Статті в журналах: "Child leukaemia"

1

Ivanov, E. P., G. Tolochko, V. S. Lazarev, and L. Shuvaeva. "Child leukaemia after Chernobyl." Nature 365, no. 6448 (October 1993): 702. http://dx.doi.org/10.1038/365702a0.

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2

WOLFF, SIMON P. "Child leukaemia — curies or cars?" Nature 346, no. 6284 (August 1990): 517. http://dx.doi.org/10.1038/346517b0.

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3

Russo, Filippo, Francesco Buda, Concetta Buda, Pietro Aragona, Giovanni Tessitori, Giorgio Simon, Sergio Chillemi, Nicola Caristi, and Alfonso Faiella. "Acute megakaryoblastic leukaemia in a child." European Journal of Cancer and Clinical Oncology 27, no. 12 (December 1991): 1713–14. http://dx.doi.org/10.1016/0277-5379(91)90457-o.

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4

Zuna, Jan, Tatiana Burjanivova, Zuzana Zemanova, Sharon Horsley, Lyndal Kearney, Katerina Muzikova, Claus Meyer, et al. "MLL Translocation in a Multipotent Progenitor Causing Acute Lymphoblastic Leukaemia - Two-Step Model of the Disease." Blood 108, no. 11 (November 1, 2006): 2295. http://dx.doi.org/10.1182/blood.v108.11.2295.2295.

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Abstract Leukaemias with MLL gene rearrangement are usually considered prognostically unfavourable and the clinical symptoms typically follow the translocation formation rapidly. MLL rearrangement is thus thought to be a major hit in leukaemogenesis that is either sufficient to cause the disease or it is a very strong and rapid inducer of the subsequent hit(s) required for the malignant transformation. We report an unusual presentation of secondary acute lymphoblastic leukaemia (sALL) with MLL rearrangement. Our patient was diagnosed originally with acute myeloid leukaemia (AML-M3) characterised by PML/RARα fusion and an internal tandem duplication of FLT3 (FLT3/ITD). After 30 months of complete remission of AML, she developed sALL with MLL/FOXO3A fusion gene. Bone marrow (BM) samples taken during AML therapy were analysed for the presence of these aberrations. Both the PML/RARα fusion and FLT3/ITD disappeared shortly after AML onset and did not reappear. However, FISH and quantitative RT-PCR showed the presence of the MLL/FOXO3A fusion 20 months before the diagnosis of sALL, present in 10–90% of BM cells. Morphological examination showed no blast infiltration of the BM at this time. Experiments combining FISH and morphology confirmed the presence of an MLL rearrangement in myeloid as well as lymphoid cells, indicating that the fusion arose in a multipotent progenitor. In order to identify potential secondary genetic events precipitating sALL in this patient, we used Affymetrix 50K single nucleotide polymorphism (SNP) array analysis on DNA from the diagnostic sALL sample versus the "preleukaemic" (remission AML) sample taken 16 months before. This analysis revealed a 10 Mb amplification on 19q13.32 in the sALL sample, not present in the preleukaemic sample: this was confirmed by FISH with a BAC from the amplified region. A difference between the pre-leukaemic and leukaemic cells is also demonstrated by the incomplete rearrangement of IgH gene (DH1/JH) present only at the diagnosis of sALL. There are about 450 genes in the amplified region on 19q and several of them might be involved in deregulation of the preleukaemic cell if overrepresented (e.g. FLT3 ligand, interleukin 11, Ras interacting protein 1, Stem cell growth factor, Aurora C). The long latency period prior to the onset of the secondary leukaemia in our case resembles the mouse model of MLL/FOXO3A. However, in contrast to the animal model and also to the previous reports of MLL/FOXO3A patients (2 cases described so far, both secondary AMLs after Hodgkin’s disease), our child developed leukaemia from the lymphoid lineage. Taken together, these results indicate that the MLL/FOXO3A fusion alone is not sufficient to cause leukaemia and that second hit is required to the onset of the disease. A responsible gene is possibly located on the telomeric part of the 19q.

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5

Saha, V., and J. S. Lilleyman. "Leukaemia." Current Paediatrics 8, no. 2 (June 1998): 73–77. http://dx.doi.org/10.1016/s0957-5839(98)80122-x.

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6

Lilleyman, J. S. "Leukaemia." Current Paediatrics 2, no. 4 (December 1992): 241–44. http://dx.doi.org/10.1016/0957-5839(92)90245-m.

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7

Mohd Radzi, Muhammad Amiro Rasheeq, Ariffin Nasir, Shatriah Ismail, Razan Hayati Zulkeflee, Juhara Haron, and Norsarwany Mohamad. "Orbital Swelling: An Unusual Case of Relapsed Acute Lymphoblastic Leukaemia in A Preschool Child." Malaysian Journal of Paediatrics and Child Health 27, no. 2 (October 3, 2021): 19–22. http://dx.doi.org/10.51407/mjpch.v27i2.139.

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Acute lymphoblastic leukaemia (ALL) is the most frequent childhood cancer. Children usually present with signs of bone marrow failure like recurrent or prolonged fever, pallor, lethargy, bleeding tendencies, bone pain and others. Occasionally they may present with sign of infiltration of leukaemic cells into other organs such as testicular and central nervous system, rarely to the periorbital or orbital region. Similarly in relapse cases, they typically presented either in bone marrow, central nervous system relapse or testicular but rarely orbital involvement. Here we report the clinical case of a five-year-old boy who developed relapsed B-ALL, presented to us with unilateral right eye swelling without other clinical findings and absence of blast cells in the peripheral blood film as well as bone marrow aspirate specimen.

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8

Cole, Andrew. "Child in gene therapy programme develops leukaemia." BMJ 336, no. 7634 (January 3, 2008): 13.2–13. http://dx.doi.org/10.1136/bmj.39436.582292.db.

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9

Sanchez-Mostiero, Daisy Olave, and Jamela Merriam Aragon Boussati. "Low back pain as an unusual presentation in a child with acute lymphoblastic leukaemia." BMJ Case Reports 15, no. 3 (March 2022): e242843. http://dx.doi.org/10.1136/bcr-2021-242843.

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Acute leukaemia is the most common childhood cancer. The clinical presentation of acute leukaemia includes fever, pallor, bleeding tendencies, hepatosplenomegaly, lymphadenopathy and bone pains. This case is about a 7-year-old boy who presented with 2 months of progressive low back pain after jumping into the sea. Radiologic workup showed compression fractures in the T6–L5 regions of the spine. Trauma and osteogenesis imperfecta were considered initially until the patient developed the classic features of leukaemia. Analysis of the bone marrow aspirate, 2 months after the sea incident, revealed B cell acute lymphoblastic leukaemia (ALL). The low back pain subsided after a week of chemotherapy. A symptom that involves bone pain in a child needs thorough evaluation because a delay in diagnosis affects the outcome of treatment. ALL has been lingering at the time of his accident and this has caused weakening of his spine that resulted in much more severe injury than would have occurred in the absence of the ALL.

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10

Bomken, Simon N., and H. Josef Vormoor. "Childhood leukaemia." Paediatrics and Child Health 19, no. 8 (August 2009): 345–50. http://dx.doi.org/10.1016/j.paed.2009.04.003.

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11

Goldman, Michael, and Chaim Kaplinsky. "Cephalhaematoma in a child with acute promyelocytic leukaemia." Pediatric Radiology 32, no. 9 (May 4, 2002): 695–96. http://dx.doi.org/10.1007/s00247-001-0575-5.

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12

Masure, O., C. Leostic, M. L. Abalain, C. Chastel, I. Yakoub-Agha, C. Berthou, and J. Briere. "Malassezia furfur septicaemia in a child with leukaemia." Journal of Infection 23, no. 3 (November 1991): 335–36. http://dx.doi.org/10.1016/0163-4453(91)93296-o.

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13

Brayley, Jessica, Lauren Katie Stanton, Lucy Jenner, and Siba Prosad Paul. "Recognition and management of leukaemia in children." British Journal of Nursing 28, no. 15 (August 8, 2019): 985–92. http://dx.doi.org/10.12968/bjon.2019.28.15.985.

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Leukaemia is the most common cancer in children. The presenting manifestations can be wide-ranging, from a relatively well child to life-threatening complications. Symptoms can be manifested in any of the bodily systems. Undertaking a thorough clinical assessment of the child, in addition to recognising and addressing parental concerns, is vital. Furthermore, recognising that children can commonly present with musculoskeletal or abdominal symptoms increases the diagnostic yield, thereby preventing missed or late diagnoses. Childhood cancer has a huge impact on the child and their family, both at diagnosis and in the long term; providing advice and signposting families to appropriate support groups is an important aspect of their management. Nurses play a vital role in managing children with cancers, starting from raising suspicion and identifying the child with leukaemia, ensuring that high-quality care is delivered throughout their treatment, managing complications, and providing support and information to children and their families. An illustrative case study is included to highlight some of the challenges that health professionals may encounter in their clinical practice.

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14

Jiang, Chang-Jen, Der-Cherng Liang, and Hwei-Fang Tien. "NEONATAL TRANSIENT LEUKAEMOID PROLIFERATION FOLLOWED BY ACUTE MYELOID LEUKAEMIA IN A PHENOTYPICALLY NORMAL CHILD." British Journal of Haematology 77, no. 2 (February 1991): 247–48. http://dx.doi.org/10.1111/j.1365-2141.1991.tb07986.x.

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15

Will, Andrew. "Update on leukaemia." Paediatrics and Child Health 18, no. 3 (March 2008): 107–11. http://dx.doi.org/10.1016/j.paed.2007.12.005.

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16

Van Bever, H., Y. Benoit, M. J. Delbeke, and E. Orye. "Meningeal leukaemia in the blastic phase of chronic granulocytic leukaemia." European Journal of Pediatrics 144, no. 4 (November 1985): 417–18. http://dx.doi.org/10.1007/bf00441794.

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17

Behjati, Sam, Amy Ruffle, Anne Kelly, and Emmy Dickens. "Fifteen-minute consultation: Initial management of suspected acute leukaemia by non-specialists." Archives of disease in childhood - Education & practice edition 105, no. 2 (July 5, 2019): 66–70. http://dx.doi.org/10.1136/archdischild-2017-314043.

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Leukaemia is the most common cancer of childhood. Most children with a new diagnosis of leukaemia are clinically stable at initial presentation. However, there are a number of life-threatening complications that have to be considered and monitored for. These complications include sepsis, tumour lysis syndrome, mediastinal masses, bleeding and pain. The aim of this article is to equip the general paediatrician with a framework for managing children with suspected leukaemia, prior to transfer to the primary treatment centre. The presentation, diagnosis and definitive treatment of acute leukaemia is not in the remit of this article.

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18

Noetzli, Jasmine, Sophie Voruz, Dorothea Wunder, Marie-Pierre Primi, Laura Crosazzo, Mathilde Gavillet, Olivier Spertini, and Sabine Blum. "Ten Year Single-Center Experience in Fertility Preservation of 459 Patients Suffering from Acute Leukaemia." Blood 126, no. 23 (December 3, 2015): 3751. http://dx.doi.org/10.1182/blood.v126.23.3751.3751.

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Abstract Patients with acute leukaemias suffer from a life threatening disease that has to be treated immediately. Fertility preservation is recommended in these patients, but quite often not possible. Methods This study is a retrospective analysis of 459 patients suffering from acute leukaemia, 221 with acute myeloid leukaemia (AML) or high risk MDS, 238 with acute lymphoblastic leukaemia (ALL) diagnosed between 2002 and 2012 in the University clinics Lausanne, Switzerland. Patients were aged between 0 and 93 years. Of course, not all of these patients were send to the preservation laboratry because of their age or their performance status. Results Of 221 AML cases, 113 were male and 108 female. 46 male patients were between 14 and 60 years of age, of these, 14 were sent for cryopreservation. 12 sperm samples could be frozen, 2 were sample failures due to azoospermia. Of the frozen samples, 7 were destroyed (6 because of death of the patient, 1 according to wish of patient), 4 are still frozen without tempting procreation and 1 was used for in vitro fertilization (IVF) resulting in a healthy child in 2010. 32 female patients were between 17 and 45. No sample of ovocytes was taken, 1 sample of ovarian tissue could be frozen, that was afterwards destroyed because of death of the patient. Of 238 ALL cases, 123 were male and 115 female. 55 male patients were between 14 and 60 years of age, of these 19 were sent for cryopreservation. 16 sperm samples could be frozen, 2 were sample failures due to azoospermia, 1 because of ejaculation failure. Of the frozen samples, 11 were destroyed (8 because of death of the patient, 2 due to missing payment and 1 according to the wish of the patient). 5 samples are still frozen, 1 was used for a IVF resulting in a healthy child in 2009. 12 female patients were between 17-45. No sample taking was tempted. Discussion In a 10-year period in our institution, of 459 patients suffering from acute leukaemia, 145 of these within the age range defined by our institution to qualifying to cryoconservation. Only 29 samples were taken (20%), non of these in paediatric patients. These samples were leading to 2 IVFs. Of note, one male patient whose samples were taken and resulted in one of the IVFs was suffering from ALL and had an allogenous stem cell transplantation with full conditioning. This patient fathered after the IVF two other healthy children without assisted fertilization. The other patient whose sperm sample was taken for a IVF suffered from AML, he too fathered a child spontaneously after the IVF. The data show that only 20% of eligible acute leukaemia patients had the opportunity to freeze sperm or ovocytes samples. Certainly, this was not possible for a lot of patients due to performance status, but more effort has to be done to improve sampling in these patients. Disclosures No relevant conflicts of interest to declare.

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19

Tweddle, Deborah A., J. Clive Graham, Gillian S. Shankland, and Jennifer Kernahan. "Cerebral candidiasis in a child 1 year after leukaemia." British Journal of Haematology 103, no. 3 (December 1998): 795–97. http://dx.doi.org/10.1046/j.1365-2141.1998.01023.x.

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20

Hanada, Takashi, Masaki Nakazawa, Hideo Sakuma, Masahiko Takahashi, Ikuko Kondo, and Hitoshi Takita. "Megakaryoblastic transformation of chronic myelogenous leukaemia in a child." Scandinavian Journal of Haematology 33, no. 5 (April 24, 2009): 476–81. http://dx.doi.org/10.1111/j.1600-0609.1984.tb00728.x.

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21

Kars, Marijke C., Mia SH Duijnstee, Aart Pool, Johannes JM van Delden, and Mieke HF Grypdonck. "Being there: parenting the child with acute lymphoblastic leukaemia." Journal of Clinical Nursing 17, no. 12 (June 2008): 1553–62. http://dx.doi.org/10.1111/j.1365-2702.2007.02235.x.

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22

Schrauder, André, Cornelia Henke-Gendo, Kathrin Seidemann, Michael Sasse, Gunnar Cario, Anja Moericke, Martin Schrappe, Albert Heim, and Armin Wessel. "Varicella vaccination in a child with acute lymphoblastic leukaemia." Lancet 369, no. 9568 (April 2007): 1232. http://dx.doi.org/10.1016/s0140-6736(07)60567-4.

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23

Khamsi, Roxanne. "Link to infection raises hope of preventing child leukaemia." Nature 434, no. 7037 (April 2005): 1058. http://dx.doi.org/10.1038/4341058b.

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24

Martinez-Climent, Jose A., Juan A. López-Andreu, Josep Ferris-Tortajada, María L. Pérez-Sirvent, and Victoria Castel-Sanchez. "Acute lymphoblastic leukaemia in a child with hereditary spherocytosis." European Journal of Pediatrics 154, no. 9 (September 1995): 753–54. http://dx.doi.org/10.1007/bf02276723.

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25

Khera, Sanjeev, Ashish Kumar Simalti, Dhanalakshmi Balasubramaniam, and Nikhil Tiwari. "Rasmussen’s aneurysm in a child with acute lymphoblastic leukaemia." BMJ Case Reports 13, no. 6 (June 2020): e235399. http://dx.doi.org/10.1136/bcr-2020-235399.

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26

Ivanov, D. О., Y. V. Petrenko, V. А. Reznik, V. N. Timchenko, Е. B. Pavlova, Т. М. Chernova, С. L. Bannova, et al. "COVID-19 i in the setting of acute lymphoblastic leukaemia (case analysis, resulting in death)." HIV Infection and Immunosuppressive Disorders 14, no. 2 (August 31, 2022): 73–82. http://dx.doi.org/10.22328/2077-9828-2022-14-2-73-82.

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A new coronaviral infection in the Russian Federation is registered less in a child treatment than in an adult one. Children’s COVID-19 is mainly asymptomatic or in mild, severe form occurs rarely. The percentage of paediatric-age patients that require in-patient medical care is from 5,7% to 20% of children with COVID-19. However, clinical observations show that children’s COVID-19 may be severe and extremely severe, also resulting in death. A risk group of unsmooth course of the new coronaviral infection is patients with serious comorbide pathology, in particular oncohematological disease, passing radiation, chemotherapy, transplantation of hematopoietic stem cells. Acute lymphoblastic leukaemia, the most frequent paediatric-age oncological disease, may be one of the factors, predisposing to severe course of the new coronaviral infection. However, COVID-19 is likely to cause the deterioration of leukaemia treatment and an adverse outcome. The article presents a clinical observation of a 12-year-old child with a critical form of the new coronaviral infection and acute lymphoblastic leukaemia in the post-transplantation period. The accumulation of COVID-19 was accompanied by deterioration in the underlying disease. Despite high-quality medical care, using modern technologies, the child had progressive deterioration with a poor outcome.

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27

Rajendran, Prasanth Varikkattu, Priya kumari Thankamony, Manjusha Nair, Guruprasad Chellappan Sojamani, Jayasudha Arundhathi Vasudevan, and Arun Gopalakrishnan. "Chronic eosinophilic leukaemia NOS transforming to B Lymphoblastic Leukaemia presenting as Myocardial Infarction in a child." Pediatric Hematology Oncology Journal 4, no. 2 (2019): S30—S31. http://dx.doi.org/10.1016/j.phoj.2019.08.086.

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28

Domínguez-Rojas, Jesús Angel, Ninoska Rojas-Soto, Pablo Vásquez-Hoyos, and Alvaro J. Coronado Munoz. "Difficult acute lymphoblastic leukaemia diagnosis in a paediatric patient with mixed presentation of COVID-19 acute respiratory failure and multisystemic inflammatory syndrome." BMJ Case Reports 15, no. 5 (May 2022): e248478. http://dx.doi.org/10.1136/bcr-2021-248478.

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New diagnoses of leukaemia and other malignancies are recently being made in paediatric patients with COVID-19. The rates of mortality and morbidity in some of these children are expected to be higher. In new cases, concurrent diagnosis can be difficult because multisystemic inflammatory syndrome (MIS-C) and malignancies have similar clinical presentations. We present the case of a preteenage child where the diagnosis of leukaemia was complicated and delayed by a multisystem involvement and an inconclusive bone marrow study. Clinical teams managing children with COVID-19 and MIS-C should suspect leukaemia and other malignancies when the clinical course is complicated and bone marrow suppression is persistent. Prompt diagnosis will allow start of treatment on time, minimising complications.

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29

Sen, Ethan S., John P. Moppett, and A. V. Ramanan. "Are you missing leukaemia?" Archives of Disease in Childhood 100, no. 9 (July 21, 2015): 811–12. http://dx.doi.org/10.1136/archdischild-2015-308607.

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30

Foot, A. B., A. Oakhill, and M. G. Mott. "Cryptosporidiosis and acute leukaemia." Archives of Disease in Childhood 65, no. 2 (February 1, 1990): 236–37. http://dx.doi.org/10.1136/adc.65.2.236.

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31

SCOTT, B., and J. M. HUTSON. "Peptic ulceration in leukaemia." Journal of Paediatrics and Child Health 23, no. 2 (April 1987): 115–16. http://dx.doi.org/10.1111/j.1440-1754.1987.tb02189.x.

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32

Esquembre, C., J. Ferris, A. Verdeguer, F. Prieto, L. Badia, and V. Castel. "Poland syndrome and leukaemia." European Journal of Pediatrics 146, no. 4 (July 1987): 444. http://dx.doi.org/10.1007/bf00444964.

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33

Yang, Y., XM Jin, CH Yan, Y. Tian, JY Tang, and XM Shen. "Urinary level of nickel and acute leukaemia in Chinese children." Toxicology and Industrial Health 24, no. 9 (October 2008): 603–10. http://dx.doi.org/10.1177/0748233708100091.

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The 8-hydroxy-2′-deoxyguanosine (8-OHdG), an oxidized nucleoside of DNA, not only is a widely used biomarker for the measurement of endogenous oxidative DNA damage but might also be a risk factor for many diseases including cancer. Metal exposure may play an important role in oxidative DNA damage among children. However, few studies on urinary 8-OHdG and metals have been conducted in children with acute leukemia. In the present study, urinary Ni and 8-OHdG were examined in 116 children with acute leukaemia (94 acute lymphoid leukaemia [ALL] and 22 acute myeloid leukaemia [AML]) and 51 healthy child controls. Our result showed that urinary Ni in acute leukaemia patients (ALL: 68.40 ± 133.98, AML: 41.48 ± 76.31 ng/mg creatinine) was significantly higher than that in controls (62.47 ± 124.90 vs 17.63 ± 46.17 ng/mg creatinine, P < 0.05). Similarly, the pretherapy level of urinary 8-OHdG in patients (ALL: 11.83 ± 16.23, AML: 12.36 ± 11.36 ng/mg creatinine) was significantly elevated compared with controls (11.92 ± 15.42 vs 4.03 ± 4.70 ng/mg creatinine, P < 0.05). Moreover, urinary 8-OHdG and urinary Ni showed a weak but significant association with increased risk of childhood leukaemia. The present study suggests that Ni may be an etiologic factor for childhood acute leukaemia by oxidative DNA damage.

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34

Thomas, E., M. Young, M. Wimalendra, and O. Tunstall. "PO-0168 Leukaemia Cutis: An Unusual Paediatric Presentation Of Acute Lymphoblastic Leukaemia." Archives of Disease in Childhood 99, Suppl 2 (October 2014): A302.2—A302. http://dx.doi.org/10.1136/archdischild-2014-307384.831.

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35

MEHROTRA, R., V. CHOUDHRY, R. SAXENA, K. KAPILA, and A. SARAYA. "Asymptomatic visceral leishmaniasis in a child with acute lymphoblastic leukaemia." Journal of Infection 30, no. 2 (March 1995): 157–59. http://dx.doi.org/10.1016/s0163-4453(95)80012-3.

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36

Petit, Arnaud, Emmanuelle Levine, Ralph Epaud, Hubert Ducou Le Pointe, and Adela Angoulvant. "Scopulariopsis brevicaulis abscess in a child treated for myeloblastic leukaemia." Lancet Infectious Diseases 11, no. 5 (May 2011): 416. http://dx.doi.org/10.1016/s1473-3099(10)70249-8.

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37

Kowatari, Ryosuke, Yasuyuki Suzuki, Kazuyuki Daitoku, and Ikuo Fukuda. "Cryptococcal infective endocarditis in a child with acute lymphocytic leukaemia." Interactive CardioVascular and Thoracic Surgery 28, no. 4 (October 29, 2018): 642–44. http://dx.doi.org/10.1093/icvts/ivy291.

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38

O’Rafferty, C., J. Kelly, L. Storey, C. Ryan, A. O’Marcaigh, and O. Smith. "Child and adolescent Down syndrome-associated leukaemia: the Irish experience." Irish Journal of Medical Science (1971 -) 184, no. 4 (October 25, 2014): 877–82. http://dx.doi.org/10.1007/s11845-014-1212-2.

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39

Heath, JA. "Leukaemia presenting as respiratory distress in a child with asthma." Journal of Paediatrics and Child Health 37, no. 4 (August 31, 2001): 397–99. http://dx.doi.org/10.1046/j.1440-1754.2001.00665.x.

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40

Staebler, Melanie, Nadira Azzi, Tayeb Sekhara, Isabelle Delpierre, Nash Damry, and Catherine Christophe. "Complications of lumbar puncture in a child treated for leukaemia." Pediatric Radiology 35, no. 11 (May 19, 2005): 1121–24. http://dx.doi.org/10.1007/s00247-005-1509-4.

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41

Gokce, M., D. Bulus, Y. Bilginer, F. Gumruk, N. Besbas, and M. Cetin. "Acute lymphoblastic leukaemia in a child with systemic lupus erythematosus." Lupus 21, no. 8 (February 13, 2012): 910–13. http://dx.doi.org/10.1177/0961203312436859.

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42

Kwan, Rui, Mei Yoke Chan, Yee Low, and Joyce Ching Mei Lam. "Leukaemia cutis of the scalp." Archives of Disease in Childhood 103, no. 6 (September 5, 2017): 578. http://dx.doi.org/10.1136/archdischild-2017-313284.

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43

Taylor, C. E., A. W. Craft, J. Kernahan, M. M. Reid, and G. L. Toms. "Nasal interferon responses in leukaemia." Archives of Disease in Childhood 60, no. 9 (September 1, 1985): 829–31. http://dx.doi.org/10.1136/adc.60.9.829.

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Chessells, J. M. "Bone marrow transplantation for leukaemia." Archives of Disease in Childhood 63, no. 8 (August 1, 1988): 879–82. http://dx.doi.org/10.1136/adc.63.8.879.

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Lie, S. O. "Acute myelogenous leukaemia in children." European Journal of Pediatrics 148, no. 5 (February 1989): 382–88. http://dx.doi.org/10.1007/bf00595892.

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von Mühlendahl, K. E., and M. Otto. "Electromagnetic fields and childhood leukaemia." European Journal of Pediatrics 154, no. 11 (November 1995): 933–34. http://dx.doi.org/10.1007/bf01957509.

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Stahnke, N., and H. J. Zeisel. "Growth hormone therapy and leukaemia." European Journal of Pediatrics 148, no. 7 (June 1989): 591–96. http://dx.doi.org/10.1007/bf00441506.

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Wang, Shuye, Haobo Xu, Yabo Liu, Wanting He, and Wei Wang. "Leukaemia cutis as the initial manifestation in a child with brachydactyly in chronic phase of chronic myeloid leukaemia." Pathology 46, no. 6 (October 2014): 569–70. http://dx.doi.org/10.1097/pat.0000000000000155.

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Hanada, T., I. Ono, N. Moriyama, and K. Koike. "Cytoplasmic granules in leukaemic cells of the cerebrospinal fluid in a child with non-granular acute lymphocytic leukaemia." European Journal of Pediatrics 150, no. 12 (October 1991): 839–40. http://dx.doi.org/10.1007/bf01955003.

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50

Zuna, Jan, Marketa Zaliova, Katerina Muzikova, Claus Meyer, Libuse Lizcova, Zuzana Zemanova, Jana Brezinova, et al. "Acute Leukaemias with TEL/ABL Fusion: a Subgroup with Poor Prognosis and Prenatal Origin." Blood 114, no. 22 (November 20, 2009): 2596. http://dx.doi.org/10.1182/blood.v114.22.2596.2596.

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Анотація:

Abstract Abstract 2596 Poster Board II-572 The TEL/ABL (ETV6/ABL1) fusion gene is a rare aberration in human oncology. Only 19 cases of TEL/ABL-positive haematological malignancy were published so far, diagnosed as chronic myeloid leukaemia (n=9) or other type of chronic myeloproliferative disease (n=3), acute myeloid leukaemia (n=4) or acute lymphoblastic leukaemia (ALL) (n=3). Median age at diagnosis in the published cases was 48 years, with only 2 children (aged 22 months and 4 years) diagnosed thus far, both with ALL. Altogether, the TEL/ABL-positive leukaemias tend to be diagnosed at higher age suggesting post-natal origin and aetiology of this aberration - at least in a vast majority of cases. In the present study we report 3 new cases (aged 8 months, 5 years and 33 years) of ALL with TEL/ABL fusion gene revealed by screening of 392 newly diagnosed ALL patients (335 children and 57 adults). In two patients the mechanism of the TEL/ABL fusion was probably identical - part of the 9q34 including C-terminus of the ABL gene was inserted (in inverse orientation) into the TEL gene at the 12p13. The mechanism of changes was probably more complicated in the infant patient. Our data suggest that in this case part of the TEL gene was inserted into ABL and, moreover, the chromosome 1 was included in the complex cytogenetic changes. In all 3 patients array-CGH analysis was performed showing short deletion in the CDKN2A/CDKN2B locus at 9p21 in 2/3 cases. Analysis of all published data including our cases reveals poor prognosis of the TEL/ABL-positive acute leukaemias - overall survival in 2 years reaches only 15%. In particular, 4 patients (including 2 in the present study) were children (0-5 years), all of them diagnosed as ALL. Despite the prognosis of childhood ALL is generally better (overall survival reaching 80–90%) than the outcome of other haematological malignancies, only 1 out of the 4 reported paediatric cases survived more than 13 months from diagnosis (the 5 year old patient from the present study is now in complete remission for 16 months). On the other hand, survival of chronic leukaemias exceeds 50% corresponding to the outcome of TEL/ABL-negative chronic leukaemias in adults. Eosinophilia was suggested as a clinical hallmark of the TEL/ABL-positive leukaemia. However, we can not confirm the 100% correlation as 2/3 patients in this report lack this feature. In the two paediatric cases the course of the leukaemia was monitored using minimal residual disease (MRD). The data demonstrate excellent correlation of the MRD levels assessed by TEL/ABL transcript and immunoreceptor genes rearrangements quantification. Scrutiny of the neonatal blood spot (Guthrie card) revealed that in the 5 year old child the TEL/ABL rearrangement initiating the ALL was originated prenatally. The relatively long latency period suggests that secondary genetic hit(s) were required for the overt disease in this patient. The ALL diagnosed in the infant case at the age of 8 months was also very likely initiated prenatally, however, we were not able to locate the genomic breakpoint between the two genes and prove this hypothesis. The deletion at the CDKN2A/CDKN2B region in 2/3 presented cases (described also previously in TEL/ABL-positive ALL) suggests that loss of function in this region or in other tumour-suppressor loci (not necessarily detectable by cytogenetics) might contribute to leukaemogenesis of the primary aberration. In conclusion, we report three new cases of ALL characterised by TEL/ABL fusion and we integrate the new patients into already published data. For the first time we show detailed characterisation of the course of the disease including MRD data, we assess prognostic impact of the aberration using “meta-analysis” and we demonstrate prenatal origin of the TEL/ABL fusion. The work was supported by grants MSM0021620813 and IGA-MZ NS1000-4. Disclosures: No relevant conflicts of interest to declare.

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