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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A possible causal association between chromosome structural change and neoplastic transformation has long been mooted, particularly since chromosomal changes occur frequently in the cells of a variety of malignancies. Only in recent years, however, has the evidence in support of this contention begun to appear convincing, and this has followed from the application of developments in cytogenetic techniques. The advent of methods for revealing specific bands in the human metaphase complement has enabled all the chromosomes and many chromosomal regions to be unambiguously identified, and the recent application of prophase banding methods gives further improvements in resolution. With these techniques, specific constitutional chromosomal deletions or translocations have been discovered in inherited cases of retinoblastoma (del.13q14), Wilms' tumour with aniridia (del.11p13) and renal-cell carcinoma (t(3:8) (p21:q24)), in which each of the chromosomal changes appears to be a dominant factor in inheriting a predisposition to a tissue-specific tumour. A heritability for cancer predisposition is also associated with the inherited chromosomal instability syndromes of Bloom's, Fanconi's anaemia and ataxia telangiectasia, although specific chromosomal changes have not been reported to be associated with the neoplasms in such individuals, except in some cases of lymphoma and leukaemia in ataxia telangiectasia. Specific chromosomal translocations have, however, been recorded in a variety of malignancies, with a particular involvement of chromosomes 22, 14, 8, 15, 17 and 21. However, although many hundreds of patients with the specific 9/22 rearrangement seen in chronic myeloid leukaemia and also those with the 14/8 rearrangement in Burkitt's, and other, lymphomas have been described, no single case in which these rearrangements were present as constitutional changes has been reported. The possible nature of the changes seen at the cytogenetic level in terms of gene content of the chromosomes involved is discussed.
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PMID:Cytogenetics of heritability in cancer. 629 35

A case is described which illustrates an acute non-lymphocytic leukemia following multimodal control and apparent cure of Wilms' tumor. Literature cases are reviewed, and therapeutic inadequacies according to present protocols and their importance for the subsequent development of secondary leukemia are discussed.
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PMID:Leukemia in a child with Wilms' tumor. 630 56

Non-random tumour-specific chromosomal abnormalities have been observed in cells of many different human tumours. In Wilms' tumour (WT) and retinoblastoma, a chromosomal deletion occurs germinally or somatically and has been considered an important step in tumour development. One class of potential cellular transforming genes comprises the cellular homologues of the transforming genes of highly oncogenic retroviruses. A remarkable concordance between the chromosomal location of human cellular oncogenes and the breakpoints involved in acquired chromosomal translocations is becoming apparent in various cancers: the oncogenes c-mos, c-myc and c-abl are located at the breakpoints that occur in acute myeloblastic leukaemia, Burkitt's lymphoma and chronic myelocytic leukaemia respectively. Thus when the oncogene c-Ha-ras1 was localized to the short arm of human chromosome 11 (refs 6-8; region 11p11 leads to p15 and not 11p13 as stated in ref. 5), it was proposed as a possible aetiological agent in the aniridia-WT association (AWTA) that results from a deletion of 11p13 (although a transforming gene recently isolated from a WT cell line (G401) was shown not to be homologous to either c-Ha-ras or c-Ki-ras9). We have now looked for deletion or rearrangement of c-Ha-ras1 in the DNA from four subjects with del(11p13)-associated predisposition to Wilms' tumour, aniridia, genitourinary abnormalities and mental retardation. We report here that in no case is c-Ha-ras1 deleted, and we have further refined its location to 11p15.1 leads to 11p15.5. On the basis of enzyme studies and direct gene dosage determination for c-Ha-ras1 and beta-globin in neoplastic and non-neoplastic tissues from one patient, we conclude that deletion of the normal counterpart of 11p cannot account for the development of the tumour.
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PMID:c-Ha-ras1 is not deleted in aniridia-Wilms' tumour association. 631 28

Data from the first four volumes of Cancer Incidence in Five Continents (CI-5) and from the first 5 years of the US Surveillance, Epidemiology and End Results (SEER) program were analyzed for evidence of geographical and temporal variations in the incidence of selected childhood tumors. Only lymphoid leukemia and glial neoplasms are common enough for the observed differences between US registries to be distinguished from sampling variation. Internationally, kidney and eye tumors and leukemia show less geographical variation than do lymphomas and brain tumors, but for none of the tumors examined is the incidence constant. Wilms' tumor rates among Japanese, Singapore Chinese and Indians (Bombay) are approximately 60% of the rates in North America and Britain, whereas in Scandinavia the rates are up to 30% higher. This lessens the status of Wilms' tumor as an "index tumor" of childhood. Areas or countries with especially high or low rates of other tumors are identified. Rates for glial neoplasms (SEER data) and Hodgkin's disease (CI-5) are increasing with time in the US, while brain tumors are being diagnosed more frequently worldwide. However, the results for brain tumors may largely reflect changes in pathology diagnosis or reporting practices, and those for Hodgkin's disease may reflect improvements in case ascertainment. Otherwise, there is a remarkable stability in the incidence of selected childhood cancers over time.
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PMID:Childhood cancer incidence: geographical and temporal variations. 631 78

The frequency of second neoplasms was examined among 487 Wilms' tumor patients treated at the Dana-Farber Cancer Institute and Children's Hospital of Boston, 1927-81. Thirty study patients (6%) developed second primary tumors: 11 cancers, 16 benign tumors, and 3 borderline neoplasms. Cumulative probability of a second cancer was 18% (standard error, 6%) in 34 years after diagnosis of Wilms' tumor. The subgroup of 412 patients who had received radiotherapy for Wilms' tumor developed all 11 second cancers, which included 1 skin carcinoma, 1 acute leukemia, and 9 solid internal cancers (expected, 0.7 cancers other than skin carcinoma; P less than .001). After exclusion of the secondary leukemia, all but 1 second cancer arose within the radiotherapy field. Concurrent therapy with dactinomycin did not reduce the risk of a radiation-associated cancer. Second cancer was the cause of death in 7 patients.
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PMID:Second neoplasms after Wilms' tumor in childhood. 631 34

Since there was no position for a full-time pediatric hematologist, Dr. Wolff practiced general pediatrics for 10 years while he volunteered as director of the hematology clinic at the Babies Hospital. He was appointed full-time Director of Pediatric Hematology in 1959. His early clinical studies were concerned with treatment of erythroblastosis fetalis and use of frequent transfusions and desferroxamine in children with thalassemia. The combined tumor clinic at the Babies Hospital, established in 1952, was one of the first to use the multidisciplinary approach to treatment of the child with cancer. In 1957, the Children's Leukemia Group A, later called the Children's Cancer Study Group, was established by Dr. Joseph Burchenal. Dr. Wolff was one of the first members. This group led to the establishment of various national intergroup committees for clinical study of cancers in children. In 1954, Farber began to use dactinomycin for treatment of Wilms' tumor. At first this drug was used only for treatment of metastatic tumors, but later it was also used to prevent metastases. Subsequently, other childhood tumors were found to be amenable to chemotherapy.
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PMID:Dr. James A. Wolff. III. First pediatric hematologist at Babies Hospital. 639 33

The true survival rates for the various forms of childhood cancer are best determined from a population-based study rather than from the results of clinical trials. Population-based survival rates have been calculated for four periods between 1956 and 1980 in Queensland. There was a significant improvement in survival for children who developed cancer after 1973 compared with those diagnosed before this date. There has however been no significant improvement in the survival rate for childhood cancer overall, or for acute lymphoblastic leukaemia since 1973. Over the 25 year period significant trends in survival rates were seen in acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin's disease, Wilms' tumour, medulloblastoma, and retinoblastoma. No such trend was seen for acute non-lymphoblastic leukaemia, neuroblastoma, rhabdomyosarcoma, juvenile or anaplastic astrocytoma, brain stem glioma, histiocytosis X, or bone tumours. There is a need for continuing research into better methods of treatment of childhood cancer.
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PMID:Childhood cancer survival trends in Queensland 1956-80. 658 17

Contrary to other tumors in children, e.g. leukemia and Wilms tumor the prognosis of which has been considerably improved by the application of surgery, radiotherapy, and chemotherapy, the treatment results of one of the most frequent tumors, namely the neuroblastoma, have not essentially ameliorated during the last few years. The authors present 28 own case records of irradiated patients and describe the clinical symptoms, diagnosis and therapy, especially radiotherapy of the neuroblastoma. A prolongation of the survival time by several months could be achieved in a small group of eight patients treated additionally with an aggressive chemotherapy. The overall long-term prognosis, however, could not be improved hitherto.
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PMID:[Clinical aspects and radiotherapy of stage III and IV neuroblastomas]. 665 53

A retrospective cohort study was conducted on the risk of radiation-induced cancer mortality following cardiac catheterization. The study included 4,891 children with congenital heart disease who were assessed by cardiac catheterization during 1946 to 1968 at The Hospital for Sick Children, Toronto. The cohort was matched against the Ontario cancer death file from 1950 to 1975. The average period of follow-up was 13 years and more than 66,000 person-years have been accrued from the cohort. No deaths from breast cancer or thyroid cancer were identified. Five cancer deaths were observed and compared with 4.8 expected deaths based on Ontario cancer death rates. The five cancer deaths resulted from three leukemias, one Wilms' tumor, and one unspecified nervous system tumor. The preliminary findings did not demonstrate a significant leukemia risk arising from diagnostic cardiac catheterizations. Continued follow-up of this cohort is required to evaluate the risk of breast and thyroid cancers which can occur more than 20 years following radiation exposure.
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PMID:Cancer mortality following cardiac catheterization: a preliminary follow-up study on 4,891 irradiated children. 682 26

A review of the literature indicates that black children in the United States have a lower overall incidence of cancer and are less prone to leukemia and certain solid tumors, including neuroblastoma, rhabdomyosarcoma, Ewing's sarcoma, testicular tumors, liver tumors, and malignant melanoma, than are white children. Black children with acute lymphoblastic leukemia and retinoblastoma, but not with neuroblastoma, Wilms' tumor, and rhabdomyosarcoma, have poorer survival rates than white children. Socioeconomic status appears to be an important reason for the discrepant outlook, but genetic differences may also play a role. Consideration of these issues will assist in planning appropriate treatment regimens.
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PMID:Cancer in black children. 698 10


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