Pediatric cancers. Pediatric Oncology Workgroup, Legislative Task Force on Cancer in Texas.
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Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
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Chemotherapy with Platinum Compounds: Current Status and Future Directions. Volume 3: Dosing, Head and Neck Cancer, Genitourinary Cancer, Pediatric Cancer, Tumor of Unknown Origin, Dose Intensity, Future Directions. Kona, Hawaii, February 24-28, 1993.
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Oncology Nursing Society position paper on cancer pain. Pediatric cancer pain.
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The Pediatric Cancer Quality of Life Inventory: a modular approach to measuring health-related quality of life in children with cancer.
Measurement of pediatric cancer patients' health-related quality of life (HRQL) in phase III randomized, controlled clinical trials is being recognized increasingly as an essential component in evaluating the comprehensive health outcomes of modern anti-neoplastic treatment protocols. Use of a brief core measure of HRQL plus disease-specific symptom modules is a way to assess specific HRQL outcomes with a minimum of subject burden. Demonstrating a measure's feasibility, reliability and validity also represents children's ability to provide reliable and valid responses to HRQL questions. The Pediatric Cancer Quality of Life Inventory (PCQL) Modular Approach consists of a 15-item core measure of HRQL and 2 specific symptom modules: pain and nausea. To validate a patient-report form and a parent-report form, the PCQL was administered to 291 pediatric cancer patients and to their parents. Feasibility and range of measurement, as well as patient-parent concordance, were assessed. Internal consistency reliability was assessed via Cronbach's alpha. Validity was determined by the known-groups approach and by correlating PCQL scores with days missed from school. Patients had minimal missing data, and the range of measurement for the items was good. Patient-parent concordance was large but not perfect. For both patient and parent forms, internal consistency reliability of the PCQL core scale (0.83 and 0. 86, respectively) was strong. The internal consistency reliabilities of the 2 symptom modules for both patient and parent forms were in the acceptable range for group comparisons. Regarding clinical validity, the core scale and the 2 symptom modules distinguished between patients on and off treatment for both patient and parent reports. Further, both patient and parent reports correlated with days of missed school in the past 6 and 12 months. The PCQL Modular Approach has demonstrated acceptable internal consistency reliability and clinical validity for both patient-report and parent-report forms. By implication, children are capable of providing reliable and valid responses to these HRQL questions.
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The future of pediatric cancer and complex diseases: aren't they all?
Over the past decade, the investigation of human genetics and disease has pursued both common and uncommon germ-line variation and shown that both can be associated with altered risk for cancer and its outcomes. This line of investigation has not only begun to generate markers for disease but also insights into the biological pathways that are altered in cancer. Already, there is emerging evidence that germ-line genetic variation can alter susceptibility to different types of cancers, including pediatric cancers. It is evident that common genetic variation has emerged as a key component of a comprehensive understanding of pediatric cancer and its outcome. Future studies should unravel the complex interaction between genes and the environment.
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Pediatric cancer in the United States. A preliminary report of a collaborative study of the Childrens Cancer Group and the Pediatric Oncology Group.
BACKGROUND: Cancer is the second leading cause of death in children younger than 15 years. Although 5-year survival rates have increased dramatically for many childhood tumors, more than 100,000 person-years of life are lost to childhood cancer each year. The exact proportion of pediatric patients with cancer who receive care at centers that use up-to-date therapeutic protocols (such as those affiliated with the Childrens Cancer Group (CCG) or the Pediatric Oncology Group (POG) is unknown. METHODS: Based on residence at the time of diagnosis, observed numbers of pediatric cancer cases seen by member institutions of the CCG and the POG in 1989 and 1990 were compared with the expected number of cases. Expected values were calculated from incidence rates obtained from the Surveillance, Epidemiology and End Results Program and population counts obtained from the US Census Bureau. RESULTS: Results indicate that more than 90% of children younger than 15 years who have a diagnosis of malignant neoplasm are seen at an institution that is a member of either CCG or POG. The highest proportion seen occurs in the youngest (0-4 years) age group, and the proportion declines steadily with increasing age. CONCLUSIONS: There are specific regions within the United States where the observed number of cases was substantially less than the expected number, including areas of Texas, Idaho, and Virginia. Although the exact reasons for these potential deficits are unknown, additional study of these areas is recommended.
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Pediatric cancer in Kentucky: good news.
Pediatric cancer is one of the more poignant aspects associated with the occurrence of this prominent chronic disease. Nationally, pediatric cancers occur with vastly lesser frequency than does adult disease, about 1:40 ratio. Nationally the rate is 14.6 per 100,000 population, age, 0-14 years. In Kentucky, all pediatric cancer rates are consistently lower, a statewide rate of 11.3 per 100,000. A rigorous examination was made for any evidence of unusual risk for pediatric cancer within the state; none was found. The population center of Jefferson County was examined with a bit greater detail, owing simply to the larger number. Again, no basis for public health or follow-back was identified. Among the most frequent pediatric cancers, leukemia, central nervous system, and brain were studied for implications of residential proximity to environmental hazards; no evidence of increased risk was identified. In all of the state, only Hardin County evinced any excess pediatric cancer risk, i.e., was significantly greater than the national rates. Yet this highly mobile population [owing to a large military population] may simply represent rates that are more compatible with those of the nation. For the Kentucky comprehensive disease control efforts, then, no emphasis need be placed with pediatric cancer beyond the intense personal tragedy that it poses.
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Tumorigenicity and oncogene expression in pediatric cancers.
Cytogenetic and epidemiological studies of pediatric cancers have implicated a loss of genetic information in the development of these tumors. In contrast, other studies have shown that activation of endogenous oncogenes is a common event in these cancer cells. The technique of somatic cell hybridization provides a model for investigating the interaction between loss of genetic elements and oncogene activation in pediatric cancers. A variety of human-human cell hybrids were formed between a tumorigenic adult carcinoma and representative tumorigenic pediatric cell lines. All hybrid cells were completely suppressed for tumor-forming ability when assayed in nu/nu (nude) mice. When the expression of the N-myc, c-myc, and sis oncogenes and tumorigenicity were examined in the same hybrid cells, no correlation was found, suggesting that the expression of these oncogenes in these hybrid cells did not appear to be controlled by putative "tumor suppressor" genes. Thus, tumorigenicity behaves as a recessive genetic trait in pediatric cancers. Furthermore, different genetic elements may be lost during tumor development of adult cancers as opposed to pediatric cancers.
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The PedsQL in pediatric cancer: reliability and validity of the Pediatric Quality of Life Inventory Generic Core Scales, Multidimensional Fatigue Scale, and Cancer Module.
BACKGROUND: The Pediatric Quality of Life Inventory (PedsQL) is a modular instrument designed to measure health-related quality of life (HRQOL) in children and adolescents ages 2-18 years. The PedsQL 4.0 Generic Core Scales are multidimensional child self-report and parent proxy-report scales developed as the generic core measure to be integrated with the PedsQL disease specific modules. The PedsQL Multidimensional Fatigue Scale was designed to measure fatigue in pediatric patients. The PedsQL 3.0 Cancer Module was designed to measure pediatric cancer specific HRQOL. METHODS: The PedsQL Generic Core Scales, Multidimensional Fatigue Scale, and Cancer Module were administered to 339 families (220 child self-reports; 337 parent proxy-reports). RESULTS: Internal consistency reliability for the PedsQL Generic Core Total Scale Score (alpha = 0.88 child, 0.93 parent report), Multidimensional Fatigue Total Scale Score (alpha = 0.89 child, 0.92 parent report) and most Cancer Module Scales (average alpha = 0.72 child, 0.87 parent report) demonstrated reliability acceptable for group comparisons. Validity was demonstrated using the known-groups method. The PedsQL distinguished between healthy children and children with cancer as a group, and among children on-treatment versus off-treatment. The validity of the PedsQL Multidimensional Fatigue Scale was further demonstrated through hypothesized intercorrelations with dimensions of generic and cancer specific HRQOL. CONCLUSIONS: The results demonstrate the reliability and validity of the PedsQL Generic Core Scales, Multidimensional Fatigue Scale, and Cancer Module in pediatric cancer. The PedsQL may be utilized as an outcome measure in clinical trials, research, and clinical practice.
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Clinical utility of bronchoalveolar lavage in pediatric cancer patients.
BACKGROUND: Pulmonary disease in the pediatric cancer patient continues to pose a difficult clinical dilemma. Bronchoalveolar lavage (BAL) is commonly utilized for the diagnosis of pulmonary complications in the immunocompromised child. PROCEDURE: We retrospectively reviewed 53 BAL procedures performed in pediatric cancer patients with pulmonary disease between 1988 and 1998 to determine the diagnostic and clinical utility of BAL. Patients who had undergone prior myeloablative therapy were excluded from analysis. RESULTS: The majority of patients (83%) had an underlying diagnosis of acute leukemia or lymphoma. BAL yielded a specific diagnosis in 16 patients (30%), including 15 infections and 1 malignant infiltration. Medical management was altered in an additional 14 patients (26%) as a consequence of a negative BAL result. Severe but transient complications associated with the BAL procedure occurred in four patients (8%). Minor complications following the BAL occurred in 21 patients (40%) and included transiently increased oxygen requirement and anesthesia-related gastrointestinal complaints. The mortality from lung disease in this patient population was 7.5%. CONCLUSIONS: Both positive and negative BAL results contribute to the management of pediatric cancer patients with pulmonary disease. The low incidence of significant complications associated with BAL and the high mortality rate in this patient population support the choice of BAL as an initial diagnostic test in pediatric cancer patients with pulmonary disease.
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Generation of CD3+ CD56+ cytokine-induced killer cells and their in vitro cytotoxicity against pediatric cancer cells.
A certain number of pediatric cancer patients still succumb to relapse following conventional treatment of their malignancies. One of the mechanisms of relapse is escape from immunity. Adoptive cellular immunotherapy with effector cells has the potential to overcome this escape. In adults, the CD3+ CD56+ cell, a cytokine-induced killer (CIK) cell, appears to be a promising effector cell type with the greatest cytotoxicity. This effector cell type may work in children as well. No similar studies with children have been published. We speculated that expanded CD3+ CD56+ cells obtained from pediatric cancer patients during remission would act similarly against various pediatric tumor cell lines; therefore, we undertook the present study to find support for our speculation. This study was undertaken to generate and expand CD3+ CD56+ CIK cells from normal peripheral blood mononuclear cells (PBL) obtained from 6 children with cancer (2 with acute lymphoblastic leukemia, 2 with large cell lymphoma, and 2 with osteosarcoma) in remission after intensive chemotherapy and to study the cytotoxic activities of these cells against chronic myeloid leukemia cell line K562 t(9;22), 4 pediatric tumor cell lines [infant acute lymphoblastic leukemia RS4 t(4;11), TEL/AML acute lymphoblastic leukemia REH t(12;21), alveolar rhabdomyosarcoma Rh-Cr t(2;13), and Ewing sarcoma EW-Le t(11;22)], and 2 pediatric glioblastoma multiforme cultured cell lines (G74 and G77). CIK cells were generated and expanded in culture medium to which interferon gamma, monoclonal antibody against CD3, and interleukin 2 were added at appropriate times. Cells were counted by flow cytometry. Net lactate dehydrogenase release from target cells incubated with CIK cells was used as an index of CIK cell cytotoxicity against various pediatric tumor cell lines. The results show that after 21 days in culture CD3+ CD56+ CIK cells derived from the 6 pediatric patients accounted for a median of 28.3% of the entire culture (range, 10.7%-36.4%). Before expansion no such cells were found in any of the 6 children. Median lytic activity rates of CIK cells were 45.5% to 64.5%, rates that contrasted drastically to the lytic activity rates of PBL, which were only 8% to 12%. The findings of the present study are encouraging. They provide information for developing adoptive immunotherapy for future clinical trials with pediatric cancer patients, particularly those patients with minimal residual disease after intensive chemotherapy or stem cell transplantation (especially nonmyeloablative transplantation procedures).
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Pediatric cancer survivors: assessment of late effects.
As pediatric cancer treatment technology continues to progress, so does the increasing pool of pediatric cancer survivors. In the past, survival studies were based on the fifth year following the diagnosis. Currently, follow-up care is imperative beyond the first 5 years. Although cure is achieved for many children, late effects from treatment occur in many survivors. As this population continues to increase, so does the need for health care providers to monitor and treat these individuals. Pediatric cancer survivors require specific screening to determine the late effects of treatment. Many treatment consequences can be alleviated through proper assessment and treatment.
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The landscape of structural variation in pediatric cancer.
Structural variants (SVs) account for over 60% of the driver variants in pediatric cancer, and in many cases act as the cancer initiating event. To study SVs from a pan-cancer perspective, we analyzed 1,616 pediatric cancer genomes in 16 major cancer types of hematological malignancies (n = 908), brain tumors (n = 183), and solid tumors (n = 525) and compared their profiles to those of 2,203 adult cancers. The SV burden varied ~100-fold across pediatric cancer types and demonstrated an 8- to 16-fold reduction compared to adult brain and solid tumors but was comparable in pediatric versus adult hematological malignancies. Recurrent SV hotspots occurred uniquely in pediatric acute lymphoblastic leukemias (ALLs) in proximity to RAG-mediated recombination signal sequences (RSS) and disrupted multiple immune-related loci as well as 69 genes, which often involved cryptic RSS sites. By contrast, such hotspots affected only immune-related loci but not driver genes in adult lymphoid cancers. Eight SV signatures extracted from the cohort had varying distributions across cancer types, with clustered translocations reflecting templated insertions in osteosarcoma, and medium-sized deletions (10 kb to 1 Mb) enriched in cancers with RAG-mediated deletions. Intra-patient evolutionary analysis in 13 patients with multiple spatiotemporally distinct samples revealed that RAG-mediated recombination in leukemia and complex rearrangements in solid tumors occurred both early in disease initiation and continuously during later diversification, contributing to clonal heterogeneity. Finally, we found that both driver genes and fragile sites were the two genomic regions most frequently disrupted by SVs. The unique and diverse SV landscapes that emerged from this comprehensive analysis expand the scope of RSS-mediated mutagenesis in pediatric ALL and will be a valuable resource for guiding future functional studies and the design of clinical genomic testing in pediatric cancer.
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[Evidence based chemotherapy for pediatric cancers].
The curability of pediatric cancer has been improved to nearly seventy percent. This change has been achieved by refinements in treatment strategy and supportive care. More than seventy percent of patients with ALL can be cured by modern chemo-radiotherapy with reduced late effects. The stratification of the patients by risk factor, introduction of CNS prophylaxis, shortening of the duration of chemotherapy and intensification of the chemotherapy with agents such as HD-MTX have contributed to this remarkable success. Burkitt's lymphoma is a tumor for which the curability has improved from almost zero to ninety percent. With Wilms' tumor, clinical trials have been used to optimally refine the treatment strategy. The NWTS first compared the efficacy of combined VCR and Act-D with the single use of each drug. The difference was significant. The results of the systematic trials were then used to improve the survival rate of patients with Wilms' tumor from twenty to ninety percent and shorten the duration of chemotherapy to six months. On the other hand, tumors remain with which less than half of patients can survive for long. Advanced neuroblastoma and AML are typical such tumors. With these diseases, refinements in the treatment based on evidence derived from clinical trials have been insufficient. Further intensification of the treatment or novel approaches to control tumor growth are warranted for these diseases. In this article, I would like to describe the "standard" therapy for each tumor and the evidence on which improvements in those strategies have been based.
Antineoplastic Combined Chemotherapy Protocols↗
Conditioned aversions in pediatric cancer patients receiving chemotherapy.
Pediatric cancer patients experiencing nausea/vomiting in anticipation of chemotherapy were studied in comparison to a matched group of patients with no history of anticipatory nausea/vomiting (ANV). Patients with ANV were characteristically more anxious and tended to screen sensory information less selectively than patients without ANV. Parents of patients with ANV relied more heavily on threat of punishment and less on modeling and reassurance when managing their children in fearful situations than did parents of patients with no ANV. ANV was related to an increased incidence of experimentally conditioned taste aversions. The contribution of patient variables to the prediction of ANV and implications for research are discussed.
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The pediatric cancer quality of life inventory-32 (PCQL-32): I. Reliability and validity.
BACKGROUND: Multidimensional measurement of pediatric cancer patients' health-related quality of life (HRQOL) in Phase III randomized controlled clinical trials is being recognized increasingly as an essential component in evaluating the comprehensive health outcomes of modern antineoplastic treatment protocols. The Pediatric Cancer Quality of Life Inventory-32 (PCQL-32) is a standardized patient self-report and parent proxy-report assessment instrument designed to assess systematically pediatric cancer patients' HRQOL outcomes. METHODS: To validate a patient-report form and a parent-report form, the PCQL-32 was administered to 291 pediatric cancer patients and to their parents. Both forms yield a total score and five a priori multidimensional scales. Clinical validity was determined by the known-groups approach by comparing patients classified as either on or off treatment. To determine construct validity, a battery of standardized psychosocial measures was administered and a multitrait-multimethod matrix was constructed. RESULTS: For both patient and parent forms, internal consistency reliability of the PCQL-32 total scale was high (0.91 and 0.92, respectively). The internal consistency reliabilities of the five component scales for both patient and parent forms were in the acceptable range for group comparisons. With regard to clinical validity, the PCQL-32 total scale and the disease/treatment and physical functioning scales of the PCQL-32 distinguished between patients on and off treatment for both patient- and parent-report. The results of the multitrait-multimethod matrix approach were consistent with hypotheses and lent evidence for the construct validity of the patient and parent forms of the PCQL-32 total scale and the psychological functioning, social functioning, cognitive functioning, physical functioning, and disease/treatment scales. CONCLUSIONS: The PCQL-32 has demonstrated acceptable internal consistency reliability, clinical validity, and construct validity for both patient-report and parent-report forms. Further field testing of the PCQL-32 will determine its practicality and utility in multisite pediatric cancer randomized controlled clinical trials.
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The Pediatric Cancer Quality of Life Inventory (PCQL). I. Instrument development, descriptive statistics, and cross-informant variance.
Intensive antineoplastic treatment protocols have been developed and implemented in controlled clinical trials with the goal of improving the survival of pediatric cancer patients. Multidimensional health outcome evaluation of this cohort of pediatric cancer patients being treated with these modern regimens is essential in order to enhance health-related quality of life. The Pediatric Cancer Quality of Life Inventory (PCQL) was developed to be a standardized assessment instrument to assess systematically pediatric cancer patient's health-related quality of life outcomes. The PCQL was administered to 291 pediatric cancer patients and their parents at various stages of treatment. The aim of the present study was to present the development, descriptive statistics, and cross-informant variance for the PCQL items. Large variability in symptoms and health-related problems were found as expected given the wide heterogeneity in the patient population sampled. Patient/parent concordance on individual items averaged in the medium effect size range. The findings underscore the importance of measuring both patient report and parent report of patient symptoms and problems in pediatric cancer health-related quality of life assessment.
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Challenges identifying genetic determinants of pediatric cancers--the childhood leukemia experience.
Pediatric cancers affect approximately 1 in every 500 children before the age of 15. Little is known about the etiology of this heterogeneous group of diseases despite the fact they constitute the major cause of death by disease among this population. Because of its relatively high prevalence, most of the work done in pediatric oncogenetics has been focused on leukemias, particularly acute lymphoblastic leukemia (ALL). Although it is now well accepted that genetic variation plays a significant role in determining individual's cancer susceptibility, few studies have explored genetic susceptibility to childhood leukemia with respect to common polymorphisms. The biochemical and genetic mechanisms contributing to cancer susceptibility are numerous and can be grouped into broad categories: (1) cellular growth and differentiation, (2) DNA replication and repair, (3) metabolism of carcinogens (4) apoptosis, (5) oxidative stress response and (6) cell cycle. To evaluate whether candidate genes in these pathways are involved in childhood leukemogenesis, we conducted case-control studies. We showed that leukemogenesis in children may be associated with DNA variants in some of these genes and that the combination of genotypes seems to be more predictive of risk than either of them independently. We also observed that, at least at some loci, the parental genetics might be important in predicting the risk of cancer in this pediatric model of a complex disease. Taken together, these results indicate that the investigation of a single enzyme and/or a single genotype might not be sufficient to explain the etiology of childhood leukemia because of the complexity of the environment and that of the inter-individual variability in cancer susceptibility.
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