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Journal articles on the topic 'Acute Leukaemia - Treatment'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2023

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1

Kuzmits, Rudolf, Paul Aiginger, Matthias M. Müller, Günter Steurer, and Werner Linkesch. "Assessment of the sensitivity of leukaemic cells to cytotoxic drugs by bioluminescence measurement of ATP in cultured cells." Clinical Science 71, no. 1 (July 1, 1986): 81–88. http://dx.doi.org/10.1042/cs0710081.

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1. A short-term test in vitro is described, which can be used to detect resistance to cytostatic agents in leukaemic cells. Leukaemic cell suspensions were incubated with cytostatic agents and the resulting intracellular ATP concentrations were measured by a bioluminescence ATP assay. 2. There was a clear dose-effect relationship in acute leukaemia and chronic lymphocytic leukaemia cells for drugs used in the treatment of leukaemias. A good correlation was found between the ATP content of leukaemic cells and cell viability as determined by the trypan blue dye exclusion test. 3. Preliminary ind

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2

Ivanovic, Mirjana, Olivera Jovicic, Jelena Mandic, Dusko Bogetic, and Marcello Maddalone. "Oral manifestations of acute leukaemia." Srpski arhiv za celokupno lekarstvo 139, no. 1-2 (2011): 103–6. http://dx.doi.org/10.2298/sarh1102103i.

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Acute leukaemia is the most common form of chilhood cancer. The aim of this paper was to underline the importance of oral manifestations in children with acute leukaemia. The disease and its treatment can directly or indirectly affect oral health. Oral manifestations are gingival inflammation and enlargement. Leukaemic cells are capable of infiltrating the gingiva and the deeper periodontal tissues which leads to ulceration and infection of oral tissues. Gingival bleeding is a common sign in patients with leukaemia. Symptoms include local lymphadenopathy, mucous membrane Petechiae and ecchymos

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3

Skarsgård, Lisa Stenman, Mattias K. Andersson, Marta Persson, Ann-Cathrine Larsen, Sarah E. Coupland, Göran Stenman, and Steffen Heegaard. "Clinical and genomic features of adult and paediatric acute leukaemias with ophthalmic manifestations." BMJ Open Ophthalmology 4, no. 1 (October 2019): e000362. http://dx.doi.org/10.1136/bmjophth-2019-000362.

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ObjectiveTo describe the clinicopathological and genomic features of nine patients with primary and secondary orbital/ocular manifestations of leukaemia.MethodsAll orbital/ocular leukaemic specimens from 1980 to 2009 were collected from the Danish Register of Pathology. In six cases, medical records and formalin-fixed, paraffin-embedded blocks were available. Three cases from the Department of Pathology, Royal Liverpool University Hospital, were also included. Immunophenotypes and MYB oncoprotein expression were ascertained by immunohistochemistry. Genomic imbalances were analysed with compara

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4

Arruda, Walter Oleschko, María Belén Montú, Marcelo de Souza R. de Oliveira, and Ricardo Ramina. "Acute myeloid leukaemia induced by mitoxantrone: case report." Arquivos de Neuro-Psiquiatria 63, no. 2a (June 2005): 327–29. http://dx.doi.org/10.1590/s0004-282x2005000200024.

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Mitoxantrone (MX) is an immunosupressant drug used in secondarily progressive multiple sclerosis (SPMS) and in relapsing-remitting multiple sclerosis (RRMS). It has a leukemogenesis potential induced by cytogenetic abnormalities, though with a low incidence. Promyelocitic leukaemia (type M3) and other forms of acute myeloblastic leukaemias (M4 and M5) have been described in a few MS patients who received MX during their treatment. We describe a white female patient, 47 year-old, with SPMS (EDSS = 4) with 14 years of disease. She received MX during her disease and developed acute promyelocytic

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5

Bhalla, Amit. "Clofarabine: a next-generation deoxyadenosine analogue." International Journal of Basic & Clinical Pharmacology 7, no. 5 (April 23, 2018): 1048. http://dx.doi.org/10.18203/2319-2003.ijbcp20181660.

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Acute lymphoblastic leukaemia (ALL) is the most common of the paediatric leukaemias. It is estimated that the use of modern combination chemotherapy results in long-term remission in nearly 80% of children diagnosed with ALL. Despite therapy advances, approximately 20% of children with ALL, experience leukaemia relapse. Clofarabine (2-chloro-2’-fluoro-2’-deoxy-9-β-D-arabinofuranosyladenine) is a second-generation nucleoside analogue and is structurally related to fludarabine and cladribine which are widely used in the treatment of lymphoproliferative disorders. Clofarabine exhibits greater aff

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6

Burnett, Alan K. "Treatment of acute myeloid leukaemia." Clinical Medicine 13, Suppl 6 (December 2013): s58—s61. http://dx.doi.org/10.7861/clinmedicine.13-6-s58.

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7

Apostolidou, Effrosyni, Ronan Swords, Yesid Alvarado, and Francis J. Giles. "Treatment of Acute Lymphoblastic Leukaemia." Drugs 67, no. 15 (2007): 2153–71. http://dx.doi.org/10.2165/00003495-200767150-00004.

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8

LÖWENBERG, B. "Treatment of acute myelogenous leukaemia." Journal of Internal Medicine 242 (July 1997): 17–22. http://dx.doi.org/10.1111/joim.1997.242.s740.17.

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9

Omura, GeorgeA. ""MAINTENANCE TREATMENT" FOR ACUTE LEUKAEMIA." Lancet 328, no. 8516 (November 1986): 1154. http://dx.doi.org/10.1016/s0140-6736(86)90553-2.

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10

Burnett, AK, and OB Eden. "The treatment of acute leukaemia." Lancet 349, no. 9047 (January 1997): 270–75. http://dx.doi.org/10.1016/s0140-6736(96)08086-5.

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11

Fenaux, Pierre, Christine Chomienne, and Laurent Degos. "Treatment of acute promyelocytic leukaemia." Best Practice & Research Clinical Haematology 14, no. 1 (March 2001): 153–74. http://dx.doi.org/10.1053/beha.2000.0121.

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12

Sørensen, Dag Reidar, Mouldy Sioud, and Per Ole Iversen. "A combined immunostimulatory and immunoinhibitory short interference RNA reduces hypercoagulability in a rat model of acute promyelocytic leukaemia." Thrombosis and Haemostasis 104, no. 08 (2010): 350–54. http://dx.doi.org/10.1160/th09-12-0816.

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SummaryAcute promyelocytic leukaemia (APL) confers an increased risk of thrombosis and bleeding. Current treatments are insufficient to inhibit these complications. We recently showed that a combined immunoinhibitory and immunostimulatory short interference (si) RNA effectively inhibited leukaemic growth and metastasis in rats with APL. We now asked if the reported anti-leukaemic effects of siRNA treatment could be explained by inhibition of hypercoagulability. We measured markers of coagulation and fibrinolysis in plasma collected from APL rats with overt leukaemia using conventional assays.

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13

Kuek, Vincent, Anastasia M. Hughes, Rishi S. Kotecha, and Laurence C. Cheung. "Therapeutic Targeting of the Leukaemia Microenvironment." International Journal of Molecular Sciences 22, no. 13 (June 26, 2021): 6888. http://dx.doi.org/10.3390/ijms22136888.

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In recent decades, the conduct of uniform prospective clinical trials has led to improved remission rates and survival for patients with acute myeloid leukaemia and acute lymphoblastic leukaemia. However, high-risk patients continue to have inferior outcomes, where chemoresistance and relapse are common due to the survival mechanisms utilised by leukaemic cells. One such mechanism is through hijacking of the bone marrow microenvironment, where healthy haematopoietic machinery is transformed or remodelled into a hiding ground or “sanctuary” where leukaemic cells can escape chemotherapy-induced

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14

Yook, Hwa Jung, Joon Ho Son, Yeong Ho Kim, Ju Hee Han, Ji Hyun Lee, Young Min Park, Nack-Gyun Chung, Hee Je Kim, and Chul Hwan Bang. "Leukaemia Cutis: Clinical Features and Outcomes of 56 Patients." Acta Dermato-Venereologica 102 (February 11, 2022): adv00647. http://dx.doi.org/10.2340/actadv.v102.1123.

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Leukaemia is a malignant neoplasm of the haematopoietic system. Cutaneous manifestations of leukaemia are called leukaemia cutis, and are regarded as a sign of poorer prognosis and shorter survival time. A single-institution retrospective review was performed of medical records of patients diagnosed with leukaemia cutis in the dermatology department of Seoul St Mary’s Hospital between January 2012 and April 2021. Fifty-six cases with cutaneous leukaemic involvement and underlying haematological malignancy were included (40 acute myelogenous leukaemia, 8 acute lymphoblastic leukaemia, 3 chronic

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15

Dachi. "Acute Leukaemias in Bauchi State, Northeastern Nigeria: Pattern of Presentations and Clinical Entities." West Africa Journal of Medicine 39, no. 5 (June 26, 2022): 497–500. http://dx.doi.org/10.55891/wajm.v39i5.122.

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Background: Acute leukaemias are very aggressive diseases that run a rapidly fatal course if not promptly diagnosed and appropriately treated. The clinical presentations range from bone marrow failure such as anaemia, neutropenia or thrombocytopenia to features of organ infiltrations such as lymphadenopathy, splenomegaly, etc, but presentations may be non-specific. Misdiagnosis is very common with delay in diagnosis and prompt treatment being the causes of high morbidity and mortality in acute leukaemias. This study aims to determine the pattern of presentation and various clinical entities of

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16

Onoja, AM, SA Otene, AT Onoja, IN Ibrahim, A. Mke, I. Okolie, R. Okoli, et al. "Prevalence and Nature of Adult Hematological Malignancies Using Bone Marrow Aspiration Cytology in a Tertiary Health Facility: A Seven Year Retrospective Review." Western Journal of Medical and Biomedical Sciences 2, no. 1 (April 12, 2021): 39–45. http://dx.doi.org/10.46912/wjmbs.39.

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Bone Marrow Aspiration (BMA) is a procedure that is often used to evaluate patients with haematological disorders including haematological malignancies (HMs) which account for about 6.5% of all cancers worldwide. There is paucity of data on the prevalence and pattern of HMs from BMA cytology in Nigeria. We carried out a retrospective review to determine the prevalence and distribution of HMs among adult patients who had BMA cytology at Benue State University Teaching Hospital (BSUTH) from June 2012 to July 2019. A total of 158 BMA reports extracted from the marrow and clinic medical records we

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17

Okamoto, Y., T. Tsuda, M. Matsunami, T. Hirose, R. Sakaguchi, N. Katayama, and K. Ota. "Treatment of Acute Myeloblastic Leukaemia in a Patient with Bombay Blood Type: A Case Report." Journal of International Medical Research 29, no. 2 (April 2001): 140–46. http://dx.doi.org/10.1177/147323000102900211.

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A 62-year-old female was admitted to our hospital with suspected acute leukaemia and after investigation we diagnosed acute myeloblastic leukaemia (AML-M1). The patient's blood type was found to be the very rare Bombay type and surveillance of her relatives showed the same blood type in her male cousin on her mother's side. Alongside chemotherapy the patient received 4000 ml of frozen Bombay-type red cells, 1400 ml of concentrated red cells in manitol adenine phosphate solutions and 360 units of type O concentrated platelets without marked effects. The anti-H antibody was initially at 128 dilu

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18

Skelding, Kathryn A., Daniel L. Barry, Danielle Z. Theron, and Lisa F. Lincz. "Bone Marrow Microenvironment as a Source of New Drug Targets for the Treatment of Acute Myeloid Leukaemia." International Journal of Molecular Sciences 24, no. 1 (December 29, 2022): 563. http://dx.doi.org/10.3390/ijms24010563.

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Acute myeloid leukaemia (AML) is a heterogeneous disease with one of the worst survival rates of all cancers. The bone marrow microenvironment is increasingly being recognised as an important mediator of AML chemoresistance and relapse, supporting leukaemia stem cell survival through interactions among stromal, haematopoietic progenitor and leukaemic cells. Traditional therapies targeting leukaemic cells have failed to improve long term survival rates, and as such, the bone marrow niche has become a promising new source of potential therapeutic targets, particularly for relapsed and refractory

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19

Lam, Stephen S. Y., and Anskar Y. H. Leung. "Overcoming Resistance to FLT3 Inhibitors in the Treatment of FLT3-Mutated AML." International Journal of Molecular Sciences 21, no. 4 (February 24, 2020): 1537. http://dx.doi.org/10.3390/ijms21041537.

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Acute myeloid leukaemia (AML) carrying internal tandem duplication (ITD) of Fms-Like Tyrosine kinase 3 (FLT3) gene is associated with high risk of relapse and poor clinical outcome upon treatment with conventional chemotherapy. FLT3 inhibitors have been approved for the treatment of this AML subtype but leukaemia relapse remains to be a major cause of treatment failure. Mechanisms of drug resistance have been proposed, including evolution of resistant leukaemic clones; adaptive cellular mechanisms and a protective leukaemic microenvironment. These models have provided important leads that may

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20

Kell, Jonathan. "Treatment of Relapsed Acute Myeloid Leukaemia." Reviews on Recent Clinical Trials 1, no. 2 (May 1, 2006): 103–11. http://dx.doi.org/10.2174/157488706776876445.

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21

Ninomiya, Haruhiko, Masaki Nakazawa, Akira Shibuya, Yasuko Aoki, Toshiro Nagasawa, and Tsukasa Abe. "Successful treatment of acute megakaryoblastic leukaemia." Scandinavian Journal of Haematology 36, no. 2 (April 24, 2009): 147–53. http://dx.doi.org/10.1111/j.1600-0609.1986.tb00819.x.

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22

Jacobs, Peter, and Lucille Wood. "Treatment of acute lymphoblastic leukaemia (ALL)." European Journal of Haematology 49, no. 2 (April 24, 2009): 53–58. http://dx.doi.org/10.1111/j.1600-0609.1992.tb00030.x.

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23

Tanday, Sanjay. "Combination treatment for acute myeloid leukaemia." Lancet Oncology 13, no. 12 (December 2012): e524. http://dx.doi.org/10.1016/s1470-2045(12)70478-3.

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24

Fenaux, Pierre, and Laurent Degos. "6 Treatment of acute promyelocytic leukaemia." Baillière's Clinical Haematology 9, no. 1 (March 1996): 107–28. http://dx.doi.org/10.1016/s0950-3536(96)80039-4.

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25

Stankovic, Tatjana, and Eliot Marston. "Molecular mechanisms involved in chemoresistance in paediatric acute lymphoblastic leukaemia." Srpski arhiv za celokupno lekarstvo 136, no. 3-4 (2008): 187–92. http://dx.doi.org/10.2298/sarh0804187s.

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Acute lymphoblastic leukaemia (ALL) is the most common paediatric cancer. Despite cure rates approaching 80%, resistance to treatment and disease relapse remain a significant clinical problem. Identification of the genes and biological pathways responsible for chemoresistance is therefore crucial for the design of novel therapeutic approaches aiming to improve patient survival. Mutations in the membrane transporter P-glycoprotein genes, genetic variations in drug-metabolising enzymes and defects in apoptotic pathways are mechanisms of chemoresistance common to a wide spectrum of cancers and al

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26

Víctor, Galán-Gómez, Matamala Nerea, Ruz-Caracuel Beatriz, Valle-Simón Paula, Ochoa-Fernández Bárbara, Guerra-García Pilar, Pernas-Sánchez Alicia, et al. "Advanced Molecular Characterisation in Relapsed and Refractory Paediatric Acute Leukaemia, the Key for Personalised Medicine." Journal of Personalized Medicine 12, no. 6 (May 27, 2022): 881. http://dx.doi.org/10.3390/jpm12060881.

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Relapsed and refractory (R/r) disease in paediatric acute leukaemia remains the first reason for treatment failure. Advances in molecular characterisation can ameliorate the identification of genetic biomarkers treatment strategies for this disease, especially in high-risk patients. The purpose of this study was to analyse a cohort of R/r children diagnosed with acute lymphoblastic (ALL) or myeloid (AML) leukaemia in order to offer them a targeted treatment if available. Advanced molecular characterisation of 26 patients diagnosed with R/r disease was performed using NGS, MLPA, and RT-qPCR. Th

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27

Cox, Charlotte V., Paraskevi Diamanti, Pamela R. Kearns, and Allison Blair. "Effects of Steroid Treatment on Childhood ALL Stem Cells." Blood 110, no. 11 (November 16, 2007): 3462. http://dx.doi.org/10.1182/blood.v110.11.3462.3462.

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Abstract Several lines of evidence indicate a central role for stem cells in the pathogenesis of human leukaemias and exemplify the need to develop strategies that target this sub-population of cells. It is proposed that these cells may exhibit different chemo-sensitivity and consequently may be resistant to drug regimens designed to kill the bulk leukaemia population. Inherently resistant leukaemia stem cells may contribute to subsequent disease relapse. Clearly, there is a need to assess the relative efficacy of therapeutic agents on the sub-populations of cells in addition to the bulk leuka

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28

Popovic, Stevan. "Individualisation of therapy in acute nonlymphoblastic leukaemia." Srpski arhiv za celokupno lekarstvo 134, Suppl. 1 (2006): 72–77. http://dx.doi.org/10.2298/sarh06s1072p.

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Acute nonlymphoblastic leukaemia involves the dynamic and individual coupling of four groups of significant prognostic factors: biological potential of the patient, leukaemic clone, normal haematopoiesis, and therapy. The active, dynamic, and timely prognosis of an unfavourable outcome represents a solid basis for the individual adaptation of antileukaemic and supportive therapy. A part of the ANLL NS 03 programme for the individualised therapy of acute nonlymphoblastic leukaemia in patients no older than 60 years will be described. The programme is based on a network of prognostic models, ide

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29

Kacanski, Natasa, Nada Konstantinidis, Jovanka Kolarovic, Bojana Slavkovic, and Dragana Vujic. "Biphenotypic acute leukaemia: Case reports of two paediatric patients." Medical review 63, no. 11-12 (2010): 867–69. http://dx.doi.org/10.2298/mpns1012867k.

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Introduction. Biphenotypic acute leukaemia is an uncommon type of leukaemia whose blasts co-express myeloid and B-or T-lymphoid antigens. Case report. We describe two cases of paediatric patients with biphenotypic acute leukaemia. A four-year-old female patient was found to have myeloid and B-lymphoid associated antigens in the same blast cells. Cytogenetic analysis showed a Philadelphia (Ph) positivity t (9;22) (q34;q11) with rearrangements of M.bcr-Abl (p210). She was treated with combined acute myeloid leukaemia/acute lymphoblastic leukaemia induction therapy followed by autologous stem cel

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30

Balasubramanian, Priyavadhana, Prashant Ramteke, Saumyaranjan Mallick, Lalit Kumar, and Pranay Tanwar. "Diffuse Large B-Cell Lymphoma Relapsing in Leukaemic Phase Presenting as Acute Leukaemia." Clinical Medicine Insights: Blood Disorders 12 (January 2019): 1179545X1882116. http://dx.doi.org/10.1177/1179545x18821160.

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Diffuse large B-cell lymphoma (DLBCL) accounts for 30% to 40% of the newly diagnosed adult non-Hodgkin lymphomas, but rarely presents in leukaemic phase. Here in, we report a case of DLBCL presenting in leukaemic phase and masquerading as acute leukaemia. A 28-year-old woman presented to our outpatient department with complaints of fever for 1 week. Her peripheral blood smear showed 5% to 8% blasts. Bone marrow aspirate showed an infiltration by ~30% blasts. Flow cytometry and immunohistochemistry confirmed relapse of DLBCL. Also, patient’s poor response to therapeutic regimen for DLBCL prompt

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31

Telek, Béla, László Rejtő, Attila Kiss, Péter Batár, Gyula Reményi, Róbert Szász, Zsófia Ágnes Ujj, and Miklós Udvardy. "Current treatment of acute myeloid leukaemia in adults." Orvosi Hetilap 153, no. 7 (February 2012): 243–49. http://dx.doi.org/10.1556/oh.2012.29304.

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Recent cytogenetical findings and novel molecular biology results of acute myeloid leukaemia have shed new lights of our understanding in the diagnosis and treatment of the disease. Acute myeloid leukaemia is not only represented by the wide variety of morphological and immunophenotypic diversity but also demonstrates cytogenetical and molecular biological heterogeneity of its own. It has an unfavorable prognosis, especially in the elderly. Overall survival of younger patients (<50–60 years) has increased in the past years due to high dose chemotherapy (daunorubicine, cytarabine). But in ca

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32

Kline, Justin P., and Richard A. Larson. "Clofarabine in the treatment of acute myeloid leukaemia and acute lymphoblastic leukaemia: a review." Expert Opinion on Pharmacotherapy 6, no. 15 (November 30, 2005): 2711–18. http://dx.doi.org/10.1517/14656566.6.15.2711.

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33

Spielberger, Ricardo T., Jerome I. Dickstein, Michelle M. Le Beau, Richard A. Larson, Karen M. Daly, James W. Vardiman, and Harvey M. Golomb. "ACUTE MYELOID LEUKAEMIA FOLLOWING INTERFERON-ALFA TREATMENT OF HAIRY CELL LEUKAEMIA." British Journal of Haematology 83, no. 3 (March 1993): 519–20. http://dx.doi.org/10.1111/j.1365-2141.1993.tb04680.x.

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34

&NA;. "Challenges in the treatment of acute leukaemia." Inpharma Weekly &NA;, no. 1072 (February 1997): 4. http://dx.doi.org/10.2165/00128413-199710720-00005.

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35

Donohue, S. M., and C. P. J. Charlton. "Drug Treatment of Acute Leukaemia Current Status." Drugs 37, no. 6 (June 1989): 926–38. http://dx.doi.org/10.2165/00003495-198937060-00006.

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36

Bishop, James F. "Adult acute myeloid leukaemia: update on treatment." Medical Journal of Australia 170, no. 1 (January 1999): 39–43. http://dx.doi.org/10.5694/j.1326-5377.1999.tb126866.x.

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37

Estey, Elihu H. "Treatment options for relapsed acute promyelocytic leukaemia." Best Practice & Research Clinical Haematology 16, no. 3 (September 2003): 521–34. http://dx.doi.org/10.1016/s1521-6926(03)00039-2.

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38

Cavenagh, J. D., D. S. Richardson, M. R. Cahill, T. Bernard, S. M. Kelsey, and A. C. Newland. "Treatment of acute myeloid leukaemia in pregnancy." Lancet 346, no. 8972 (August 1995): 441–42. http://dx.doi.org/10.1016/s0140-6736(95)92813-8.

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39

Taub, Jeffrey W., and Yaddanapudi Ravindranath. "7 Treatment of childhood acute myeloid leukaemia." Baillière's Clinical Haematology 9, no. 1 (March 1996): 129–46. http://dx.doi.org/10.1016/s0950-3536(96)80040-0.

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40

Lokody, Isabel. "Overcoming resistance in acute myeloid leukaemia treatment." Nature Reviews Cancer 14, no. 7 (June 24, 2014): 453. http://dx.doi.org/10.1038/nrc3776.

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41

CAFFREY, E. A., M. G. DAKER, and J. J. HORTON. "Acute myeloid leukaemia after treatment with razoxane." British Journal of Dermatology 113, no. 2 (August 1985): 131–34. http://dx.doi.org/10.1111/j.1365-2133.1985.tb02054.x.

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42

Barnett, M. J., M. F. Greaves, J. A. L. Amess, W. M. Gregory, A. Z. S. Rohatiner, H. S. Dhaliwal, M. L. Slevin, R. Biruls, J. S. Malpas, and T. A. Lister. "Treatment of acute lymphoblastic leukaemia in adults." British Journal of Haematology 64, no. 3 (November 1986): 455–68. http://dx.doi.org/10.1111/j.1365-2141.1986.tb02201.x.

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43

Rodgers, J., P. G. Britton, R. G. Morris, J. Kernahan, and A. W. Craft. "Memory after treatment for acute lymphoblastic leukaemia." Archives of Disease in Childhood 67, no. 3 (March 1, 1992): 266–68. http://dx.doi.org/10.1136/adc.67.3.266.

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44

Mulford, Deborah A., and Joseph G. Jurcic. "Antibody-based treatment of acute myeloid leukaemia." Expert Opinion on Biological Therapy 4, no. 1 (January 2004): 95–105. http://dx.doi.org/10.1517/14712598.4.1.95.

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45

Darbyshire, P. J., C. R. Pinkerton, R. F. Stevens, and A. Oakhill. "Treatment of acute lymphoblastic leukaemia after relapse." Lancet 335, no. 8691 (March 1990): 733. http://dx.doi.org/10.1016/0140-6736(90)90853-w.

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46

Ng, Chin-Hin, and Wee-Joo Chng. "Recent advances in acute promyelocytic leukaemia." F1000Research 6 (July 28, 2017): 1273. http://dx.doi.org/10.12688/f1000research.10736.1.

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Acute promyelocytic leukaemia (APML) is a subtype of leukaemia arising from a distinct reciprocal translocation involving chromosomes 15 and 17, which results in thePML-RARAfusion gene. Over the past three decades, APML has been transformed from a highly fatal disease to a highly curable one. This drastic improvement is because of the introduction of a new treatment strategy with all-trans retinoic acid and, more recently, arsenic trioxide. The revolutionary treatment of APML has also paved the way for a new cancer treatment, which is genetically targeted therapy. In this review, we look into

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47

W Aworanti, Oladapo, Foluke A Fasola, Taiwo R Kotila, John A Olaniyi, and Biobele J Brown. "Acute leukemia in sickle cell disease patients in a tertiary health facility in Nigeria: a case series." African Health Sciences 20, no. 3 (October 7, 2020): 1304–12. http://dx.doi.org/10.4314/ahs.v20i3.36.

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Background and objectives: Sickle cell disease(SCD) is a disorder of red cells resulting from the co-inheritance of hae- moglobin S (HbS) with another abnormal haemoglobin. The diagnosis of acute leukaemia is uncommon in our patients with sickle cell disease more so the patients have high morbidity and mortality due to the sickling process.Acute leukemia is a malignant clonal disorder of haemopoietic precursor cells resulting in accumulation of immature blood cells in the bone marrow and blood.The objective of the case series was to highlight the challenges of diagnosis and management of SCD p

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48

Hoffmann, H., C. Thiede, I. Glauche, M. Bornhaeuser, and I. Roeder. "Differential response to cytotoxic therapy explains treatment dynamics of acute myeloid leukaemia patients: insights from a mathematical modelling approach." Journal of The Royal Society Interface 17, no. 170 (September 2020): 20200091. http://dx.doi.org/10.1098/rsif.2020.0091.

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Disease response and durability of remission are very heterogeneous in patients with acute myeloid leukaemia (AML). There is increasing evidence that the individual risk of early relapse can be predicted based on the initial treatment response. However, it is unclear how such a correlation is linked to functional aspects of AML progression and treatment. We suggest a mathematical model in which leukaemia-initiating cells and normal/healthy haematopoietic stem and progenitor cells reversibly change between an active state characterized by proliferation and chemosensitivity and a quiescent state

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Whiting, P. H., D. J. King, A. Ireland, M. A. Ratcliffe та A. A. Dawson. "N-Acetyl-β-D-Glucosaminidase Enzymuria in Leukaemia and Myelomatosis: Effect of Treatment in Acute Myeloblastic Leukaemia and Myelomatosis in Adults". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 23, № 6 (листопад 1986): 676–80. http://dx.doi.org/10.1177/000456328602300609.

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The activity of the lysosomal hydrolase N-acetyl-β-d-glucosaminidase (NAG) was measured in the urine of patients with leukaemia or myeloma. Elevated pre-treatment enzymuria was noted in all patient groups with acute myeloblastic leukaemias (AML) FAB type M4 or 5 displaying higher activities than AML patients FAB types M1–3, which in turn were higher than those found in patients with myelomatosis and chronic lymphocytic leukaemia. The ratio of the major isoenzymes of NAG, A/B was reduced significantly only in patients with AML. Following treatment, AML patients who entered remission demonstrate

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Vey, Norbert, and Daniel Olive. "Anti-natural Killer Inhibitory Receptors in Elderly Patients with Acute Myeloid Leukaemia." European Oncology & Haematology 06, no. 01 (2010): 86. http://dx.doi.org/10.17925/eoh.2010.06.1.86.

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Treatment with anti-killer-cell immunoglobulin-like receptor (KIR) monoclonal antibody (mAb) is a new approach aimed at harnessing the antileukaemic potential of natural killer (NK) cells for the treatment of acute myeloid leukaemia (AML). NK cell antitumour activity is regulated by a balance between activating and inhibitory receptors (KIR). 1-7F9/IPH2101 is a fully human immunoglobulin G4 (IgG4) mAb that binds to inhibitory KIR and blocks binding with its ligand (human leukocyte antigen C [HLA-C] molecule) on leukaemic cells.In vitro,and in a surrogatein vivomodel in mice, treatment with 1-7

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