Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ewing's sarcoma occurs most often in young males of caucasian type and affects the medio-diaphysis of a long bone of the lower extremity, the pelvis and the humerus. Radiologically there is bone destruction, onion skin appearance, a Codman triangle and extension into the surrounding soft tissues. Microscopically, this tumor is composed of small round cells and it can be differentiated from non Hodgkin lymphoma, metastatic neuroblastoma and embryonal rhabdomyosarcoma. Recent immunological studies suspect a neuroectodermal origin. Ewing's sarcoma growths rapidly and spreads to lung and other bone locations. Without treatment, survival at 5 years is less than 5%. The actual therapeutic approach is multidisciplinary including surgery, chemotherapy and if necessary radiotherapy. With this approach actual survival rates at 5 years reaches 75%.
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PMID:[Ewing's sarcoma: literature review and presentation of 4 cases]. 186 78

Lag time (the interval between symptom onset and diagnosis) was described for 2665 children with lymphoma or a solid tumor who participated in Pediatric Oncology Group therapeutic protocols from 1982 until 1988. Median lag time ranged from 21 days for neuroblastoma to 72 days for Ewing sarcoma. Significant differences in lag time were found among diagnostic groups (p less than 0.001), even after adjustment for age, gender, and race. Age was significantly associated with lag time for all diagnoses (p less than 0.05) except Hodgkin disease. Girls had increased lag times for non-Hodgkin lymphoma (p = 0.02) but decreased lag times for Ewing sarcoma (p = 0.02). Differences in lag time related to race were significant only for children with osteosarcoma (p = 0.02), for which white children had longer lag times. Type of tumor and age were strongly associated with lag time. Within diagnostic groups, age, gender, and race failed to explain more than 16% of the variance in lag time, suggesting that other factors may play more prominent roles. Further study is necessary to identify these factors and to assess the relationship between lag time, stage of disease at diagnosis, and prognosis, especially before designing early-detection interventions for childhood cancer.
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PMID:Interval between symptom onset and diagnosis of pediatric solid tumors. 194 78

Eight children (1-17 yr) underwent bone marrow harvesting while in cytostatic-induced remission of their disease (leukemia [n = 6], Ewing sarcoma, and non-Hodgkin lymphoma). After the induction of general anesthesia, all patients were loaded with 10 mL/kg of a 6% high-molecular dextran solution (Macrodex--Pharmacia), which resulted in a significant preoperative decrease in hematocrit (Hct) from 32% +/- 6% to 28% +/- 5% (hypervolemic hemodilution) and also allowed the procedure to be performed without systemic heparinization. The blood aspirated during the harvest (24 +/- 6 mL/kg; mean +/- SD) was replaced with a solution of 6% dextran and Ringer's acetate solution, and the Hct decreased from 28% +/- 5% to a minimum of 18% +/- 3%. Immediately after the harvest, 10 mL/kg of homologous packed red blood cells was transfused, increasing Hct to 25% +/- 3%. Oxygen saturation in the superior caval vein (ScvO2) decreased from 79% +/- 4% before the harvest to 70% +/- 3% (P less than 0.01) at the end of it, and then increased to 74% +/- 3% after the transfusion of homologous packed red blood cells. There was a strong linear correlation between mean values for Hct and ScvO2 during the various stages (r = 0.99). Mean heart rate decreased gradually during the procedure, from 106 +/- 10 to 86 +/- 7 beats/min. There was no significant change in arterial pressure, but cardiac output measured by impedance cardiography was about 30% greater during harvesting than during undisturbed anesthesia. Pulse oximetric saturation was 99% or 100% throughout. Caval venous blood lactate and pyruvate concentrations remained within normal limits in all children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodilution during bone marrow harvesting in children. 201 22

Between 1965 and 1988, at the Children's Hospital of Buenos Aires, 22 children developed two successive malignant tumors of different histology. The first tumor was diagnosed between 3 months and 12 years of age: 13 retinoblastoma, 2 rhabdomyosarcoma, 2 non-Hodgkin lymphoma, 2 Hodgkin disease, 1 brain stem glioma, 1 endodermal sinus tumor and 1 Ewing sarcoma. Familial cancer was registered in 6 patients. Children were treated with surgery, intensive chemo and radiotherapy. The second malignancy developed after 2 to 13 years: 10 osteosarcoma, 2 Ewing sarcoma, 2 rhabdomyosarcoma, 2 glioblastoma, 1 medulloblastoma, 1 synoviosarcoma, 1 fibrosarcoma, 1 thyroid carcinoma, 1 acute lymphoblastic leukemia and 1 acute myeloblastic leukemia. In 17 patients, the tumor developed in irradiated field. There was no evidence of the first tumor and only 1 patient was still under chemotherapy. Oncologic treatment was frustrating for these second tumors and 18 children died. Three are alive with no evidence of disease at 2 years, 2 years and 4 months and 3 years after diagnosis. One patient was lost to follow-up. It if postulated that second malignant tumors are consecutive to genetic predisposition and/or to the oncogenic effect of chemo and radiotherapy. The intensity of each treatment modality must be reduced as much as possible to obtain survival while limiting the secondary effects.
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PMID:[Second malignant tumor in children. Report of 22 cases]. 210 57

We have examined expression of the smg p25A (a ras p21-like GTP-binding protein) gene in neural crest-derived tumor cell lines and neuroblastoma tissues. The human neuroblastoma cell lines GOTO, IMR-32, NB-1, and SK-N-SH expressed the 1.6-kilobase smg-25A mRNA. SH-SY5Y and SH-IN, variant cell lines with a neuronal phenotype derived from SK-N-SH, expressed much more smg-25A mRNA than did SH-EP1, a variant line with an epithelium-like phenotype also derived from SK-N-SH. The primitive neuroectodermal tumor cell lines SK-N-MC and KU-SN and the Ewing's sarcoma cell lines RD-ES and SK-ES expressed the smg-25A mRNA to a much smaller extent than did neuroblastoma cell lines. Of 15 human neuroblastoma specimens tested, 13 expressed the smg-25A mRNA to various extents. When the relative ratio of the smg-25A mRNA level to the glyceraldehyde-3-phosphate dehydrogenase mRNA level was compared among neuroblastoma tumor tissues, the value was significantly higher in tumors histologically diagnosed as ganglioneuroblastoma. The smg-25A mRNA was not detected in the tissues of Hodgkin's lymphoma, Wilms' tumor, Ewing's sarcoma, or undifferentiated sarcoma of the liver. These results suggest that the smg-25A mRNA level is closely related to the neuronal differentiation state of tumors derived from the neural crest.
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PMID:Expression of the smg p25A (a ras p21-like GTP-binding protein) gene in human neuroblastoma cell lines and tumor tissues. 212 31

Studies were made on the appearance of second malignant tumors (SMT) in children followed in a pediatric hospital at metropolitan Santiago, Chile, between years 1968 and 1987. A retrospective analysis identified SMT in 7 of 430 patients who survived a childhood cancer (incidence 1.62%). An 8th patient was added, whose first neoplasm was treated in another hospital. The initial diagnosis in the affected children were medulloblastoma, neuroblastoma, Wilm's tumor retinoblastoma, Ewing's sarcoma, Hodgkin's disease and, in two cases, acute lymphocytic leukemias. The age range was 6 months to 11 years. Treatment was done by surgery in 5/8, chemotherapy in 7/8 and radiotherapy in all patients. The latent period between the diagnosis of the first cancer and the diagnosis of the SMT was 3.5 to 12 years (median 8.5 years). Osteosarcomas were the most frequent SMT (5/8). The other SMT were a rhabdomyosarcoma, a non Hodgkin lymphoma and an astrocytoma. The majority of SMT were located in the area of prior radiotherapy (6/8). In the other two cases, one had an osteosarcoma, after a bilateral retinoblastoma, which grew outside the previously treated area, and the last one consisted of a lymphoma which was identified 9 years after an acute lymphocytic leukemia. Only 3/8 SMT patients are alive after 14.21 and 34 months follow up. The other children died between 11 and 20 months after diagnosis of SMT. Notwithstanding these kinds of outcome, benefits of therapy for patients with primary tumors greatly outweight the later risk of cancer induction in a small proportion of them.
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PMID:[Second cancer in pediatric patients]. 213 86

One hundred forty-three patients who received radiation therapy for childhood tumors, and survived to the age of skeletal maturity, were studied by retrospective review of oncology records and roentgenograms. Diagnoses for the patients were the following: Hodgkin's lymphoma (44), Wilms's tumor (30), acute lymphocytic leukemia (26), non-Hodgkin's lymphoma (18), Ewing's sarcoma (nine), rhabdomyosarcoma (six), neuroblastoma (six), and others (four). Age at the follow-up examination averaged 18 years (range, 14-28 years). Average length of follow-up study was 9.9 years (range, two to 18 years). Asymmetry of the chest and ribs was seen in 51 (36%) of these children. Fifty (35%) had scoliosis; 14 had kyphosis. In two children, the scoliosis was treated with a brace, while one developed significant kyphosing scoliosis after laminectomy and had spinal fusion. Twenty-three (16%) patients complained of significant pain at the radiation sites. Twelve of the patients developed leg-length inequality; eight of those were symptomatic. Three patients developed second primary tumors. Currently, the incidence of significant skeletal sequelae is lower and the manifestations are less severe than reported in the years from 1940 to 1970. The reduction in skeletal complications may be attributed to shielding of growth centers, symmetric field selection, decreased total radiation doses, and sequence changes in chemotherapy.
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PMID:Skeletal sequelae of radiation therapy for malignant childhood tumors. 213 23

Survival rates were analysed for a population-based series of over 15,000 childhood cancers registered in Great Britain during 1971-85. There were highly significant improvements (P less than 0.001 for trend) in survival for many major diagnostic groups. Between 1971-73 and 1983-85 the actuarial 5-year survival rates increased from 37% to 70% for acute lymphoblastic leukaemia, from 4% to 26% for acute non-lymphoblastic leukaemia, from 76% to 88% for Hodgkin's disease, from 22% to 70% for non-Hodgkin's lymphoma, from 61% to 72% for astrocytoma, from 24% to 42% for medulloblastoma, from 15% to 43% for neuroblastoma, from 58% to 79% for Wilms' tumour, from 17% to 54% for osteosarcoma, from 26% to 61% for rhabdomyosarcoma, from 59% to 94% for malignant testicular germ-cell tumours and from 43% to 77% for malignant ovarian germ-cell tumours. These increases in population-based survival rates reflect the substantial advances in treatment of a wide range of childhood cancers since 1970. The two principal diagnostic groups for which there was no evidence of any trend were retinoblastoma, which already had an excellent prognosis with a 5-year survival rate of over 85%, and Ewing's sarcoma, for which the survival rate remained below 45%.
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PMID:Trends in survival for childhood cancer in Britain diagnosed 1971-85. 217 43

Transcripts for the muscle regulatory gene MyoD1 are expressed during normal skeletal muscle myogenesis and in rhabdomyosarcomas but not in other tissues or in soft-tissue sarcomas. Here we report the distribution of MyoD1 protein, determined by reactivity with anti-MyoD1 polyclonal sera in normal tissues, rhabdomyosarcoma cell lines, and in a variety of pediatric solid tumors. The distribution of MyoD1 protein was highly restricted in normal tissues and was detected only in fetal skeletal muscle and more faintly in adult skeletal muscle. All six human rhabdomyosarcoma cell lines analyzed expressed MyoD1 mRNA transcripts as well as immunoreactive protein. The immunohistochemical expression of MyoD1 protein was then examined in 49 surgical specimens from a variety of pediatric solid tumors. Each of 16 rhabdomyosarcoma specimens was positive for MyoD1, including four that did not express the intermediate filament protein desmin. Two of five specimens originally designated sarcoma type indeterminate (STI) and two of three specimens originally designated extraosseous Ewing's sarcoma (EOE) were positive for MyoD1, suggesting commitment to myogenic differentiation. Three of eight Wilms' tumors, which also expressed desmin and had clearly evident myogenic elements, also were positive for MyoD1. Tumors that failed to express MyoD1 protein included neuroblastoma, primitive neuroectodermal tumor, non-Hodgkins lymphoma, embryonal sarcoma of the liver, malignant fibrous histiocytoma, malignant rhabdoid tumor, and Ewing's sarcoma of the bone. These results indicate that expression of MyoD1 protein is highly restricted in normal human tissues and that expression of this gene product in malignant tissue may be diagnostic for rhabdomyosarcoma. Furthermore MyoD1 staining may be a valuable adjunct in the classification of pediatric soft-tissue sarcomas.
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PMID:Myogenic regulatory protein (MyoD1) expression in childhood solid tumors: diagnostic utility in rhabdomyosarcoma. 226 Jun 21

An investigation of 749 deaths occurring among 4082 patients surviving at least five years after the diagnosis of childhood cancer in Britain before 1971 has been undertaken. Of the 738 with sufficient information the numbers of deaths attributable to the following causes were: recurrent tumour, 550 (74%), a second primary tumour, 61 (8%), a medical condition related to treatment of the tumour, 49 (7%), an traumatic death unrelated to the tumour or its treatment, 34 (5%), finally, any other cause unrelated to the tumour or its treatment, 44 (6%). Less than 10% of five year survivors of non-Hodgkin lymphomas, neuroblastoma, retinoblastoma, Wilms' tumour, or a soft tissue sarcoma died of recurrent tumour during the next 15 years, while more than 25% of five year survivors of Hodgkin's disease, ependymoma, medulloblastoma, and Ewing's tumour died of recurrent tumour during the corresponding period. Almost 50% of five year survivors of acute lymphoblastic leukaemia died of recurrent disease during the corresponding 15 years, a large proportion of deaths being due to central nervous system relapse in an era before central nervous system prophylaxis was routinely given. Comparison of the mortality observed with that expected from mortality rates in the general population indicated three times the expected number of deaths from non-neoplastic causes. Five times the expected number of deaths from cardiovascular causes were observed, these were predominantly myocardial infarction and cerebrovascular accidents. There was no evidence of an excess in the number of suicides observed, but there were three times the expected number of deaths from accidents observed after central nervous system tumours. Two groups of patients were identified whose deaths were potentially avoidable. Seven patients with craniopharyngioma and panhypopituitarism presented with addisonian crises during periods of stress not adequately covered by exogenous corticosteroids. In the other group were children who received radiotherapy and later developed problems related to radiation fibrosis. We emphasize that our investigation relates to patients diagnosed with childhood cancer before 1971. The pattern of mortality that will emerge after recent treatment regimens, in which chemotherapy is being used more extensively, is likely to be different from that observed in our study.
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PMID:Late deaths after treatment for childhood cancer. 227 Sep 44


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