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1. Leone G, Fianchi L, Pagano L, Voso MT: Incidence and susceptibility to therapy-related myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):39-45
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  • Therapy-related myeloid neoplasms (t-MN) include acute myeloid leukemias and myelodysplastic syndromes arising in patients who have been treated with chemotherapy, radiation therapy, immunosuppressive agents or after documented exposure to environmental carcinogen. t-MN are defined according to the primary treatment and the corresponding genetic and molecular lesions.
  • Chromosome(s) 7 and/or 5 monosomies or deletions are typical of alkylating agent-induced AML, while balanced translocations involving chromosome bands 11q23 and 21q22 are associated to preceeding therapy with DNA-topoisomerase II inhibitors.
  • Antimetabolites, and in particular the immunosuppressive agents azathioprine and fludarabine, have also been recently associated to t-MN.
  • Combination of polymorphisms impairing detoxification and DNA repair may significantly increase therapy-related myeloid neoplasm risk.
  • Patients with lymphoma are at highest risk if total body irradiation followed by autologous stem cell transplantation is used as rescue or consolidation.
  • The addition of granulocyte-colony stimulating factor (G-CSF) and radiotherapy plays a significant role in t-MN following treatment of childhood acute lymphoblastic leukemia.
  • In solid tumors, treatment for breast cancer and germ-cell tumors has been associated with a 1-5% lifetime risk of t-MN.
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Benzene / adverse effects. Disease Susceptibility / etiology. Humans. Incidence. Radiotherapy / adverse effects. Topoisomerase II Inhibitors

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20026017.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Topoisomerase II Inhibitors; J64922108F / Benzene
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2. Konar H: Clinical experience of ovarian neoplasm in childhood and adolescence. J Indian Med Assoc; 2006 Jun;104(6):317-8, 320-1
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  • [Title] Clinical experience of ovarian neoplasm in childhood and adolescence.
  • Clinical behaviour of 12 cases of ovarian neoplasm in childhood and adolescence was reviewed.
  • Diagnostic work-up required a great deal of time, gentleness and patience.
  • Of all ovarian tumours, 58.4% were epithelial, 33.3% were germ cell group and 8.3% were sex cord stromal tumours.
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Child. Cisplatin / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Drug Therapy, Combination. Early Diagnosis. Female. Hospitals, University. Humans. India. Physician-Patient Relations

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  • (PMID = 17058549.001).
  • [ISSN] 0019-5847
  • [Journal-full-title] Journal of the Indian Medical Association
  • [ISO-abbreviation] J Indian Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin
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3. Lopes LF, Macedo CR, Pontes EM, Dos Santos Aguiar S, Mastellaro MJ, Melaragno R, Vianna SM, Lopes PA, Mendonça N, de Assis Almeida MT, Sonaglio V, Ribeiro KB, Santana VM, Schneider DT, de Camargo B: Cisplatin and etoposide in childhood germ cell tumor: brazilian pediatric oncology society protocol GCT-91. J Clin Oncol; 2009 Mar 10;27(8):1297-303
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  • [Title] Cisplatin and etoposide in childhood germ cell tumor: brazilian pediatric oncology society protocol GCT-91.
  • PURPOSE: In 1988, we formed a consortium of Brazilian institutions to develop uniform standards for the diagnostic assessment and multidisciplinary treatment of children and adolescents with germ cell tumors.
  • We also implemented the first childhood Brazilian germ cell tumor protocol, GCT-91, evaluating two-agent chemotherapy with cisplatin and etoposide (PE).
  • We now report on the clinical characteristics and survival of children and adolescents with germ cell tumors treated on this protocol.
  • PATIENTS AND METHODS: From May 1991 to April 2000, 115 patients (106 assessable patients) were enrolled onto the Brazilian protocol with a diagnosis of germ cell tumor.
  • This is of particular importance for smaller institutions with previous limited experience in the treatment of childhood germ cell tumors.
  • In addition, the results of a two-agent regimen with PE were favorable (5-year overall survival rate is 83.3% for patients in the high-risk group [n = 36] who received PE v 58.8% for patients in the high-risk patients group who received PE plus ifosfamide, vinblastine, and bleomycin [n = 17; P = .017]).
  • Thus for selected patients, complex three-agent regimens may not be necessary to achieve long-term survival, even for some patients with advanced disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Germ Cell and Embryonal / drug therapy

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  • (PMID = 19164215.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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4. Kremens B: [Systemic therapy in children and adolescents]. Urologe A; 2007 Oct;46(10):1404-6
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  • Urologic malignancies in childhood and adolescence are mainly nephroblastomas, neuroblastomas, soft tissue sarcomas, and germ cell tumors.
  • National and supranational treatment studies are the standard of care for pediatric cancer in Germany; they yield 5-year survival rates of almost 90% for nephroblastoma and germ cell tumors and 60% for neuroblastoma (all stages) and rhabdomyosarcoma.
  • The principles of antineoplastic therapy are the same as in adult cancer medicine; the drugs used depend upon the disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoadjuvant Therapy. Urogenital Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / mortality. Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / surgery. Adrenal Medulla. Chemotherapy, Adjuvant. Child. Child, Preschool. Combined Modality Therapy. Humans. Infant. Kidney Neoplasms / drug therapy. Kidney Neoplasms / mortality. Kidney Neoplasms / pathology. Kidney Neoplasms / surgery. Neoplasm Staging. Neoplasms, Germ Cell and Embryonal / drug therapy. Neoplasms, Germ Cell and Embryonal / mortality. Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Germ Cell and Embryonal / surgery. Neuroblastoma / drug therapy. Neuroblastoma / mortality. Neuroblastoma / pathology. Neuroblastoma / surgery. Prognosis. Radiotherapy, Adjuvant. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / mortality. Rhabdomyosarcoma / pathology. Rhabdomyosarcoma / surgery. Survival Rate. Wilms Tumor / drug therapy. Wilms Tumor / mortality. Wilms Tumor / pathology. Wilms Tumor / surgery

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  • (PMID = 17823786.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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5. Schneider DT, Calaminus G, Wessalowski R, Pathmanathan R, Harms D, Göbel U: Therapy of advanced ovarian juvenile granulosa cell tumors. Klin Padiatr; 2002 Jul-Aug;214(4):173-8
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  • [Title] Therapy of advanced ovarian juvenile granulosa cell tumors.
  • BACKGROUND: Gonadal sex cord-stromal tumors are rare tumors that develop from the gonadal non-germ cell component such as granulosa, Sertoli or Leydig cells.
  • Among these, juvenile granulosa cell tumors (JGCT) constitute the largest subgroup of ovarian sex cord-stromal tumors during childhood and adolescence.
  • In local disease (FIGO stage I), the beneficial role of tumor-ovarectomy is well established.
  • In contrast, life expectancy in patients with advanced JGCT (FIGO stage >/= II) is short even after complete tumor resection.
  • PATIENTS AND METHODS: Therefore, we analyzed the patients with FIGO stage >/= II JGCT who were prospectively documented as follow-up patients of the German MAKEI trials for non-testicular germ cell tumors and received the recommended cisplatin-based chemotherapy in an adjuvant setting.
  • Two patients received laparoscopic tumor resection, which was incomplete in both.
  • All patients received 4 or 6 cycles of adjuvant cisplatin-based three-agent chemotherapy in analogy to the current therapeutic concept applied in malignant germ cell tumors.
  • One patient with a large tumor and multiple peritoneal metastases additionally received 40 Gy abdominal irradiation.
  • One patient developed a metachronous tumor of the contralateral ovary after 126 months follow-up and is still alive but currently in therapy of another recurrence.
  • Another patient suffered a tumor recurrence after 12 months but achieved a second complete remission with cisplatin chemotherapy after a follow-up of currently 4 months.
  • One patient achieved complete clinical remission but suffered a diffuse peritoneal tumor recurrence with massive ascites and finally died as a result of tumor progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulosa Cell Tumor / drug therapy. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Cisplatin / administration & dosage. Cisplatin / adverse effects. Combined Modality Therapy. Female. Follow-Up Studies. Germany. Humans. Neoplasm Staging. Prospective Studies. Survival Rate

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  • (PMID = 12165898.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin
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6. Ishibashi M, Nakayama K, Oride A, Yeasmin S, Katagiri A, Iida K, Nakayama N, Miyazaki K: [A case of PEP(BEP)-resistant ovarian dysgerminoma successfully treated by VeIP therapy]. Gan To Kagaku Ryoho; 2009 Mar;36(3):513-7
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  • Ovarian germ cell tumors are malignant tumors which commonly develop during childhood, and which are sensitive to chemotherapy.
  • We have had a case of germ cell tumors which showed resistance to first-line PEP(BEP)chemotherapy.
  • As second-line chemotherapy, VeIP therapy was used, because it is possible that this therapy is effective against recurrent testicular germ cell tumors.
  • She experienced acute abdominal pain and visited the hospital, where she was diagnosed with torsion of an ovarian tumor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / drug effects. Dysgerminoma / drug therapy. Dysgerminoma / pathology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / pathology

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  • (PMID = 19295284.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; Q20Q21Q62J / Cisplatin
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7. Holleman A, den Boer ML, de Menezes RX, Cheok MH, Cheng C, Kazemier KM, Janka-Schaub GE, Göbel U, Graubner UB, Evans WE, Pieters R: The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia. Blood; 2006 Jan 15;107(2):769-76
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  • [Title] The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) consists of various subtypes that respond differently to cytotoxic drugs and therefore have a markedly different clinical outcome.
  • We used microarrays to investigate, in 190 children with ALL at initial diagnosis, whether 70 key apoptosis genes were differentially expressed between leukemic subgroups defined by lineage, genetic subtype, in vitro drug resistance, and clinical outcome.
  • The expression of 44 of 70 genes was significantly different in T-versus B-lineage ALL, 22 genes differed in hyperdiploid versus nonhyperdiploid, 16 in TEL-AML1-positive versus-negative, and 13 in E2A-rearranged versus germ-line B-lineage ALL.
  • In conclusion, ALL subtypes have a unique expression pattern of apoptosis genes and our data suggest that selective genes are linked to cellular drug resistance and prognosis in childhood B-lineage ALL.
  • [MeSH-major] Apoptosis. Cell Lineage. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


8. Yang JJ, Cheng C, Yang W, Pei D, Cao X, Fan Y, Pounds SB, Neale G, Treviño LR, French D, Campana D, Downing JR, Evans WE, Pui CH, Devidas M, Bowman WP, Camitta BM, Willman CL, Davies SM, Borowitz MJ, Carroll WL, Hunger SP, Relling MV: Genome-wide interrogation of germline genetic variation associated with treatment response in childhood acute lymphoblastic leukemia. JAMA; 2009 Jan 28;301(4):393-403
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  • [Title] Genome-wide interrogation of germline genetic variation associated with treatment response in childhood acute lymphoblastic leukemia.
  • CONTEXT: Pediatric acute lymphoblastic leukemia (ALL) is the prototype for a drug-responsive malignancy.
  • Of 102 SNPs, 21 were also associated with antileukemic drug disposition, generally linking MRD eradication with greater drug exposure.
  • In total, 63 of 102 SNPs were associated with early response, relapse, or drug disposition.
  • CONCLUSION: Host genetic variations are associated with treatment response for childhood ALL, with polymorphisms related to leukemia cell biology and host drug disposition associated with lower risk of residual disease.

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  • (PMID = 19176441.001).
  • [ISSN] 1538-3598
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA021765-259006; United States / NCI NIH HHS / CA / U10 CA098413-07; None / None / / U10 CA029139-22; None / None / / U10 CA098413-07; United States / NCI NIH HHS / CA / CA 29139; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / P30 CA021765-259006; United States / NCI NIH HHS / CA / R37 CA036401-24; United States / NIGMS NIH HHS / GM / GM061374-03; United States / NCI NIH HHS / CA / CA 086011; United States / NIGMS NIH HHS / GM / U01 GM061393-08; United States / NCI NIH HHS / CA / CA093552-02; United States / NCI NIH HHS / CA / R01 CA060419-13; United States / NCI NIH HHS / CA / CA 51001; United States / NCI NIH HHS / CA / CA 60419; United States / NCI NIH HHS / CA / CA078224-10; United States / NCI NIH HHS / CA / CA 093552-02; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / U10 CA098413; None / None / / R01 CA051001-15; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / CA 78224; United States / NCI NIH HHS / CA / CA098543-05; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA R3736401; United States / NIGMS NIH HHS / GM / GM061393-08; United States / NCI NIH HHS / CA / CA086011-08; United States / NCI NIH HHS / CA / CA036401-24; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / R01 CA051001-15; United States / NIGMS NIH HHS / GM / U01 GM061374-03; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061374; United States / NCI NIH HHS / CA / R01 CA078224-10; United States / NCI NIH HHS / CA / U10 CA098543-05; United States / NCI NIH HHS / CA / R01 CA086011-08; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA051001; United States / NIGMS NIH HHS / GM / U01 GM61374; None / None / / R01 CA060419-13; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / R01 CA086011; United States / NCI NIH HHS / CA / U10 CA029139-22; United States / NCI NIH HHS / CA / R01 CA093552-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS89586; NLM/ PMC2664534
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9. Schmidt P, Haas RJ, Göbel U, Calaminus G: [Results of the German studies (MAHO) for treatment of testicular germ cell tumors in children--an update]. Klin Padiatr; 2002 Jul-Aug;214(4):167-72
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  • [Title] [Results of the German studies (MAHO) for treatment of testicular germ cell tumors in children--an update].
  • BACKGROUND: The MAHO studies for treatment of testicular germ cell tumors in childhood and adolescence registered between 1982 and 1/2001 260 patients (pts.).
  • 17 pts. had stage III or IV, 5 of these died despite receiving salvage therapy, 9 pts. survived in complete remission, 3 pts. had partial remission.
  • For YST pts. of stages greater than stage I A and all other malignant testicular tumors in childhood effective chemotherapy exists with an overall cure rate of about 95 %.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Germ Cell and Embryonal / drug therapy. Testicular Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Combined Modality Therapy. Drug Administration Schedule. Follow-Up Studies. Humans. Lymph Node Excision. Lymph Nodes / pathology. Male. Neoplasm Staging. Orchiectomy. Salvage Therapy. Survival Rate

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  • (PMID = 12165897.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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10. Yang JJ, Bhojwani D, Yang W, Cai X, Stocco G, Crews K, Wang J, Morrison D, Devidas M, Hunger SP, Willman CL, Raetz EA, Pui CH, Evans WE, Relling MV, Carroll WL: Genome-wide copy number profiling reveals molecular evolution from diagnosis to relapse in childhood acute lymphoblastic leukemia. Blood; 2008 Nov 15;112(10):4178-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide copy number profiling reveals molecular evolution from diagnosis to relapse in childhood acute lymphoblastic leukemia.
  • The underlying pathways that lead to relapse in childhood acute lymphoblastic leukemia (ALL) are unknown.
  • To comprehensively characterize the molecular evolution of relapsed childhood B-precursor ALL, we used human 500K single-nucleotide polymorphism arrays to identify somatic copy number alterations (CNAs) in 20 diagnosis/relapse pairs relative to germ line.
  • In an independent cohort of children with ALL, reduced expression of MSH6 was associated with resistance to mercaptopurine and prednisone, thereby providing a plausible mechanism by which this acquired deletion contributes to drug resistance at relapse.

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  • (PMID = 18768390.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / NCI CA 51 001; United States / NIGMS NIH HHS / GM / U01GM61374; United States / NCI NIH HHS / CA / CA21765; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061374; United States / NCI NIH HHS / CA / CA 78 224; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / CA093552-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; 0 / DNA-Binding Proteins; 0 / EBF1 protein, human; 0 / G-T mismatch-binding protein; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Trans-Activators; 148971-36-2 / Ikaros Transcription Factor; 9PHQ9Y1OLM / Prednisolone; E7WED276I5 / 6-Mercaptopurine
  • [Other-IDs] NLM/ PMC2581992
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