma and leukaemia were those most frequently observed to develop a second malignancy whilst osteosarcoma was the most common second tumour. The patterns of second neoplasms appear to be changing and a recent increase in the number of children with leukaemia and lymphoma who develop second primary tumours has been observed. In this series, the two most frequent associations of tumours were retinoblastoma followed by osteosarcoma and the combination of acute leukaemia with a tumour of the central nervous system. Genetic factors which may have contributed to the development of the second primary tumour were identified in 53 patients (33%), 33 of whom had the genetic form of retinoblastoma. In an analysis of the treatment of 151 patients, for whom the interval between the two neoplasms was greater than 12 months, the second malignancy was considered to be 'radiation associated' in 93 (61%). Fifty children (33%) had been treated with either single or multiple agent chemotherapy which included an alkylating agent in 38. Forty five children had received a combination of chemotherapy and radiotherapy and of these, 10 developed leukaemia as their second tumour. Of the 19 secondary leukaemias, 16 have occurred in patients treated since 1970.
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PMID:Patterns of multiple primary tumours in patients treated for cancer during childhood. 347 72

Recently, the National Cancer Institute published a comprehensive monograph on multiple primary cancers in Connecticut and Denmark. This paper summarizes some of the observations made on the Connecticut population. Data compiled by the Connecticut Tumor Registry have extended our knowledge about the patterns of multiple primary cancers, especially among long-term survivors of cancer and among patients with relatively rare tumors about which little information currently exists. When compared with the general Connecticut population, cancer patients had a 31 percent (RR = 1.31) increased risk of developing a second cancer and a 23 percent (RR = 1.23) elevated risk of second cancer at a different site from the first. Common environmental exposures seemed responsible for the excess occurrence of many second cancers, particularly those related to cigarette smoking, alcohol consumption, or both. For example, persons with epithelial cancers of the lung, larynx, esophagus, buccal cavity, and pharynx were particularly prone to develop new cancers in the same or contiguous tissue throughout their lifetimes. Cancers of the colon, uterine corpus, breast, and ovary frequently occurred together, suggesting underlying hormonal or dietary influences. Only patients with prostate cancer were at significantly low risk for second cancer development; this might be an artifact of case finding, since advanced age at initial diagnosis was generally associated with an underascertainment of second cancers. Radiotherapy may have caused rectal and other cancer among patients with cancers of the female genital tract, and leukemia among patients with uterine corpus cancer. Chemotherapy with alkylating agents probably contributed to the excess of acute nonlymphocytic leukemia following multiple myeloma or cancers of the breast and ovary. Genetic susceptibility seemed to explain some tumor complexes, such as the multiple occurrences of cutaneous melanoma and the excess of bone cancer following retinoblastoma. Research into multiple cancer syndromes should enhance our understanding of carcinogenic factors and mechanisms and the development of strategies for cancer prevention and control.
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PMID:Multiple primary cancers in Connecticut, 1935-82. 354 9

Neuroblastoma (NB) arises from primitive sympathetic neuroblasts in the adrenal gland or the sympathetic ganglion. NB in situ, sometimes observed in the adrenal glands of autopsied infants, is considered to be a premalignant lesion that may develop into NB. Little is understood about the morphological and biochemical changes that accompany this malignant progression. In this study, a unique monoclonal antibody, KP-NAC8, raised against a human NB cell line is described. This binds to NB cells but not to fetal neuroblasts. The antibody recognizes a Mr 200,000 surface protein on NB cells. KP-NAC8 binds to 15 of 17 human NB cell lines and all 26 fresh NB samples either from tumor tissues or from marrow aspirates involved with tumor. The antibody was found to cross-react with some other tumor cell lines, namely, Ewing's sarcoma (1 of 2), melanoma (1 of 4), lung cancer (3 of 3), and leukemia (2 of 14) cell lines. However, KP-NAC8 did not bind to any rhabdomyosarcoma (0 of 4), Wilms' tumor (0 of 4), retinoblastoma (0 of 2), glioma (0 of 4), and gastric cancer (0 of 2) cell lines examined. Among fetal tissues, KP-NAC8 did not react with normal neuroblasts in the adrenal glands of 5 fetuses. In a further study, the membrane phenotype of fetal adrenal neuroblasts was analyzed by a panel of 12 monoclonal antibodies including KP-NAC8. A comparison of the binding of the same panel of antibodies to fresh NB revealed that antibodies UJ13A, UJ127:11, PI153/3, anti-Thy-1, A2B5, BA-1, BA-2, HSAN1.2, and Leu-7 bound to both fetal adrenal neuroblasts and NB cells. Monoclonal antibodies OKIa-1 and J5 did not bind to either tissues. The only antibody that could distinguish fetal adrenal neuroblasts from NB cells was KP-NAC8. KP-NAC8 may, therefore, define a differentiation-related antigen that may prove helpful in understanding the biological nature of NB and NB in situ.
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PMID:Cell surface membrane antigen present on neuroblastoma cells but not fetal neuroblasts recognized by a monoclonal antibody (KP-NAC8). 356 10


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