J U Cope

National Cancer Institute (USA), 베서스다, Maryland, United States

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Publications (4)6.55 Total impact

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    ABSTRACT: Researchers have speculated that surgical excision of lymphoid tissue, such as appendectomy, early in life might confer an increased risk of cancer. In this study, we determined the risks of cancer for people who had appendectomy performed during childhood. We studied the risk of cancer in a large Swedish cohort of children who had appendectomy performed during the period of 1965-1993. Standardized incidence ratios (SIRs) were computed using age-, gender-, and period-specific incidence rates derived from the entire Swedish population as comparison. Hospital discharge diagnosis data were used to examine cancer risks by categories of surgery, medical conditions, and type of appendicitis. The average length of follow-up was 11.2 years. We found no excess overall cancer risk but noted a significant excess for stomach cancer (SIR: 2.45; 95% confidence interval [CI]: 1.1-4.8) and a borderline increase of non-Hodgkin's lymphoma (NHL; SIR: 1.55; 95% CI: 1.0-2.3). The elevated risks for both cancers were only evident 15 or more years after appendectomy (stomach cancer, SIR: 3.82; 95% CI: 1.7-7.5; NHL, SIR: 2.49; 95% CI: 1.4-4.2). It is reassuring that there was no overall increase of cancer several years after childhood appendectomy. Increased risks for NHL and stomach cancer, occurring 15 or more years after appendectomy, were based on small absolute numbers of excess cancers. As 95% of the subjects were younger than 40 years at exit, this cohort requires continuing follow-up and monitoring.
    No preview · Article · Jul 2003 · PEDIATRICS
  • Judith U. Cope · Maria Tsokos · Robert W. Miller
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    ABSTRACT: Excesses of various childhood cancers have been reported after retinoblastoma, including a trickle of Ewing sarcoma (ES) and perhaps histologically similar olfactory neuroblastoma, both of which are neural tumors. To update and advance this information, case reports were sought by an extensive review of the literature. The search was made through the use of PubMed, and the Web of Science (Citation Index Expanded), keying on primary references. Three sinonasal cancers diagnosed as ES were immunohistochemically stained for MIC-2 protein (positive in ES). Retinoblastoma occurred before ES in ten cases (seven bilateral). In four others, retinoblastoma (three bilateral) developed before sinonasal neural tumors (poorly differentiated). ES also occurred after 14 cancers other than retinoblastoma (five lymphomas, four leukemias, and one each of five miscellaneous cancers). The predominance of retinoblastoma prior to ES differs markedly from the low-frequency of retinoblastoma among childhood cancers in the general population. On the contrary, cancers other than retinoblastoma were proportionate to those in the general population. Previously, retinoblastoma followed by excesses of osteosarcoma and soft tissue sarcomas has been attributed to the action of the inherited RB-1 gene. The sinonasal tumors stained negative for MIC-2 protein. Heritable retinoblastoma may predispose to ES and perhaps to a subset of poorly differentiated neuroectodermal tumors in the sinonasal region that may be related to olfactory neuroblastoma.
    No preview · Article · Feb 2001 · Medical and Pediatric Oncology
  • J U Cope
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    ABSTRACT: Despite the finding of characteristic somatic mutations in the tumor tissue and efforts to identify risk factors, the etiology of Ewing's sarcoma (ES) is still unknown. ES is very different from other childhood bone cancers. It rarely occurs in the black population and has no animal model. Recently studies indicate that ES may have a neural, not mesenchymal, origin. It has a distinctive unimodal age-incidence peak at adolescence. Because its incidence curve pattern has a striking resemblance to that of DES-related clear cell adenocarcinoma of the vagina, an in utero exposure might be considered. Although in utero chemical and hormonal exposures have not been found to be associated with ES in epidemiologic studies, we suggest that its etiology could be an in utero viral infection. We hypothesize that the epidemiological characteristics of ES suggest an association with cytomegalovirus (CMV).
    No preview · Article · Dec 2000 · Medical Hypotheses
  • J U Cope · M Tsokos · L J Helman · G Gridley · M A Tucker
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    ABSTRACT: Various congenital anomalies have been associated with childhood cancer, but as yet no anomaly has been consistently found with Ewing sarcoma (ES). Recently a large case-control study of ES patients reported a greater number of hernias in both cases and their sibling controls than in population controls. Most of these hernias were inguinal. Because these anomalies were also reported previously in two case series, we looked for inguinal hernias in a different population of ES patients. We abstracted medical records for 306 pathologically confirmed ES/primitive neuroectodermal tumor (PNET) patients seen at NIH between 1960 and 1992. Epidemiological data on demographics and medical conditions were analyzed. The frequency of anomalies was compared to expected rates to calculate relative risk and confidence intervals. Anomalies were present in 67 (22%) cases. A particular anomaly, inguinal hernia, was reported for 13 (5%) NIH cases. Compared to population estimates for white children, the relative risk of inguinal hernia among white NIH cases was 13.3 (95% CI 3.60-34.1) for females and 6.67 (95% CI 2.67-13.7) for males. The findings of inguinal hernias in some patients with ES suggest that a disruption in normal embryological development occurred. This may provide an important clue to the etiology of ES. We hypothesize that these hernias may relate to an in utero exposure or indicate an underlying genetic disorder. Future studies should carefully evaluate ES families for genetic disease and explore environmental factors. Med. Pediatr. Oncol. 34:195-199, 2000. Published 2000 Wiley-Liss, Inc.
    No preview · Article · Apr 2000 · Medical and Pediatric Oncology

Publication Stats

45 Citations
6.55 Total Impact Points


  • 2000-2003
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Genetic Epidemiology
      베서스다, Maryland, United States