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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 individual clinical correlations suggest a correlation between the chemosensitivity in vitro and the response patterns in vivo in leukaemia patients. This simple, fast and sensitive method may have application for determination of drug-induced cytotoxicity in leukaemic cells in vitro.

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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 ecchymoses. Cytotoxic drugs have direct effects like mucositis, involving atrophy, desquamation and ulceration of the mucosa, with increasing the risk for local and systemic infections. Leukaemia can directly influence dental care and dental treatment, while oral lesions may have life-threatening consequences. Knowledge and skills among dentists may also not be adequate to treat children with acute leukaemia. It is therefore imperative that all stomatologists be aware of dental problems that occur in leukaemia in order to be able to effectively carry out appropriate measures to mitigate these problems.

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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 comparative genomic hybridisation arrays and oncogene rearrangements with fluorescence in situ hybridisation.ResultsFour patients had B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) and five had acute myeloid leukaemia (AML). Two patients with BCP-ALL and one with AML had primary orbital manifestations of leukaemia. Common symptoms were proptosis, displacement of the eye, and reduced eye mobility in patients with orbital leukaemias and pain, and reduced visual acuity in patients with ocular leukaemias. All patients with primary orbital lesions were alive up to 18 years after diagnosis. All but one patient with secondary ophthalmic manifestations died of relapse/disseminated disease. ETV6 and RUNX1 were rearranged in BCP-ALL, and RUNX1 and KMT2A in AML. Genomic profiling revealed quiet genomes (0–7 aberrations/case). The MYB oncoprotein was overexpressed in the majority of cases.ConclusionsLeukaemias with and without ophthalmic manifestations have similar immunophenotypes, translocations/gene fusions and copy number alterations. Awareness of the clinical spectrum of leukaemic lesions of the eye or ocular region is important to quickly establish the correct diagnosis and commence prompt treatment.

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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 leukaemia (M3), with severe thrombocytopenia 30 months later. She ultimately died due to intracerebral hemorrhage. Other cases of treatment related to AML are reviewed and discussed.

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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 affinity to deoxycytidine kinase (dCyd kinase) and prolonged retention in leukaemic blasts compared to fludarabine and cladribine. Clofarabine inhibits both DNA polymerases and ribonucleotide reductase (RNR). This results in impaired DNA synthesis through inhibition of DNA elongation as well as depletion of deoxyribonucleotides. Accumulation of clofarabine triphosphate, in the blasts of patients with refractory leukemia has been demonstrated. Prolonged intracellular half-life of 24 hours for clofarabine triphosphate. Clofarabine is indicated for the treatment of pediatric patients 1 to 21 years old with relapsed or refractory acute lymphoblastic leukemia after at least two prior regimens.

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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. Coagulopathy developed in untreated leukaemic rats evidenced by increase in several haemostatic markers. Treatment of leukaemic rats with the siRNA reduced (p < 0.05) the concentration of thrombin-anti-thrombin complex (a marker of coagulation) by 40% compared with rats treated with an inactive, control siRNA. Substantial reductions (p < 0.05) were also obtained for two markers of fibrinolysis: D-dimer (72%) and plasminogen activator inhibitor type 1 (51%). The activity of tissue factor, the main initiator of coagulation, was not increased (p > 0.05) in untreated leukaemic rats compared with healthy rats, and did not change (p > 0.05) upon treatment with the siRNA. The bifunctional siRNA reduces the hypercoagulable state in APL in addition to its direct anti-leukaemic properties, supporting testing of this small molecule in human APL.

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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 cytotoxicity. The bone marrow microenvironment, which consists of endosteal and vascular niches, can support leukaemogenesis through intercellular “crosstalk” with niche cells, including mesenchymal stem cells, endothelial cells, osteoblasts, and osteoclasts. Here, we summarise the regulatory mechanisms associated with leukaemia–bone marrow niche interaction and provide a comprehensive review of the key therapeutics that target CXCL12/CXCR4, Notch, Wnt/b-catenin, and hypoxia-related signalling pathways within the leukaemic niches and agents involved in remodelling of niche bone and vasculature. From a therapeutic perspective, targeting these cellular interactions is an exciting novel strategy for enhancing treatment efficacy, and further clinical application has significant potential to improve the outcome of patients with leukaemia.

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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 myeloid leukaemia, 2 chronic lymphocytic leukaemia, and 3 myelodysplastic syndrome). Male-female ratio 1.9:1, mean age at diagnosis 45.8 years. Plaques (28%) and papules (27%) were the most common skin lesions, followed by patches (18%) and nodules (16%). Mean time from diagnosis of leukaemia to development of leukaemia cutis was 12.3 months. Forty-six patients (84%) died during the 7-year follow-up; mean time from diagnosis of leukaemia cutis to death was 5.4 months. The results suggest that leukaemia cutis is associated with poor outcomes in patients with leukaemia. Comprehensive skin examination of these patients may help diagnose leukaemia cutis early, enabling prompt treatment.

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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 acute leukaemias in Bauchi State, North-Eastern Nigeria. Subjects, materials and methods: This was a three year retrospective study in which records of cases of acute leukaemias diagnosed in the Haematology Department of Abubakar Tafawa Balewa University Teaching Hospital (ATBUTH) Bauchi from the bone marrow aspiration cytology register from 1st January, 2018 to 31st December, 2020 were collected. Data on socio-demographic characteristics of the patients that include age, gender, diagnosis as well as subtypes of some of the malignancies diagnosed were also collated. The collated data were analyzed using SPSS Version 20.0. A p-value of < 0.05 was considered significant. Results: Twenty-nine cases of acute leukaemias were diagnosed during the period under review. Majority of cases had acute lymphoblastic leukaemia (ALL) 19/29 (65.5%) while acute myeloid leukaemia (AML) was seen in 10/29 (34.5%). The mean ± SD age of the patients was 22.2±9.2 years with a range 6 months to 60 years. Males constituted 75.9% (22/29) of the cases of acute leukaemias diagnosed. The male to female ratios for AML and ALL were 2:1 and 2.6:1 respectively. The mean±SD ages for AML and ALL were 27±9.2years and 17.3±11.3 years respectively. The most common form of presentation of acute leukaemia in this study is recurrent anaemia necessitating blood transfusion while proptosis and epistaxis were the least forms of presentation. Conclusion: Acute lymphoblastic leukaemia is the commonest form of acute leukaemias while recurrent anaemia is the commonest form of clinical presentations in our setting. Early referral of patients with clinical features suggestive of acute leukaemias is recommended. Author R A Dachi 1, F G Mustapha 1, M Mahdi 1, H Abbas 2

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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 were reviewed. Out of 158 adult BMA cytology reports, HMs accounted for 78(49.4%) of all haematological disorders. There was no significant gender difference. The Male 38(48.7%) to Female 40(51.3%) ratio (M:F) was 1:1.1. Their ages ranged from 16 to 85 years with the median age of 54.0 years. Out of the 78 HMs, Lymphoid neoplasms were the most prevalent 47(60.3%), the leukaemias were higher 53/78(67.9%) compared to the non-leukaemic neoplasms. Of the 53 leukaemias, those of chronic lymphoid types were more 24/53(45.3%), followed by the chronic myeloid 15/53(28.3%). Chronic lymphocytic leukaemia (CLL) was the predominant leukaemia 24/53(45.3%) as well as the most prevalent HM 24/78(30.8%), followed by chronic myeloid leukaemia (CML) 19.2%(15/78). Others were myelodysplastic syndrome (MDS) 11.5%(9/78), acute lymphoblastic leukaemia (ALL) 10.3% (8/78), multiple myeloma (MM) 10.3%(8/78), acute myeloblastic leukaemia (AML) 7.7%(6/78), non-Hodgkin's lymphoma (NHL) 6.4%(5/78), Small lymphocytic lymphoma (SLL) 2.6%(2/78) and Hodgkin's lymphoma (HL) 1.3%(1/78). In conclusion, we established high prevalence of HMs among patients who had BMA cytology evaluation at BSUTH with the preponderance of lymphoid malignancies. We advocate for inclusion of HMs in the National Health Insurance Scheme (NHIS) for full implementation and to prioritise provision of modern diagnostic equipment and treatment options for quality and optimal management of leukaemias in the center.

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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 dilution but for unknown reasons increased to 2048 dilution after remission of AML-M1. About 3 months after hospitalization the patient died of Cryptococcus neoformans pneumonia despite strict precautions against infection. Although AML-M1 is a common adult leukaemia and is chemosensitive to anti-leukaemic drugs, neither AML-M1 in a patient with Bombay-type red cells nor its treatment with chemotherapy and transfusion with type Oh frozen red cells have previously been reported.

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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 AML. This review briefly discusses the role of the bone marrow microenvironment in AML development and progression, and as a source of novel therapeutic targets for AML. The main focus of this review is on drugs that modulate/target this bone marrow microenvironment and have been examined in in vivo models or clinically.

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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 inform design of clinical trials. Clinically, FLT3 inhibitors in combination with conventional chemotherapy as induction treatment for fit patients; with low-intensity treatment as salvage treatment or induction for unfit patients as well as maintenance treatment with FLT3 inhibitors post HSCT hold promise to improve survival in this AML subtype.

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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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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 also play a role in paediatric ALL. In addition, several recent microarray studies have identified transcriptional profiles specifically associated with chemoresistance and pointed to a number of potentially novel therapeutic targets. These microarray studies have shown that genes discriminating between clinically responsive and resistant leukaemias tend to be involved in cellular processes such as regulation of cell cycle, proliferation, and DNA repair. Here we review the outcomes of these microarray studies and also present our own investigations into apoptotic resistance to DNA double strand breaks (DSBs) in paediatric ALL. We present stratification of paediatric ALL by the profile of DNA damage response following ionising radiation (IR) in vitro. This approach allows classification of ALL tumours at presentation into IR-apoptotic sensitive and IR-apoptotic resistant. Furthermore, apoptotic resistant leukaemias exhibit abnormal response of NFkB pathway following irradiation and inhibition of this pathway can sensitise leukaemic cells to IR-induced DSBs.

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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. The clinical relevance of the identified alterations was discussed in a multidisciplinary molecular tumour board (MTB). A total of 18 (69.2%) patients were diagnosed with B-ALL, 4 (15.4%) with T-ALL, 3 (11.5%) with AML and 1 patient (3.8%) with a mixed-phenotype acute leukaemia (MPL). Most of the patients had relapsed disease (88%) at the time of sample collection. A total of 17 patients (65.4%) were found to be carriers of a druggable molecular alteration, 8 of whom (47%) received targeted therapy, 7 (87.5%) of them in addition to hematopoietic stem cell transplantation (HSCT). Treatment response and disease control were achieved in 4 patients (50%). In conclusion, advanced molecular characterisation and MTB can improve treatment and outcome in paediatric R/r acute leukaemias.

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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 leukaemia. We have previously demonstrated that the sub-population of childhood acute lymphoblastic leukaemia (ALL) cells, capable of serially engrafting NOD/SCID mice, have a CD34+/CD19− or CD34+/CD7− phenotype in B cell precursor (BCP) ALL and T-ALL, respectively. In this investigation we have compared the efficacy of a current glucocorticoid therapeutic agent on these putative ALL stem cells with their effects on the bulk leukaemia population. The effect of dexamethasone (dex), a key component of the treatment of childhood ALL, on primary ALL cells from 13 paediatric cases was examined. Unsorted ALL cells were co-cultured with and without dex for 48 hours. Subsequently, cell viability and apoptosis were evaluated by flow cytometry using propidium iodide and annexin V staining, with Flow-Count fluorospheres to directly determine absolute cell counts. Primary cells from 11 patients with BCP ALL were sorted for expression of CD34/CD19 and cells from 2 T-ALL cases were sorted for expression of CD34/CD7. The unsorted cells and the sorted sub-fractions were co-cultured with increasing concentrations of dex (0.05 to 500 μM) to compare the relative chemosensitivity of the bulk and putative leukaemia stem cell populations. The unsorted leukaemia populations were completely refractory to dex with no significant difference in the levels of apoptosis observed or the absolute number of viable cells in the treated samples and in the untreated controls. Interestingly, when the sorted populations were assessed, an increase in the absolute numbers of viable CD34+/CD19− (1.2–9.7 fold, P<0.02) and CD34+/CD7− (2.6–5 fold, P<0.04) leukaemia cells were observed even at the highest steroid dose, compared to the respective untreated sub-fractions. The other leukaemic sub-fractions did not show a significant increase in the number of viable cells following dex exposure. These data show that 10 out of 11 drug treated primary leukaemia cells were resistant to dex. The putative CD34+/CD19− BCP ALL cells and CD34+/CD7− T-ALL cells showed a significantly enhanced proliferative potential when exposed to the drug, suggesting that it is these cells that may be responsible for disease relapse.

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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, identifying predictors and preventive measures against an unfavourable outcome. The crucial point of the ANLL NS 03 programme is to determine the optimal timing for the transplantation of allogeneic and autologous haematopoietic stem cells. Indicators of early death include the age of the patient, infection, and hemorrhagic syndrome. According to our models, the predictors of fatal bleeding and fatal infection are hyperleukocytosis, leucopenia, and granulocytopenia, respectively. Resistance to cytostatics can be predicted on day 14 from the onset of therapy using two original cytological-mathematical parameters: the absolute blast count (ABC) forming the intensity dimension, and parameter S forming the selectivity dimension, of the early effects of the first induction treatment. The ABC and S values determine the structure and timing of the second induction treatment. Transplantation of autologous and allogeneic haematopoietic stem cells within the ANLL NS 03 programme is applied selectively during the early stages of the first remission in patients at high risk of an early relapse. Predictors of early relapse are leukocyte counts higher than 30x109/l, remission induction during the second treatment, and the presence of myelodysplasia. In all other patient categories and in patients with cytogenetically favourable forms of acute nonlymphoblastic leukaemia, transplantation is postponed until the second remission of the disease.

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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 cell transplantation. The patient died due to the complications of stem cell transplantation procedure. Another patient was a 20-month-old girl with myeloid and T-lymphoid associated antigens in the blast cells and with normal karyotype. She received acute myeloid leukaemia induction therapy. She has never achieved remission. Discussion. Immunophenotype is essential to establish the diagnosis of biphenotypic acute leukaemia according to the scoring system adopted by the European Group of Immunological Classification of Leukaemia. There is no agreement about uniformity in treatment for the patients with this type of leukaemia. Biphenotypic acute leukaemia is a high risk leukaemia which requires a more intensive treatment. Conclusion. Therapy for every patient with biphenotypic acute leukaemia should depend on their immunophenotype and gene rearrangement profiles.

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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 prompted to consider second differential diagnosis of acute leukaemia. This case is a learning case, as it emphasizes the combined role of diagnostic ancillary techniques along with clinical judgments for management. The case also makes us more vigilant towards the pathobiology of DLBCL and dynamics of personalized individual treatment response.

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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 case of unfavorable prognostic factors (not only cytogenetical but also molecular biological characters of the disease), allogeneic stem cell transplantation is needed for successful overall outcome. Better understanding the biology of acute myeloid leukaemia could establish novel targeted therapies and help us eventually to cure the disease. Orv.Hetil., 2012, 153, 243–249.

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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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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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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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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 this amazing journey of transformation and provide recent advances in the management of APML.

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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 patients with acute leukaemia, the importance of peripheral blood film review and propound a possible risk factor. Methods: Records of 58 patients diagnosed and managed for acute leukaemia over a 7 year period at the University College Hospital, Ibadan were reviewed. The diagnosis of acute leukaemia was based on clinical features in addition to peripheral and bone marrow smears findings. Microsoft excel version 2013 was used for statistical analysis. Results: Five (8.6%) of the patients with acute leukaemia also had sickle cell disease: 3 males and 2 females were described. Recurrent fever and anaemia were the most consistent presenting features in the patients. All the patients were not on any routine medications meant for SCD patients and had poor history of clinic attendance prior to the diagnosis of acute leu- kaemia. The diagnosis of acute leukaemia was not made until the patients were seen by a haematologist. The principal tool of diagnosis in all the patients was peripheral blood film review. Two patients were discharged against medical advice.The treatment period ranged between one month and one year in the remaining three patients. Conclusion: SCD patients are not exempted from developing acute leukaemias and the diagnoses of the two conditions overwhelms the social and economic support of patients and care givers.The study also underscores the relevance of high level of suspicion and prompt review of peripheral blood film of SCD patients particularly when patients present with un- remitting symptoms associated with anaemia and fever. Keywords: Acute leukaemia; sickle cell disease; anaemia.

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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, in which the cells do not divide, but are also insensitive to chemotherapy. Applying this model to 275 molecular time courses of nucleophosmin 1 -mutated patients, we conclude that the differential chemosensitivity of the leukaemia-initiating cells together with the cells’ intrinsic proliferative capacity is sufficient to reproduce both, early relapse as well as long-lasting remission. We can, furthermore, show that the model parameters associated with individual chemosensitivity and proliferative advantage of the leukaemic cells are closely linked to the patients’ time to relapse, while a reliable prediction based on early response only is not possible based on the currently available data. Although we demonstrate with our approach, that the complete response data is sufficient to quantify the aggressiveness of the disease, further investigations are necessary to study how an intensive early sampling strategy may prospectively improve risk assessment and help to optimize individual treatments.

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Whiting, P. H., D. J. King, A. Ireland, M. A. Ratcliffe, and 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, no. 6 (November 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 demonstrated NAG levels which approached normal values. In those AML patients who were either in relapse, in the terminal phase of their illness or treated with aminoglycoside antibiotics, NAG enzymuria was similar to pre-treatment values. A reduction in urinary NAG levels and both serum and urine β2 microglobulin concentrations was also observed following treatment in myeloma patients. The use of enzymuria both as a guide to progress towards remission in AML patients and for assessing prognosis and progress in myeloma patients is discussed.

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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 1-7F9/IPH2101 was able to induce NK cell activation and cytotoxicity against leukaemic cells. Patients with AML often display abnormal NK cell function, while evidence of an impact of NK cell status on AML outcome has been reported in allogeneic transplantation. 1-7F9/IPH2101 is currently under clinical investigation in patients with AML. This article reviews the mechanisms of NK cell antileukaemic activity and its role and defects in AML. Currently available data on the pre-clinical and clinical development of 1-7F9/IPH2101 are presented, and the rationale for its future use as a single agent or in combination is discussed.

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