bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immuno‐ and cytochemical characterization of congenital leukemia: A case report
Authors: Heikinheimo Markku , Pakkala Seppo , Juvonen Eeva , Saarinen Ulla M. 
Published: February 2007

AbstractCongenital leukemia (CL) is a rare disorder, which usually presents as a myelocytic leukemia based on morphological features. Very few reports include data on cyto‐ or immunochemical parameters. A case of CL with detailed description of immunochemical, cytochemical features, and colony formation properties of the progenitor cells is reported. This leukemia was classified as an M4 in FAB classification based on the morphological features and special stains. Two different cell populations were identified by flow cytometry. One consisted of small cells expressing early T‐ and early B‐cell associating antigens as well as early myeloid‐associated antigens, but not CD10 (CALLA antigen), which is normally present in cord blood lymphocytes. The other was a population of large cells expressing myeloid‐associated antigens and a pan‐T‐antigen. The growth pattern of hematopoietic progenitors in the patient was compatible with both acute myeloid and acute lymphatic leukemia as well as erythroleukemia. © 1994 Wiley‐Liss, Inc.
Primary lymphoma of the pericardium: Report on a „Cured”︁ case and review of the literature
Authors: Pavlidis Nicholas A. , Elisaf Moses , Bai Mary , Tolis Christos , Papadimitriou Constantine 
Published: February 2007

AbstractThis report describes a 62‐year‐old man with a primary diffuse, immunohistochemically proven B‐cell lymphoma of large non‐cleaved cell (centroblastic) type of the pericardium. The patient responded completely to systemic chemotherapy and remains free of disease 30 months after diagnosis. The use of non‐cardiotoxic drugs in divided doses as initial treatment is emphasized. In addition, the authors reviewed the literature of the last decade regarding the management and outcome of patients with primary cardiac lymphomas. © 1994 Wiley‐Liss, Inc.
Neonatal tumours: A thirty‐year population‐based study
Authors: Parkes S. E. , Muir K. R. , Southern L. , Cameron A. H. , Darbyshire P. J. , Stevens M. C. G. 
Published: February 2007

AbstractEstimates of the incidence and outcome of tumours in neonates are uncertain and most reports relate to selected experience in single centres. The definition of neonatal tumour is also unclear and histology is not always an accurate predictor of outcome. This report documents the incidence, clinical features, and outcome of neonatal tumours (birth‐3 months) in a population‐based paediatric register over a 30‐year period from 1960‐89. Case note and pathology review identified 170 cases for analysis, of which 21 were leukaemias, 14 CNS tumours, and 135 solid tumours of differing types. Fifty‐eight percent were diagnosed in the first month and mature teratoma was the most common diagnosis (29%). Overall incidence increased over the period of the study. Important family medical history was identified in 16% of cases and 15% of patients had associated congenital abnormalities. Overall survival at 1 year was 55%, with leukaemia having the poorest prognosis. Treatment strategies must be individualised but many patients may have a better prognosis than expected and would benefit from assessment at a designated paediatric oncology centre. © 1994 Wiley‐Liss, Inc.
Multicentric angiofollicular lymph node hyperplasia and associated carcinoma
Authors: Baker William J. , Vukelja Svetislava J. , Weiss Raymond B. , Dich Nguyen 
Published: February 2007

AbstractThere is a well described association between multicentric angiofollicular hyperplasia and non‐Hodgkin's lymphoma and/or Kaposi's sarcoma. Two cases of multifocal angiofollicular hyperplasia and associated carcinomas and non‐Hodgkin's lymphoma are reported. We suggest that underlying immunological defects in patients with multicentric angiofollicular hyperplasia make them susceptible to the development of carcinomas, as well as non‐Hodgkin's lymphoma and Kaposi's sarcoma. © 1994 Wiley‐Liss, Inc.
Pediatric hodgkin's disease in costa rica: Twelve years' experience of primary treatment by chemotherapy alone, without staging laparotomy
Authors: Lobo‐Sanahuja Francisco , García Ivette , Barrantes José C. , Barrantes Max , Gonzalez Mario , Jimenez Rafael 
Published: February 2007

AbstractThis is a prospective and nonrandomized study in which 86 children with previously untreated Hodgkin's disease (HD) were clinically staged (CS) and treated with chemotherapy (CT) alone. Fifty‐two (CS IA‐38, IIA‐7, IIB‐3, IIIA‐4) received six courses of cyclophosphamide, vinblastine, procarbazine, and prednisone (CVPP). Ten (CS IA with peripheral nodes) received only three courses of CVPP with a reinforcement of C on day 8. Twenty‐four (CS IIIB‐18, IVA‐2, IVB‐4) received six courses of CVPP alternating with six courses of epirubicine, bleomycine, and vincristine (EBO). Surgical staging was not performed in any patient. Two patients (CS IIIB) had partial remission and died from progressive disease. Seventy out of 86 children have not relapsed and are in complete remission with a median follow‐up of 65 months (range 13‐156 months); 14 children relapsed seven to 37 months from diagnosis (median 16 months); one of them (IV B) died of disease. Thirteen are in second and third remission (median 55 months). Actuarial five year survival rates and relapse‐free survival rates are 100% and 90% for CS I to IIIA and 81% and 60% for CS 1MB and IV, respectively. As a result of this study, we can conclude that in developing countries most of the children with HD staged by noninvasive diagnostic techniques can be cured with CT alone as primary treatment and thus will not suffer from the late effects of radiotherapy (RT) and the morbidity of laparotomy and splenectomy. RT alone or with other CT combinations should be considered for children who develop relapse of HD. © 1994 Wiley‐Liss, Inc.
Karyotype evolution in a patient with down syndrome and acute leukemia following a congenital leukemoid reaction
Authors: Sawyer J. R. , Roloson G. J. , Head D. R. , Becton D. 
Published: February 2007

AbstractWe report the serial cytogenetic study of a patient with Down syndrome who experienced a congenital leukemoid reaction, underwent a spontaneous remission within four months, and subsequently developed acute myeloid leukemia at 16 months. A blood chromosome study to rule out Down syndrome performed at age 24 days, during the leukemoid reaction, revealed a 47,XX,+21 karyotype. The diagnosis of acute leukemia was made at 16 months, at which time a chromosome study, on bone marrow, was performed. This analysis revealed a clonal karyotype of 47,XX,+21,‐22,+der (22)t(1;22)(q21;q13) in all but one cell studied. The single apparently nonclonal cell showed a karyotype of 49,XX,+12,‐13,‐19, +der(19)t(19;?)(q11;?)x2,+21,+22. A third chromosome study at 19 months indicated the original leukemic clone with t(1;22) (q21;q13) had been replaced by the clone represented by the single cell with 49 chromosomes seen in the previous chromosome study. This case of an infant with Down syndrome and acute leukemia illustrated rapid evolution and a transitory nature to clonal chromosome aberrations while retaining AML morphology and course. © 1994 Wiley‐Liss, Inc.
Pure dysgerminoma of the ovary in childhood: Treatment results and sequelae
Authors: Teinturier C. , Gelez J. , Flamant F. , Habrand J. L. , Lemerle J. 
Published: February 2007

AbstractThirty‐five children with pure dysgerminoma of the ovary were all treated at the Institut Gustave Roussy (IGR) from 1956–1985. The median follow‐up is 8.5 years. The crude 5‐year survival rate is 94.1% (±4.1). The disease‐free 5‐year survival rate is 81.8% (±6.7). Fourteen patients who had stage I disease were treated by unilateral salpingooophorectomy and prophylactic radiotherapy (20 Gy) to ipsilateral iliac, lumbar‐aortic, and subclavicular lymph nodes. All are alive without sequelae. Eighteen patients with stage II and III disease were treated by surgery and radiotherapy (30–40 Gy) to the tumor volume. All are alive but radio‐induced sequelae are severe. Five relapses of stage I, II, and III tumors occurred and were cured by a second line treatment. Two of the three patients with stage IV disease died.Four patients received a cisplatinum‐containing regimen for disseminated disease or because of a relapse before radiotherapy. Three achieved a complete response of measurable tumor. Given the high efficacy of this kind of chemotherapy and the severe sequelae induced by abdomino‐pelvic irradiation, we propose initial chemotherapy for widespread disease andd radiotherapy in the event of residual tumor. © 1994 Wiley‐Liss, Inc.
Therapy‐related acute myeloid leukemia following treatment with epipodophyllotoxins: Estimating the risks
Authors: Smith Malcolm A. , Rubinstein Lawrence , Ungerleider Richard S. 
Published: February 2007

AbstractIn the past decade, therapy‐related acute myeloid leukemia (t‐AML) following treatment with regimens that include inhibitors of topoisomerase‐II (TOPO‐II) has been reported with increasing frequency. These cases of t‐AML generally have a shorter latency period than t‐AML following alkylator therapy, are associated with chromosomal translocations (especially involving chromosome band 11q23), and usually present as M4 or M5 FAB subtype. Although the epipodophyllotoxins (etoposide and teniposide) have been most often implicated, similar cases of t‐AML occur following therapy with other classes of Topo‐II inhibitors (e.g., anthracyclines).There is wide variation in published studies in the estimates of risk of t‐AML following epipodophyllotoxin therapy. These varying estimates may reflect a number of factors, including: small sample size leading to large confidence intervals around risk estimates; varying susceptibility of different patient populations; varying schedules of epipodophyllotoxin administration; different cumulative doses of epipodophyllotoxins; and administration of epopodophyllotoxins with additional agents that may alter the leukemogenic effect of the epipodophyllotoxins.Available data suggest that children with acute lymphocytic leukemia (ALL) treated with high cumulative doses of epipodophyllotoxins using either weekly or twice‐weekly schedules of administration have a relatively high risk of developing t‐AML (5–12% cumulative risk). On the other hand, germ cell patients treated with relatively low cumulative doses of etoposide (usually 1,500–2,500 mg/m2) appear to have a low risk for developing t‐AML. There is inadequate experience at this time with higher cumulative doses of etoposide (e.g., 4,000–5,000 mg/m2 as used for pediatric solid tumors) given on a daily x 5 schedule to allow estimates of risk to be developed for this schedule and cumulative dose.The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan designed to obtain reliable estimates of the risk of t‐AML following epipodophyllotoxin treatment. Twelve Cooperative Group clinical trials that use epipodophyllotoxins at either low (<1,500 mg/m2), moderate (1,500–3,999 mg/m2), or higher cumulative doses (>4,000 mg/m2) are being prospectively monitored for cases of t‐AML occurring among patients entered onto the trials. © 1994 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
LCH‐I: A randomized trial of etoposide vs. vinblastine in disseminated langerhans cell histiocytosis
Authors: Ladisch Stephan , Gadner Helmut , Arico Maurizio , Broadbent Valerie , Grois Nicole , Jacobson Ake , Komp Diane , Nicholson H. Stacy 
Published: February 2007

AbstractAn international randomized trial in Langerhans cell histiocytosis (LCH) has been initiated by the Histiocyte Society. This report reviews the rationale, design, and progress of LCH‐I, which compares etoposide (VP‐16) and vinblastine in the treatment of disseminated LCH. Data on the risk of etoposide‐associated (therapy‐induced) malignancy, in the setting of histiocytosis, are reviewed. The available evidence leads to the recommendation that the study of etoposide in LCH should be continued. © 1994 Wiley‐Liss, Inc.
Liver function studies in children with acute lymphocytic leukemia after cessation of therapy
Authors: Bessho Fumio , Kinumaki Hiroshi , Yokota Shunichiro , Hayashi Yasuhide , Kobayashi Miyuki , Kamoshita Shigehiko 
Published: February 2007

AbstractWe investigated liver function in 27 children with acute lymphocytic leukemia (ALL) after cessation of therapy. Induction therapy consisted of prednisolone + vincristine (VP regimen) alone (16 patients) or with addition of daunorubicin (4 patients) or L‐asparaginase (7 patients). Patients treated with VP regimen short courses of VP regimen every 12 weeks for the first year of maintenance. Twenty‐five patients remained in first complete remission and had completed 3‐year maintenance therapy with methotrexate (MTX) and 6‐mercaptopurine (6‐MP) 1–7 years prior to this study. Twenty‐three patients had transfusions of packed red blood cells or fresh whole blood (1–11 units; median: 2 units) but none had evidence of either hepatitis B or hepatitis C. Alanine aminotransferase (ALT), which was measured every 3 months during maintenance therapy, had values more than three times the upper limit of the normal range in 25% of the measurements in more than half of the patients. However, by 3 months after the completion of maintenance therapy, ALT had normalized in all patients and remained normal in all but two patients until the time of this study. Serum bilirubin, serum albumin, and prothrombin time were all within normal limits. Fasting and 2‐hour postprandial total serum bile acids were high in 5 of 13 patients and in 6 of 13 patients, respectively. The ratio of cholic acids + deoxycholic acids to chenodeoxycholic acids + lithocholic acids was below 1 in all but two patients, whereas this ratio was above 1 in all controls. Our bile acid profile results indicate the necessity of careful long‐term follow‐up of survivors of ALL treated with hepatotoxic chemotherapy during childhood. © 1994 Wiley‐Liss, Inc.
Cytogenetic abnormalities of small round cell tumours
Authors: Bown N. P. , Reid M. M. , Malcolm A. J. , Davison E. V. , Craft A. W. , Pearson A. D. J. 
Published: February 2007

AbstractBetween 1987 and 1991, cytogenetic studies were carried out on small round cell tumours of 68 patients from the Northern Health Region of England. Clonal chromosome abnormalities were found in 30, comprising 15 neuroblastomas, 7 Ewing's tumours, 7 rhabdomyosarcomas, and 1 granular cell tumour. Characteristic rearrangements were found in five cases of Ewing's tumour [all with translocation t(11;22) (q24;q12)] and in four cases of rhabdomyosarcoma [all with evidence of translocation t(2;13) (q35–37;q14)]. In one case of Ewing's tumour and three of rhabdomyosarcoma, the cytogenetic findings were important in diagnosis. Within the neuroblastomas, examples were found of hyperdiploidy, 1p rearrangements, double minute chromosomes, and homogeneously staining regions, but too few cases were available for prognostic associations to be assessed. Our findings confirm the diagnostic importance of chromosome abnormalities in small round cell tumours and indicate that cytogenetic analysis should be an intrinsic part of the initial investigations of all patients with such tumours. © 1994 Wiley‐Liss, Inc.
Factors contributing to the prognostic significance of bone marrow involvement in childhood non‐Hodgkin lymphoma
Authors: Sandlund J. T. , Ribeiro R. , Lin J.‐S. , Ayers D. , Santana V. M. , Furman W. L. , Mahmoud H. , Berard C. W. , Hutchison R. E. , Crist W. M. , Rafferty M. , Pui C.‐H. 
Published: February 2007

AbstractTo evaluate the clinical characteristics and treatment outcome of childhood non‐Hodgkin lymphoma (NHL) cases with bone marrow involvement, we studied 13 lymphoblastic, 15 small noncleaved cell, and 8 large cell cases with tumor cells in their marrow. They represented 16%, 11%, and 9% of consecutive NHL cases with these respective histologic subtypes. The treatment outcome differed significantly according to histologic subtype—the 5‐year event‐free survivals (EFS ± SE) for large cell NHL, small non‐cleaved cell NHL, and lymphoblastic NHL cases were 11 ± 8%, 40 ± 20%, and 62 ± 15%, respectively. Increased serum lactate dehydrogenase (LDH) levels (>500 U/L) were associated with a poorer EFS (5‐year EFS, 0% vs. 50 ± 10%; P < 0.001). Children ⩽5 years of age had a poorer EFS survival than older children (5‐year EFS, 14 ± 9% vs. 44 ± 10%; P = 0.03). The degree of bone marrow involvement (<5% vs. ⩾5%) and race were not significantly associated with treatment outcome. Although intensive chemotherapy has substantially improved survival for patients with advanced stage lymphoblastic or small noncleaved cell lymphoma, patients with large cell NHL and associated marrow involvement continue to have a dismal outcome and require novel or more intensive therapy. © 1994 Wiley‐Liss, Inc.
Cerebral atrophy in an infant following treatment with ifosfamide
Authors: Bruggers Carol S. , Friedman Henry S. , Tien Robert , Delong Robert 
Published: February 2007

AbstractIfosfamide, a nitrogen mustard derived alkylating agent commonly used in the treatment of solid tumors, has been associated with neurotoxicity in 5–33% of treated patients. Encephalopathy most often occurs during or shortly following drug administration, with increased drowsiness or irritability, confusion, hallucinations, visual blurring, extrapyramidal dysfunction, cranial nerve abnormalities, incontinence, generalized muscle twitching, seizures, and coma reported in infants, children, and older adults. While most reported neurologic abnormalities associated with ifosfamide have been reversible, encephalopathy resulting in death has occurred.We now report an infant who developed ifosfamide‐induced encephalopathy, loss of developmental milestones, progressive brain atrophy, and cessation of cranial growth. This is the first case of cerebral atrophy and loss of developmental milestones that has been reported in a pediatric patient treated with ifosfamide. Given the efficacy of this anti‐neoplastic agent and its increasing use in pediatrics, further investigation is indicated, especially in infants where brain growth is ongoing. © 1994 Wiley‐Liss, Inc.
Treatment of malignant testicular tumors in childhood: Results of the german national study 1982–1992
Authors: Haas Rainer J. , Schmidt Piroska , Göbel Ulrich , Harms Dieter 
Published: February 2007

AbstractThe German Cooperative Protocol for treatment of testicular germ cell tumors in childhood registered 106 patients from January 1982 through February 1992. Sixty‐one patients suffered from yolk sac tumors (YST); 25 patients from differentiated teratomas (TD); 19 patients from malignant teratomas of either intermediate (MTI), undifferentiated (MTU), or trophoblastic type (MTT), and 1 patient from a seminoma.A stratified chemotherapy based on stage and histology was administered in addition to unilateral orchiectomy: Standard chemotherapy consisted of four treatments with vinblastine, bleomycin, and cisplatinum. If viable tumor was suspected after two treatments with standard chemotherapy, a delayed explorative laparotomy was done. There were two options based on the histological findings: In case of complete tumor regression, the standard chemotherapy was continued. In case of incomplete tumor response, patients a salvage chemotherapy consisting of three treatments with VP 16 (etoposide), ifosfamide, and cisplatinum. In addition three injections with VP 16 were given as a maintenance therapy.The following results were obtained: YST: 59 patients with stage I. Forty‐nine patients were followed according to “wait and see” policy. Eight of these needed a delayed standard chemotherapy. The relapse free survival of all 61 patients in 100%. Median observation time is 49 months.TD: Twenty‐five patients had stage I. No chemotherapy was given. The relapse free survival is 100%. Median observation time is 48 months.Malignant teratomas (MTI, MTU, MTT): 8 patients had stage I. Three of these adjuvant chemotherapy and 5 lymphadenectomy without chemotherapy. All patients survived without relapse. Nine patients had stage II and standard chemotherapy. Four of these patients had a delayed explorative laparotomy leading to a salvage therapy in two patients. All patients survived relapse free. Two patients had stage III. Of these 1 standard chemotherapy and is well. One patient suffering from MTU stage IIIA died due to candida septicemia during salvage therapy. Median observation time of the entire group is 60 months. © 1994 Wiley‐Liss, Inc.
Effects of CPT‐11 (a unique DNA topoisomerase I inhibitor) on a highly malignant xeno‐transplanted neuroblastoma
Authors: Komuro Hiroaki , Li Pai , Tsuchida Yoshiaki , Yokomori Kinji , Nakajima Katsuyoshi , Aoyama Takao , Kaneko Michio , Kaneda Norimasa 
Published: February 2007

AbstractAlthough many advances have been made in the management of neuroblastoma, the prognosis of patients with advanced neuroblastoma remains poor, and constant efforts are being made to search for newer effective drugs. CPT‐11 is a newly developed derivative of camptothecin and shows a unique anti‐tumor activity by inhibiting DNA topoisomerase I. In this study the effects of CPT‐11 on a human neuroblastoma xenograft, TNB9, were investigated according to the standard Battelle Columbus Laboratories protocol. TNB9 is one of the most malignant strains of neuroblastoma, showing a homogeneously staining resion (HSR) on chromosome 20 and 80‐fold amplification of the N‐myc gene. This study disclosed that CPT‐11 was highly effective against TNB9. Maximum inhibition rate (IR) was 72.5% at a standard dose and 52.8% even at half the dose. No nude mouse used in this study lost weight after an administration of CPT‐11. Plasma pharmacokinetics of CPT‐11 administered in this experimental model were compared to that in clinical patients. Our data suggested that CPT‐11 might be a promising new drug in the treatment of high‐risk neuroblastoma patients and encouraged us to employ CPT‐11 in the protocol of the Study Group of Japan. © 1994 Wiley‐Liss, Inc.
Etiology of neutrophilic granulocytic hypoplasia in a case of large granular lymphocytic leukemia with paraproteinemia
Authors: Friedman Henry D. , Goldberg Jack , Kurec Anthony S. , Davey Frederick R. 
Published: February 2007

AbstractThe association between large granular lymphocytic leukemia (LGLL) and neutropenia is poorly understood. We attempted to assess whether neutropenia in LGLL with paraproteinemia has a different etiology than LGLL without paraproteinemia. We found neither direct serum inhibition of granulocyte/monocyte‐colony forming units in vitro nor increased immunoglobulin binding to granulocytic neutrophils, neutrophil precursors, or granulocyte/monocyte‐colony stimulating factor. Clonogenic assay experiments suggested that suppression of the patient's granulocyte/monocyte‐colony forming units by the neoplastic T‐cells and decreased granulocyte/monocyte‐colony stimulating factor production contributed to the pathogenesis of neutropenia in this particular case. © 1994 Wiley‐Liss, Inc.