Second cancers in survivors of childhood cancer (original) (raw)
Neugut, A. I., Meadows, A. T. & Robinson, E. (eds). Multiple Primary Cancers 1999 3–10 (Lippincott Williams & Wilkins, Philadelphia, 1999). Google Scholar
Sklar, C. A. Overview of the effects of cancer therapies: the nature, scale, and breadth of the problem. Acta Paediatr Suppl88, 1–4 (1999). CASPubMed Google Scholar
Neglia, J. P. et al. Second malignant neoplasms in five-year survivors of childhood cancer: childhood cancer survivor study. J. Natl Cancer Inst.93, 618–629 (2001).In a large cohort of five-year survivors of childhood cancer, the authors describe the incidence of second cancers, characterize the second cancers and describe the risk factors associated with their development. CASPubMed Google Scholar
Bhatia, S. et al. Breast cancer and other second neoplasms after childhood Hodgkin's disease. N. Engl. J. Med.334, 745–751 (1996).The authors describe the incidence and risk factors associated with the development of second primary breast cancer and other second cancers in a large multinational cohort of childhood Hodgkin's disease survivors followed for an extended period of time. CASPubMed Google Scholar
Meadows, A. T. Risk factors for second malignant neoplasms: report from the Late Effects Study Group. Bull. Cancer75, 125–130 (1988). CASPubMed Google Scholar
Neglia, J. P. et al. Second neoplasms after acute lymphoblastic leukaemia in childhood. N. Engl. J. Med.325, 1330–1336 (1991). CASPubMed Google Scholar
Boice, J. D. Jr, Land, C. E. & Preston, D. L. in Cancer Epidemiology and Prevention (eds Schottenfeld, D. & Fraumeni, J. F. Jr) 319–354 (Oxford Univ. Press, New York, 1996). Google Scholar
Preston, D. et al. Cancer incidence in atomic bomb survivors. III. Leukaemia, lymphoma, and multiple myeloma, 1950–1987. Radiat. Res.137, S68–S97 (1994). CASPubMed Google Scholar
Thompson, D. E. et al. Cancer incidence in atomic bomb survivors. II: solid tumours, 1958–1987. Radiat. Res.137, S17–S67 (1994). CASPubMed Google Scholar
Ron, E. et al. Radiation-induced skin carcinomas of the head and neck. Radiat. Res.125, 318–325 (1991). CASPubMed Google Scholar
Wong, F. L. et al. Cancer incidence after retinoblastoma. Radiation dose and sarcoma risk. JAMA278, 1262–1267 (1997).In a large cohort of patients with retinoblastoma, diagnosed between 1914 and 1984, the authors describe the incidence and risk factors of second cancers and show that genetic predisposition has a substantial impact on the risk of subsequent cancers, which is further increased by radiation therapy. CASPubMed Google Scholar
Strong, L. C., Stine, M. & Norsted, T. L. Cancer in survivors of childhood soft tissue sarcoma and their relatives. J. Natl Cancer Inst.79, 1213–1220 (1987). CASPubMed Google Scholar
Land, C. E. et al. Incidence of salivary gland tumours among atomic bomb survivors, 1950–1987. Evaluation of radiation-related risk factors. Radiat. Res.146, 28–36 (1996). CASPubMed Google Scholar
Sankila, R., Pukkala, E. & Teppo, L. Risk of subsequent malignant neoplasms among 470,000 cancer patients in Finland, 1953–1991. Int. J. Cancer60, 464–470 (1995). CASPubMed Google Scholar
Dong, C. & Hemminki, K. Second primary neoplasms in 633,964 cancer patients in Sweden, 1958–1996. Int. J. Cancer93, 155–161 (2001). CASPubMed Google Scholar
Curtis, R. E., Boice, J. D. Jr Kleinerman, R. A., Flannery, J. T. & Fraumeni, J. F. Jr. Summary: multiple primary cancers in Connecticut, 1935–1982. Natl Cancer Inst. Monogr.68, 219–242 (1985). CASPubMed Google Scholar
Olsen, J. H. et al. Second malignant neoplasms after cancer in childhood or adolescence. Nordic Society of Paediatric Haematology and Oncology Association of the Nordic Cancer Registries. BMJ307, 1030–1036 (1993). CASPubMedPubMed Central Google Scholar
Reis, L. A. G. et al. (eds). SEER Cancer Statistics Review, 1973–1998, National Cancer Institute. (National Cancer Institute, Bethesda, Maryland, 2001).
Bhatia, S. et al. Malignant neoplasms following bone marrow transplantation. Blood87, 3633–3639 (1996). CASPubMed Google Scholar
Darrington, D. L. et al. Incidence and characterization of secondary myelodysplastic syndrome and acute myelogenous leukaemia following high-dose chemoradiotherapy and autologous stem cell transplantation for lymphoid malignancies. J. Clin. Oncol.12, 2527–2534 (1994). CASPubMed Google Scholar
Zang, E. A. & Wynder, E. L. Differences in lung cancer risk between men and women: examination of the evidence. J. Natl Cancer Inst.88, 183–192 (1996). CASPubMed Google Scholar
Breslow, N. E. et al. Second malignant neoplasms following treatment of Wilm's tumour: a report from the National Wilms' Tumour Study Group. J. Clin. Oncol.13, 1851–1859 (1995). CASPubMed Google Scholar
Hawkins, M. M. et al. Radiotherapy, alkylating agents, and risk of bone cancer after childhood cancer. J. Natl Cancer Inst.88, 270–278 (1996).In a large population-based cohort study, the authors report a low incidence of bone tumours among three-year survivors of childhood cancer, except following hereditary retinoblastoma, Ewing's sarcoma and other malignant bone tumours. They show the dose–response relationship of the second primary bone tumours with increasing doses of radiation, and the association of second primary bone tumours with alkylating agents. CASPubMed Google Scholar
Garwicz, S. et al. Second malignant neoplasms after cancer in childhood and adolescence: a population-based case–control study in the 5 Nordic countries. The Nordic Society for Pediatric Hematology and Oncology. The Association of the Nordic Cancer Registries. Int. J. Cancer88, 672–678 (2000).The authors carried out a nested case–control study within a Nordic cohort of 25,120 patients to assess the risk factors associated with the development of second primary cancers following a first primary cancer in childhood. Radiation therapy was the most important treatment-related risk factor identified. CASPubMed Google Scholar
Tucker, M. A., D'Angio, G. J., Boice, J. D. Jr et al. Bone sarcomas linked to radiotherapy and chemotherapy in children. N. Engl. J. Med.317, 588–593 (1987). CASPubMed Google Scholar
Hancock, S. L., Tucker, M. A. & Hoppe, R. T. Breast cancer after treatment of Hodgkin's disease. J. Natl Cancer Inst.85, 25–31 (1993). CASPubMed Google Scholar
Metayer, C. et al. Second cancers among long-term survivors of Hodgkin's disease diagnosed in childhood and adolescence. J. Clin. Oncol.18, 2435–2443 (2000). CASPubMed Google Scholar
Kaste, S. C. et al. Breast masses in women treated for childhood cancer: incidence and screening guidelines. Cancer82, 784–792 (1998). CASPubMed Google Scholar
Travis, L. B., Curtis, R. E. & Boice, J. D. Jr. Late effects of treatment for childhood Hodgkin's disease. N. Engl. J. Med.334, 745–751 (1996). Google Scholar
De Vathaire, F. et al. Thyroid carcinomas after irradiation for a first cancer during childhood. Arch. Intern. Med.159, 2713–2719 (1999). CASPubMed Google Scholar
Sklar, C. et al. Abnormalities of the thyroid in survivors of Hodgkin's disease: data from the Childhood Cancer Survivor Study. J. Clin. Endocrinol. Metab.85, 3227–3232 (2000). CASPubMed Google Scholar
Loning, L. et al. Secondary neoplasms subsequent to Berlin–Frankfurt–Munster therapy of acute lymphoblastic leukaemia in childhood: significantly lower risk without cranial radiotherapy. Blood95, 2770–2775 (2000).The authors followed a large cohort of patients treated for ALL in childhood on Berlin-Frankfurt–Munster (BFM) therapeutic protocols, and showed that the incidence of second cancers is relatively low, except among patients receiving cranial irradiation. CASPubMed Google Scholar
de Vathaire, F. et al. Second malignant neoplasms after a first cancer in childhood: temporal pattern of risk according to type of treatment. Br. J. Cancer79 1884–1893 (1999). CASPubMed Google Scholar
Smith, M. A. et al. Secondary leukaemia or myelodysplastic syndrome after treatment with epipodophyllotoxins. J. Clin. Oncol.17, 569–577 (1999).The Cancer Therapy Evaluation Program of the National Cancer Institute has developed a monitoring plan to describe the incidence of secondary leukaemia after epipodophyllotoxin treatment and the relationship between epipodophyllotoxin cumulative dose and risk of secondary leukaemia. The study failed to show a dose–response relationship between epipodophylltoxins and therapy-related leukaemia. CASPubMed Google Scholar
Pedersen-Bjergaard, J. et al. Carcinoma of the urinary bladder after treatment with cyclophosphamide for non-Hodgkin's lymphoma. N Engl J Med318 1028–1032 (1988). CASPubMed Google Scholar
Wolden, S. L., Lamborn, K. R., Cleary, S. F., Tate, D. J. & Donaldson, S. S. Second cancers following pediatric Hodgkin's disease. J. Clin. Oncol.16, 536–544 (1998). CAS Google Scholar
Sankila, R. et al. Risk of subsequent malignant neoplasms among 1,641 Hodgkin's disease patients diagnosed in childhood and adolescence: a population-based cohort study in the five Nordic countries — Association of the Nordic Cancer Registries and the Nordic Society of Pediatric Hematology and Oncology. J. Clin. Oncol.14, 1442–1446 (1996). CASPubMed Google Scholar
Schellong, G. et al. Low risk of secondary leukaemia after chemotherapy without mechlorethamine in childhood Hodgkin's disease: German–Austrian Pediatric Hodgkin's Disease Group. J. Clin. Oncol.15, 2247–2253 (1997). CASPubMed Google Scholar
Greene, M. H. et al. Melphalan may be a more potent leukaemogen than cyclophosphamide. Ann. Intern. Med.105, 36–67 (1986). Google Scholar
Tucker, M. A. et al. Leukaemia after therapy with alkylating agents for childhood cancer. J. Natl Cancer Inst.78, 459–464 (1987). CASPubMed Google Scholar
Chabner, B. A. & Myers, C. E. in Principles and Practice of Oncology 2nd edn (eds DeVita, V.T., Hellman, S. & Rosenberg, S. A.) 349–395 (J. B. Lippincott, Philadelphia, 1989). Google Scholar
Tew, K. D., Clovin, M. & Chabner, B. A. in Cancer Chemotherapy and Biotherapy: Principles and Practice Vol. 1 (eds Chabner, B. A. & Longo, D. L.) 297–232 (Lippincott-Raven Publishers, New York (1996). Google Scholar
Karp, J. E. & Smith, M. A. The molecular pathogenesis of treatment-induced (secondary) leukemias: foundations for treatment and prevention. Semin. Oncol.24, 103–113 (1997). CASPubMed Google Scholar
Pui, C.-H. et al. Acute myeloid leukaemia in children treated with epipodophyllotoxins for acute lymphocytic leukaemia. N. Engl. J. Med.325, 1682–1687 (1991).Puiet al. assessed the risk of therapy-related AML among children with ALL treated with epipodophyllotoxins, and showed that the risk of epipodophyllotoxin-related leukaemia depended largely on the schedule of drug administration. CASPubMed Google Scholar
Winick, N. J. et al. Secondary acute myeloid leukaemia in children with acute lymphoblastic leukaemia treated with etoposide. J. Clin. Oncol.11, 209–217 (1993). CASPubMed Google Scholar
Sugita, K. et al. High frequency of etoposide (VP-16)-related secondary leukaemia in children with non-Hodgkin's lymphoma. Am. J. Pediatr. Hematol. Oncol.15, 99–104 (1993). CASPubMed Google Scholar
Hawkins, M. M. et al. Epipodophyllotoxins, alkylating agents, and radiation and risk of secondary leukaemia after childhood cancer. BMJ304, 951–958 (1992).The authors investigated the incidence and aetiology of secondary leukaemia after childhood cancer in a cohort of 16,422 patients diagnosed and treated in the United Kingdom, and showed that epipodophyllotoxins acting alone or together with alkylating agents or radiation seem to be involved in secondary leukaemia after childhood. CASPubMedPubMed Central Google Scholar
Corbett, A. H. & Osheroff, N. When good enzymes go bad: conversion of topoisomerase II to a cellular toxin by antineoplastic drugs. Chem. Res. Toxicol.6, 585–597 (1993). CASPubMed Google Scholar
Felix, C. A. Secondary leukaemias induced by topoisomerase targeted drugs. Biochim. Biophys. Acta1400, 233–235 (1998). CASPubMed Google Scholar
Atlas, M. et al. Cloning and sequence analysis of four t(9;11) therapy-related leukaemia breakpoints. Leukemia12, 1895–1902 (1998). CASPubMed Google Scholar
Megonigal, M. D. et al. Detection of leukaemia-associated MLL-GAS7 translocation early during chemotherapy with DNA topoisomerase II inhibitors. Proc. Natl Acad. Sci. USA97, 2814–2819 (2000). CASPubMed Google Scholar
Lovett, B. D. et al. Etoposide metabolites enhance DNA topoisomerase II cleavage near leukaemia-associated MLL translocation breakpoints. Biochemistry40, 1159–1170 (2001). CASPubMed Google Scholar
Super, H. J. G. et al. Rearrangements of the MLL gene in therapy-related acute myeloid leukaemia in patients previously treated with agents targeting DNA topoisomerase II. Blood82, 3705–3711 (1993). CASPubMed Google Scholar
Felix, C. A. et al. Chromosome band 11q23 translocation breakpoints are DNA topoisomerase II cleavage sites. Cancer Res.55, 4287–4292 (1995). CASPubMed Google Scholar
Bower, M. et al. Human trithorax gene rearrangements in therapy-related acute leukaemia after etoposide treatment. Leukemia8, 226–229 (1994). CASPubMed Google Scholar
Felix, C. A. et al. Common region of ALL-1 gene disrupted in epipodophyllotoxin-related secondary acute myeloid leukaemia. Cancer Res.53, 2954–2956 (1993). CASPubMed Google Scholar
Broeker, P. L. S. et al. Distribution of 11q23 breakpoints within the MLL breakpoint cluster region in de novo acute leukaemia and therapy-related acute myeloid leukaemia: correlation with scaffold attachment regions and topoisomerase II consensus binding sites. Blood87, 1912–1922 (1996). CASPubMed Google Scholar
Hunger, S. P. et al. HRX involvement in de novo and secondary leukaemias with diverse chromosome 11q23 abnormalities. Blood81, 3197–3203 (1993). CASPubMed Google Scholar
Andersen, M. K., Johansson, B., Larsen, S. O. & Pedersen-Bjergaard, J. Chromosomal abnormalities in secondary MDS and AML. Relationship to drugs and radiation with specific emphasis on the balanced rearrangements. Haematologica83, 483–488 (1998). CASPubMed Google Scholar
Jeha, S., Jaffe, N. & Robertson, R. Secondary acute nonlymphoblastic leukaemia in two children following treatment with a _cis_-diamminechloroplatinum-II-based regimen for osteosarcoma. Med. Pediatr. Oncol.20, 71–74 (1992). CASPubMed Google Scholar
Ben-Yehuda, D. et al. Microsatellite instability and p53 mutations in therapy-related leukaemia suggest a mutator phenotype. Blood88, 4296–4303 (1996). CASPubMed Google Scholar
Gafanovich, A. et al. Microsatellite instability and p53 mutations in pediatric secondary malignant neoplasms. Cancer85, 504–510 (1999). CASPubMed Google Scholar
Hisada, M. et al. Multiple primary cancers in families with Li–Fraumeni syndrome. J. Natl Cancer Inst.90, 606–611 (1998). CASPubMed Google Scholar
Swift, M., Morrell, D., Massey, R. B. & Chase, C. L. Incidence of cancer in 161 families affected by ataxia-telangiectasia. N. Engl. J. Med.325, 1831–1836 (1991). CASPubMed Google Scholar
Nichols, K. E. et al. Heterozygous germline ATM mutations do not contribute to radiation-associated malignancies after Hodgkin's disease. J. Clin. Oncol.17, 1259 (1999).
Shafman, T. D. et al. Prevalence of germline truncating mutations in ATM in women with a second breast cancer after radiation therapy for a contalateral tumour. Genes Chromosomes Cancer27, 124–129 (2000). CASPubMed Google Scholar
Teraoka, S. N. et al. Increased frequency of ATM mutations in breast carcinoma patients with early onset disease and positive family history. Cancer92, 479–487 (2001). CASPubMed Google Scholar
Relling, M. V. et al. High incidence of secondary brain tumours after radiotherapy and antimetabolites. Lancet354, 34–39 (1999).The authors assessed the clinical, biological and pharmacokinetic features among children with ALL receiving cranial radiotherapy, and showed that underlying genetic characteristics and treatment variables might be associated with an increased risk of radiation-associated brain tumours. CASPubMed Google Scholar
Relling, M. V. et al. Etoposide and antimetabolite pharmacology in patients who develop secondary acute myeloid leukaemia. Leukemia12, 346–352 (1998).The authors assessed the pharmacological characteristics of patients who developed epipodophyllotoxin-related AML after ALL, and showed that patients with lower thiopurine methyltransferase activity were more likely to develop secondary AML in this setting. CASPubMed Google Scholar
Naoe, T. et al. Analysis of genetic polymorphism in NQO1, GST-M1, GST-T1, and CYP3A4 in 469 Japanese patients with therapy-related leukaemia/myelodysplastic syndrome and de novo acute myeloid leukaemia. Clin. Cancer Res.6, 4091–4095 (2000). CASPubMed Google Scholar
Chen, H. et al. Increased risk for myelodysplastic syndromes in individuals with glutathione transferase θ1 (GSTT1) gene defect. Lancet347, 295–297 (1996). CASPubMed Google Scholar
Felix, C. A. et al. Association of CYP3A4 genotype with treatment-related leukaemia. Proc. Natl Acad. Sci. USA95, 13176–13181 (1998).The authors showed that individuals with the CYP3A4-W genotype might be at increased risk for treatment-related leukaemia and that epipodophyllotoxin metabolism by CYP3A4 might contribute to the secondary leukaemia by increasing production of potentially DNA-damaging reactive intermediates. CASPubMed Google Scholar
Hayes, J. D. & Pulford, D. J. The glutathione _S_-transferase supergene family: regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance. Crit. Rev. Biochem. Mol. Biol.30, 445–600 (1995). CASPubMed Google Scholar
Smith, G., Stanley, L. A., Sim, E., Strange, R. C. & Wolf, C. R. Metabolic polymorphisms and cancer susceptibility. Cancer Surv.25, 27–65 (1995). CASPubMed Google Scholar
Raunio, H. et al. Diagnosis of polymorphisms in carcinogen activating and inactivating enzymes and cancer susceptibility. Gene159, 113–121 (1995). CASPubMed Google Scholar
Wrighton, S. & Stevens, J. The human hepatic cytochromes P450 involved in drug metabolism. Crit. Rev. Toxicol.22, 1–21 (1992). CASPubMed Google Scholar
Allan, J. M. et al. Polymorphism in glutathione _S_-transferase P1 is associated with susceptibility to chemotherapy-induced leukaemia. Proc. Natl Acad. Sci. USA98, 11592–11597 (2001).The authors assessed polymorphisms in glutathioneS-transferases and sought to identify an association with therapy-related leukaemia. They showed that inheritance of at least one Val allele at GSTP1 codon 105 confers a significantly increased risk of developing therapy-related leukaemia after cytotoxic chemotherapy. CASPubMed Google Scholar
Woo, M. H. et al. Glutathione _S_-transferase genotypes in children who develop treatment-related acute myeloid malignancies. Leukemia14, 226–231 (2000). Google Scholar
Van Leeuwen, F. E. et al. Roles of radiotherapy and smoking in lung cancer following Hodgkin's disease. J. Natl Cancer Inst.87, 1530–1537 (1995).This study investigated the effects of radiation dose, chemotherapy and smoking on the risk of lung cancer following treatment of Hodgkin's disease. The authors showed that the excess risk of lung cancer in patients with Hodgkin's disease who were treated with radiotherapy is related to the radiation dose received by the affected area of the lung. Moreover, smokers experience a significantly greater risk attributable to radiotherapy than non-smokers. CASPubMed Google Scholar
Boivin, J. F. Smoking, treatment for Hodgkin's disease, and subsequent lung cancer. J. Natl Cancer Inst.87, 1502–1503 (1995). CASPubMed Google Scholar
Tucker, M. A. et al. Second primary cancers related to smoking and treatment of small-cell lung cancer. J. Natl Cancer Inst.89, 1782–1788 (1997). CASPubMed Google Scholar
Inskip, P. D. & Boice, J. D. Jr. Radiotherapy-induced cancer among women who smoke. Cancer73, 1541–1543 (1994). CASPubMed Google Scholar
Neugut, A. I. et al. Increased risk of lung cancer after breast cancer radiation therapy in cigarette smokers. Cancer73, 1615–1620 (1994). CASPubMed Google Scholar
Jensen, O. M., Paine, S. L., McMichal, A. J. & Ewertz, M. in Cancer Epidemiology and Prevention 2nd edn (eds Schottenfeld, D. & Fraumeni, J. F.) 290–318 (Oxford, Oxford Univ. Press, 1996). Google Scholar
Rothman, K. & Keller, A. Z. The effect of joint exposure to alcohol and tobacco on risk of cancers of the mouth and pharynx. J. Chronic Dis.25, 711–716 (1972). CASPubMed Google Scholar
Flanders, W. D. & Rothman, K. J. Interaction of alcohol and tobacco in laryngeal cancer. Am. J. Epidemiol.115, 371–379 (1982). CASPubMed Google Scholar
LaVecchia, C. & Negri, E. The role of alcohol in esophageal cancer in nonsmokers, and the role of tobacco in nondrinkers. Int. J. Cancer43, 784–785 (1989). CAS Google Scholar
van Leeuwen, F. E. et al. Roles of radiotherapy and smoking in lung cancer following Hodgkin's disease. J. Natl Cancer Inst.87, 1530–1537 (1995). CASPubMed Google Scholar
Perera, F. P. Environment and cancer: who are susceptible? Science278, 1068–1073 (1997). CASPubMed Google Scholar
Baron, J. A. & Rohan, T. E. in Cancer Epidemiology and Prevention 2nd edn (eds Schottenfeld, D. & Fraumeni, J. F.) 269–289 (Oxford, Oxford Univ. Press, 1996). Google Scholar
Rothman, K. & Keller, A. Z. The effect of joint exposure to alcohol and tobacco on risk of cancers of the mouth and pharynx. J. Chronic Dis.25, 711–716 (1972). CASPubMed Google Scholar
Flanders, W. D. & Rothman, K. J. Interaction of alcohol and tobacco in laryngeal cancer. Am. J. Epidemiol.115, 371–379 (1982). CASPubMed Google Scholar
LaVecchia, C. & Negri, E. The role of alcohol in esophageal cancer in nonsmokers, and the role of tobacco in nondrinkers. Int. J. Cancer43, 784–785 (1989). CAS Google Scholar
Thomas, H. V., Reeves, G. K. & Key, T. J. Endogenous oestrogen and postmenopausal breast cancer: a quantitative review. Cancer Causes Control8, 922–928 (1997). CASPubMed Google Scholar
Pike, M. C., Spicer, D. V., Dahmoush, L. & Press, M. F. Oestrogens, progesterone, normal breast cell proliferation, and breast cancer risk. Epidemiol. Rev.15, 17–35 (1993). CASPubMed Google Scholar
Bosland, M. C. The role of steroid hormones in prostate carcinogenesis. J. Natl Cancer Inst. Monogr.27, 39–66 (2000). CAS Google Scholar
Yu, H. & Rohan, T. Role of the insulin-like growth factor family in cancer development and progression. J. Natl Cancer Inst.92, 1472–1489 (2000). CASPubMed Google Scholar
Sklar, C. A. Growth and neuroendocrine dysfunction following therapy for childhood cancer. Pediatr. Clin. N. Am.44, 489–503 (1997). CAS Google Scholar
Sklar, C. A. et al. Changes in body mass index and prevalence of overweight in survivors of childhood acute lymphoblastic leukaemia: role of cranial irradiation. Med. Pediatr. Oncol.35, 91–95 (2000). CASPubMed Google Scholar
Tavani, A. et al. Risk factors for breast cancer in women under 40 years. Eur. J. Cancer35, 1361–1367 (1999). CASPubMed Google Scholar
Willett, W. C., Dietz, W. H. & Colditz, G. A. Guidelines for healthy weight. N. Engl. J. Med.341, 427–434 (1999). CASPubMed Google Scholar
Sklar, C., Boulad, F., Small, T. & Kernan, N. Endocrine complications of pediatric stem cell transplantation. Front. Biosci.6, G17–G22 (2001).
Bhatia, S., Sather, H. N., Trigg, M., Gaynon, P. & Robison, L. L. Low incidence of second neoplasms following childhood ALL: follow–up of the Children's Cancer Group Cohort. Presented at the American Society of Hematology Meeting, San Francisco, California, 2000.
Bhatia, S., Krailo, M., Robison, L. L. & Meyers, P. Secondary myelodysplasia among survivors of osteosarcoma. Presented at the American society of Clinical Oncology Meeting, San Francisco, California, 2001.
Krishnan, A. et al. Predictors of therapy-related leukaemia and myelodysplasia following autologous transplantation for lymphoma: an assessment of risk factors. Blood95, 1588–1593 (2000). CASPubMed Google Scholar
Bhatia, S., Davies, S. M. & Robison, L. L. in Multiple Primary Cancers (eds Neugut, A. I., Meadows, A. T. & Robinson, E.) 257–275 (Lippincott Williams & Wilkins, Philadelphia, 1999). Google Scholar