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1

Rodriguez, W., C. Castañeda, C. Vallejos, et al. "Acute lymphatic leukemia: Peruvian experience." Journal of Clinical Oncology 23, no. 16_suppl (2005): 6726. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.6726.

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2

Sasidharan, P. K. "Case Report: A rare association between SLE and Acute Lymphatic Leukemia." General medicine and Clinical Practice 1, no. 3 (2018): 01–02. http://dx.doi.org/10.31579/2639-4162/011.

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A 30-year-old housewife with past history of acute lymphoblastic leukemia 12 years back, still in remission, was admitted with polyarthritis of 2 months duration. She was evaluated and found to have SLE with positive ANA and Anti ds DNA which were strongly positive.
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3

Bekkers, B. C. A. M., B. J. A. Denarié, and G. M. J. Bos. "Massive cardiac involvement in acute lymphatic leukemia." Heart 90, no. 3 (2004): 354. http://dx.doi.org/10.1136/hrt.2003.022699.

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4

Schröcksnadel, H., G. Busch, W. Aulitzky, and M. Tabarelli. "Bilateral breast tumours in acute lymphatic leukemia." Archives of Gynecology and Obstetrics 247, no. 1 (1990): 43–45. http://dx.doi.org/10.1007/bf02390654.

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5

Lipsanen, V., P. Leinonen, L. Alhonen, and J. Janne. "Hypomethylation of ornithine decarboxylase gene and erb-A1 oncogene in human chronic lymphatic leukemia." Blood 72, no. 6 (1988): 2042–44. http://dx.doi.org/10.1182/blood.v72.6.2042.2042.

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Abstract The methylation state of CCGG sites in and around the human ornithine decarboxylase gene, oncogenes c-myc and erb-A1, and actin genes were determined in human malignant leucocytes from patients with acute and chronic myeloid leukemia, chronic lymphatic leukemia, polycythemia vera, and multiple myeloma by means of isoschizomeric restriction endonuclease analysis. When compared with DNA from leucocytes of healthy controls, the ornithine decarboxylase and erb-A1 genes were substantially hypomethylated in all samples obtained from patients with chronic lymphatic leukemia. Hypomethylation
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6

Lipsanen, V., P. Leinonen, L. Alhonen, and J. Janne. "Hypomethylation of ornithine decarboxylase gene and erb-A1 oncogene in human chronic lymphatic leukemia." Blood 72, no. 6 (1988): 2042–44. http://dx.doi.org/10.1182/blood.v72.6.2042.bloodjournal7262042.

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The methylation state of CCGG sites in and around the human ornithine decarboxylase gene, oncogenes c-myc and erb-A1, and actin genes were determined in human malignant leucocytes from patients with acute and chronic myeloid leukemia, chronic lymphatic leukemia, polycythemia vera, and multiple myeloma by means of isoschizomeric restriction endonuclease analysis. When compared with DNA from leucocytes of healthy controls, the ornithine decarboxylase and erb-A1 genes were substantially hypomethylated in all samples obtained from patients with chronic lymphatic leukemia. Hypomethylation of genes,
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7

Journal, Baghdad Science. "5'-nucleoridase activity in sera from iraq children with leukemia." Baghdad Science Journal 3, no. 3 (2006): 449–55. http://dx.doi.org/10.21123/bsj.3.3.449-455.

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8

Al-Rubaee, Eman A., Rokzan M. Al-Saffar, and Sanad B. Al-Arrji. "5'-nucleoridase activity in sera from iraq children with leukemia." Baghdad Science Journal 3, no. 3 (2006): 449–55. http://dx.doi.org/10.21123/bsj.2006.725.

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9

Mlynek, M. L., H. K. Mahmoud, and L. D. Leder. "Relapsing acute non-lymphatic leukemia with chaning phenotypes." Klinische Wochenschrift 63, no. 21 (1985): 1129–33. http://dx.doi.org/10.1007/bf02291095.

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10

van Leeuwen, A., PI Schrier, MJ Giphart, et al. "TCA: a polymorphic genetic marker in leukemias and melanoma cell lines." Blood 67, no. 4 (1986): 1139–42. http://dx.doi.org/10.1182/blood.v67.4.1139.1139.

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Abstract TCA (T Cell system A) is a di-allelic system of HLA-like antigens encoded by genes located about 15 cM telomeric to HLA-A. In normal individuals, TCA antigens are only expressed on a subpopulation of T cells, the TG lymphocytes. We now report on the expression of TCA on leukemias and other malignancies. An increased proportion of cells carrying the TCA phenotype was encountered in testing peripheral blood lymphocytes from patients with acute lymphoblastic T-cell leukemia (T- ALL), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML). In contrast, patients with B-cell malig
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11

van Leeuwen, A., PI Schrier, MJ Giphart, et al. "TCA: a polymorphic genetic marker in leukemias and melanoma cell lines." Blood 67, no. 4 (1986): 1139–42. http://dx.doi.org/10.1182/blood.v67.4.1139.bloodjournal6741139.

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TCA (T Cell system A) is a di-allelic system of HLA-like antigens encoded by genes located about 15 cM telomeric to HLA-A. In normal individuals, TCA antigens are only expressed on a subpopulation of T cells, the TG lymphocytes. We now report on the expression of TCA on leukemias and other malignancies. An increased proportion of cells carrying the TCA phenotype was encountered in testing peripheral blood lymphocytes from patients with acute lymphoblastic T-cell leukemia (T- ALL), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML). In contrast, patients with B-cell malignancies s
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12

Patel, P. S., S. G. Adhvaryu, and B. R. Baxi. "Tumor Markers in Leukemia: Evaluation of Serum Levels of Different Forms of Sialic Acid, Regan Isoenzyme and Lactate Dehydrogenase." International Journal of Biological Markers 6, no. 3 (1991): 177–82. http://dx.doi.org/10.1177/172460089100600307.

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A sensitive and specific serum marker can greatly help in the early diagnosis of malignancy as well as in monitoring the treatment of cancer patients. The present work was initiated for determining serum levels of Total Sialic Acid (TSA), Lipid Bound Sialic Acid (LSA), Free Sialic Acid (FSA), Regan Isoenzyme (RI) and Lactate Dehydrogenase (LDH), so as to evaluate their value as potential tumor markers. Fifty patients with anemia and 78 patients with leukemia were studied. The leukemia group consisted of 32 cases of Acute Myeloid Leukemia (AML), 29 cases of Chronic Myeloid Leukemia (CML) and 17
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13

S., Hariprasath, Dharani T., and Santhi M. "Detection and Classification of Acute Lymphoblastic Leukemia from Blood Smear Images Using Supervised Pattern Classifier." Journal of Communication Engineering and Its Innovations 5, no. 2 (2019): 22–29. https://doi.org/10.5281/zenodo.3249779.

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Leukemia is a blood cancer that causes abnormalities in the lymphatic system of our body. It is considered as one of the fatal diseases in our country. Among all the types of leukemia, Acute Lymphoblastic Leukemia (ALL) is the fast growing disease. Hence, early detection of this disease is needed in order to provide the required treatment to the victims. In this paper, the detection and classification of ALL and its subtypes (L1, L2 and L3) is done by multiclass SVM classifier based on the features extracted from nucleus and cytoplasm of the blast cell (where abnormal leucocytes are known as &
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14

Sucharitha, Are. "An Overview of Cancer." Advances in Cancer Chemotherapy and Pharmacology 1, no. 1 (2023): 1–8. http://dx.doi.org/10.23880/accp-16000102.

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Cancer is defined as one of the large groups of diseases characterized by the development of abnormal cells that grow beyond their boundaries, which can invade adjoining tissues via circulation, and spread to other organs in the body. Cancer can be initiated anywhere in the body, where damaged cells grow and multiply where they shouldn't. These cells form tumors, also called neoplasm- an abnormal mass of cells. Tumors can be non-cancerous (benign) and cancerous (malignant). Cancers are grouped according to their origin of tissue or organ. Four major types of cancers- • Carcinomas – are maligna
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15

De, A., H. Mathurkar, S. Baveja, and MV Manglani. "Pseudomonas diarrhea in a child suffering from acute lymphatic leukemia." Indian Journal of Medical and Paediatric Oncology 30, no. 4 (2009): 147. http://dx.doi.org/10.4103/0971-5851.65341.

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16

Munch-Petersen, Birgitte, and Gerda Tyrsted. "Thymidine kinase isoenzymes in human acute and chronic lymphatic leukemia." Leukemia Research 10, no. 6 (1986): 637–42. http://dx.doi.org/10.1016/0145-2126(86)90266-3.

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17

Berkowicz, M., A. Toren, E. Rosner, et al. "Translocation (2;14)(p13;q32) in CD10+;CD13+ acute lymphatic leukemia." Cancer Genetics and Cytogenetics 83, no. 2 (1995): 140–43. http://dx.doi.org/10.1016/0165-4608(95)00038-q.

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18

Pestalozzi, B. C., and H. Müller. "Lymphomatous acute lymphatic leukemia with translocation t(9;13)(p22;q12)." Cancer Genetics and Cytogenetics 33, no. 1 (1988): 149–50. http://dx.doi.org/10.1016/0165-4608(88)90062-3.

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19

Kollegger, H., P. Preis, E. Maida, et al. "CSF Cytology of a Patient with Conversion of an Acute Lymphatic Leukemia to an Acute Eosinophilic Leukemia." European Neurology 25, no. 5 (1986): 320–26. http://dx.doi.org/10.1159/000116029.

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20

Haque, Shabirul, and Sarah R. Vaiselbuh. "Silencing of Exosomal miR-181a Reverses Pediatric Acute Lymphocytic Leukemia Cell Proliferation." Pharmaceuticals 13, no. 9 (2020): 241. http://dx.doi.org/10.3390/ph13090241.

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Exosomes are cell-generated nano-vesicles found in most biological fluids. Major components of their cargo are lipids, proteins, RNA, DNA, and non-coding RNAs. The miRNAs carried within exosomes reveal real-time information regarding disease status in leukemia and other cancers, and therefore exosomes have been studied as novel biomarkers for cancer. We investigated the impact of exosomes on cell proliferation in pediatric acute lymphocytic leukemia (PALL) and its reversal by silencing of exo-miR-181a. We isolated exosomes from the serum of PALL patients (Exo-PALL) and conditioned medium of le
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21

Cai, Dali, Ying Wang, Oliver G. Ottmann, Peter J. Barth, Andreas Neubauer, and Andreas Burchert. "FLT3-ITD–, but not BCR/ABL-transformed cells require concurrent Akt/mTor blockage to undergo apoptosis after histone deacetylase inhibitor treatment." Blood 107, no. 5 (2006): 2094–97. http://dx.doi.org/10.1182/blood-2005-08-3317.

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Leukemias are differentially sensitive to histone deacytelase inhibitor (HDI)–induced apoptosis, but molecular reasons for this remain unclear. We here show that BCR/ABL-, but not FMS-like tyrosine kinase 3 (FLT3)–internal tandem duplication (ITD)–transformed 32D cells or primary acute myeloid leukemia (AML) blasts undergo apoptosis after treatment with the HDI valproic acid (VPA) plus all-trans retinoic acid (VPA/ATRA). A particular VPA/ATRA responsiveness of Philadelphia chromosome–positive (Ph+) acute lymphatic leukemia (ALL) was confirmed in a therapy-refractory patient in vivo. HDI-stimul
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22

Haferlach, Torsten, Alexander Kohlmann, Susanne Schnittger, et al. "Global approach to the diagnosis of leukemia using gene expression profiling." Blood 106, no. 4 (2005): 1189–98. http://dx.doi.org/10.1182/blood-2004-12-4938.

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AbstractAccurate diagnosis and classification of leukemias are the bases for the appropriate management of patients. The diagnostic accuracy and efficiency of present methods may be improved by the use of microarrays for gene expression profiling. We analyzed gene expression profiles in 937 bone marrow and peripheral blood samples from 892 patients with all clinically relevant leukemia subtypes and from 45 nonleukemic controls by U133A and U133B GeneChip arrays. For each subgroup, differentially expressed genes were calculated. Class prediction was performed using support vector machines. Pred
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23

Slaper-Cortenbach, IC, LG Admiraal, JM Kerr, EF van Leeuwen, AE von dem Borne, and PA Tetteroo. "Flow-cytometric detection of terminal deoxynucleotidyl transferase and other intracellular antigens in combination with membrane antigens in acute lymphatic leukemias." Blood 72, no. 5 (1988): 1639–44. http://dx.doi.org/10.1182/blood.v72.5.1639.1639.

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Abstract Development of a new fixation procedure allowed flow-cytometric analysis of nuclear and other intracellular antigens in acute lymphatic leukemia (ALL). A short fixation of the cells with buffered formaldehyde acetone (BFA) rendered the cell membrane permeable, allowing the monoclonal antibodies (MoAbs) to penetrate the cell. Through this method, a rapid analysis of intracellular antigens, specific for acute lymphatic leukemia [such as terminal deoxynucleotidyl transferase (TdT), immunoglobulin M (IgM) heavy chain, and antigens recognized by the CD22 or CD3 MoAbs) was performed by flow
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24

Slaper-Cortenbach, IC, LG Admiraal, JM Kerr, EF van Leeuwen, AE von dem Borne, and PA Tetteroo. "Flow-cytometric detection of terminal deoxynucleotidyl transferase and other intracellular antigens in combination with membrane antigens in acute lymphatic leukemias." Blood 72, no. 5 (1988): 1639–44. http://dx.doi.org/10.1182/blood.v72.5.1639.bloodjournal7251639.

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Development of a new fixation procedure allowed flow-cytometric analysis of nuclear and other intracellular antigens in acute lymphatic leukemia (ALL). A short fixation of the cells with buffered formaldehyde acetone (BFA) rendered the cell membrane permeable, allowing the monoclonal antibodies (MoAbs) to penetrate the cell. Through this method, a rapid analysis of intracellular antigens, specific for acute lymphatic leukemia [such as terminal deoxynucleotidyl transferase (TdT), immunoglobulin M (IgM) heavy chain, and antigens recognized by the CD22 or CD3 MoAbs) was performed by flow cytometr
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25

Lambertenghi-Deliliers, Giorgio, Enrico Pogliani, Claudio Annaloro, Maria Adele Pacciarini, and Elio E. Polli. "Oral Idarubicin in Adult Acute Leukemia: A Preliminary Experience." Tumori Journal 72, no. 2 (1986): 157–61. http://dx.doi.org/10.1177/030089168607200207.

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Twelve patients affected by different types of acute leukemia received idarubicin (4-demethoxy-daunorubicin) by oral route at the total dosage of 45, 60 or 90 mg/m’ distributed over three consecutive days. Drug response was assessed by the decrease in blast cells in peripheral blood and showed some variations between the different types of leukemia. Acute myelogenous leukemia patients and those with blastic crisis of chronic myeloid leukemia appeared to be the more responsive groups; however, the lower dose schedule could explain the less satisfactory results obtained in lymphatic leukemia pat
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26

Bjerregaard, Lise Lotte, and Steen Rosthoøj. "Vertebral Compression and Eosinophilia in a Child With Acute Lymphatic Leukemia." Journal of Pediatric Hematology/Oncology 24, no. 4 (2002): 313–15. http://dx.doi.org/10.1097/00043426-200205000-00019.

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27

Jain, Yogesh, V. P. Choudhry, L. S. Arya, and M. Mehta. "Neuropsychological abnormalities following CNS prophylaxis in children with acute lymphatic leukemia." Indian Journal of Pediatrics 60, no. 5 (1993): 675–81. http://dx.doi.org/10.1007/bf02821732.

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28

Oka, Yoko, Ryosuke Shirasaki, Haruko Tashiro, et al. "Tcf3/Pbx1 Fusion Molecule Induces the Transcription of Prox-1 and Vascular Endothelial Growth Factor Receptor Type-3." Blood 118, no. 21 (2011): 1487. http://dx.doi.org/10.1182/blood.v118.21.1487.1487.

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Abstract Abstract 1487 Background and Aims: It is now known that, in some hematological malignancies, hematopoietic cytokines and their specific receptors work on the progression of leukemia with an autocrine stimulation of immature leukemic blasts. Vascular endothelial growth factor (VEGF)-C and VEGF receptor type-3 (VEGFR-3), which play an important role in creation of systematic lymphatic vessel systems, are also reported to work on the progression of malignant solid tumors and some of acute leukemias. We recently reported that in two cases of acute lymphocytic leukemia (ALL) with TCF3/PBX1
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29

Xu, Linwei, Xiaolei Wei, Yongqiang Wei, et al. "Coagulation Disorder after Treatment of Pegaspargase and L-Asparaginase." Blood 126, no. 23 (2015): 4876. http://dx.doi.org/10.1182/blood.v126.23.4876.4876.

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Abstract Introduction: Pegaspargase(PEG-ASP) and L-asparaginase(L-ASP) has been widely used in the treatment of acute lymphatic leukemia, changes of coagulation function after treatment are not actually the same. So we performed the present study to analyze coagulation disorder after PEG-ASP and L-ASP treatment of adults with acute lymphatic leukemia. Methods and materials: Totally 153 hospitalized patients with acute lymphatic leukemia treated with L-ASP or PEG-ASP were studied from January, 2010 to January, 2015. Of all 153 patients analyzed, they received L-ASP treatment 158 dose times and
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30

Maheshwari, G. "Unusual Presentations of Acute Lymphoblastic Leukemia in Children: A Study of 9 Patients." Journal of Global Oncology 4, Supplement 2 (2018): 87s. http://dx.doi.org/10.1200/jgo.18.42100.

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Background: Acute lymphoblastic leukemia is the most common malignancy in children below 15 years of age. Bone marrow, CNS and the gonads are the three major sites of failure or relapse in acute lymphoblastic leukemia. Occasionally, leukemic cells can infiltrate the unusual sites and present with some unusual manifestations either at initial (diagnosis) presentation or during the course of disease. This study presents 9 such rare cases of unusual manifestations of acute lymphoblastic leukemia. Aim: To report the unusual presentation and management of acute lymphatic leukemia in children either
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31

Faguet, GB, and JF Agee. "Monoclonal antibodies against the chronic lymphatic leukemia antigen cCLLa: characterization and reactivity." Blood 70, no. 2 (1987): 437–43. http://dx.doi.org/10.1182/blood.v70.2.437.437.

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Abstract Monoclonal antibodies (MoAbs) were developed against the cCLLa, a 69- kilodalton leukemia-associated antigen expressed on malignant cells of B-type chronic lymphatic leukemia (B-CLL) and its variants: prolymphocytic (PLL) and hairy cell leukemias (HCL). Two hybridomas yielded approximately 2 and approximately 7.5 mg/mL of IgG2a kappa and IgM kappa, respectively. Monoclonal surface immunoglobulin-bearing cells of all B-CLL patients studied (n = 30) reacted with the MoAbs (r greater than .99) regardless of stage or lymphocyte count. This suggests that the malignant clone in CLL can be i
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32

Faguet, GB, and JF Agee. "Monoclonal antibodies against the chronic lymphatic leukemia antigen cCLLa: characterization and reactivity." Blood 70, no. 2 (1987): 437–43. http://dx.doi.org/10.1182/blood.v70.2.437.bloodjournal702437.

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Monoclonal antibodies (MoAbs) were developed against the cCLLa, a 69- kilodalton leukemia-associated antigen expressed on malignant cells of B-type chronic lymphatic leukemia (B-CLL) and its variants: prolymphocytic (PLL) and hairy cell leukemias (HCL). Two hybridomas yielded approximately 2 and approximately 7.5 mg/mL of IgG2a kappa and IgM kappa, respectively. Monoclonal surface immunoglobulin-bearing cells of all B-CLL patients studied (n = 30) reacted with the MoAbs (r greater than .99) regardless of stage or lymphocyte count. This suggests that the malignant clone in CLL can be identified
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33

Seipel, Katja, Karin Schmitter, Ulrike Bacher, and Thomas Pabst. "Rationale for a Combination Therapy Consisting of MCL1- and MEK-Inhibitors in Acute Myeloid Leukemia." Cancers 11, no. 11 (2019): 1779. http://dx.doi.org/10.3390/cancers11111779.

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Amplification and overexpression of the myeloid cell leukemia differentiation protein MCL1 and the murine double minute protein MDM2 have been reported in various human tumors as well as hematological malignancies including acute myeloid leukemia (AML). While MCL1 is an anti-apoptotic member of the BCL-2 family proteins, MDM2 is an important cellular inhibitor of the p53 tumor suppressor. The key oncogene in AML is the FLT3 growth factor receptor gene. FLT3 signaling pathways including the MAPK cascade (RAS-RAF-MEK-ERK) are highly active in AML cells, leading to induced protein translation and
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34

Suratman, Rivani Sintia, Rudy Afriant, Drajad Priyono, Raveinal, and Fauzar. "The Role of Immunophenotyping in the Diagnosis of Acute Leukemia: A Narrative Literature Review." Bioscientia Medicina : Journal of Biomedicine and Translational Research 7, no. 2 (2023): 3085–90. http://dx.doi.org/10.37275/bsm.v7i2.772.

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Leukemia is the expansion of leukocyte cells in the bone marrow, which results in an increase in the number of leukocyte cells in the blood circulation and abnormal cell proliferation in the lymphatic tissue. The diagnosis of leukemia is established based on anamnesis, physical examination, and laboratory and confirmed by supporting examinations such as bone marrow aspiration to immunophenotyping. This literature review aimed to describe the role of immunophenotyping in the diagnosis of acute leukemia. The working process of immunophenotyping consists of a group of cells stained with a fluoroc
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35

MORISHIMA, YASUO. "Autologous bone marrow transplantation therapy of acute lymphatic leukemia using monoclonal antibody." Japanese Journal of Clinical Immunology 14, no. 5 (1991): 530–32. http://dx.doi.org/10.2177/jsci.14.530.

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36

Nilsson, A., M. Nordin, F. Chiodi, and O. Björk. "Immunity to Measles, Mumps and Rubella After Acute Lymphatic Leukemia in Childhood." Pediatric Research 45 (May 1999): 756. http://dx.doi.org/10.1203/00006450-199905010-00112.

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37

BOHM, J., A. IMMONEN, P. RIIKONEN, R. VANNINEN, and I. ALAFUZOFF. "Case report: central neurocytoma with concomitant cerebral involvement by acute lymphatic leukemia." Human Pathology 37, no. 4 (2006): 488–92. http://dx.doi.org/10.1016/j.humpath.2005.11.018.

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38

Cicogani, A., V. Vecchi, P. Pirazzoli, et al. "GROWTH AND PITUITARY FUNCTION IN CHILDREN TREATED FOR ACUTE LYMPHATIC LEUKEMIA (ALL)." Pediatric Research 23, no. 1 (1988): 119. http://dx.doi.org/10.1203/00006450-198801000-00106.

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39

Mapara, MY, K. Bommert, RC Bargou, et al. "G protein subunit G alpha 16 expression is restricted to progenitor B cells during human B-cell differentiation." Blood 85, no. 7 (1995): 1836–42. http://dx.doi.org/10.1182/blood.v85.7.1836.bloodjournal8571836.

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Recently G alpha 16, a new guanosine triphosphate (GTP) binding protein alpha subunit has been described to be specifically expressed in human hematopoietic cells. Expression of G alpha 16 was observed in human cell lines of myelomonocytic and T-lymphocytic origin, but not in human B-cell lines Raji and IM9. We studied the expression of G alpha 16 in human B cells corresponding to different stages of B-cell differentiation by means of reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. The human Burkitt's lymphoma cell lines Raji, Ramos, BJAB, the lymphoblastoid cell
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40

Lee, Ji Yoon, Heeje Kim, Sohye Park, et al. "Enriched Expression of the Lymphatic Marker VEGFR-3 in CD56+ Cells with Low Levels of Lytic Function in Acute Myeloid Leukemia,." Blood 118, no. 21 (2011): 3230. http://dx.doi.org/10.1182/blood.v118.21.3230.3230.

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Abstract Abstract 3230 Acute myeloid leukemia (AML) is heterogeneous clonal disorder, marked by the accumulation of undifferentiated myeloid blasts. Emerging data suggest that angiogenesis plays an important role in AML, and angiogenic mediators that promote the growth of leukemic blasts in an auto/paracrine manner may be promising targets for novel therapeutic strategies. Like angiogenesis, lymphangiogenesis is also involved in tumor cell dissemination and metastasis. In particular, targeting of VEGFR-3, a lymphatic marker, has been successful in treating tumors. Although lymphatic factors ca
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41

Shustov, V. Ya, N. A. Afanasyeva, P. P. Kuznetsov, and A. K. Myshkina. "Use of immunocorrectors in patients with chronic lymph leukemia." Kazan medical journal 67, no. 2 (1986): 99–101. http://dx.doi.org/10.17816/kazmj65309.

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Chronic lymphatic leukemia is second only to acute leukemia in the frequency of infectious complications. In most cases, severe infectious complications are the cause of death in these patients. Modern chemotherapy makes it possible to preserve the ability to work and the life expectancy of patients for a long time. However, the negative effect of cytostatic drugs on the already altered immune system leads to an even greater suppression of immunity and an increase in the number of infectious complications. The search for new ways to combat infections has shown the advisability of long-term out
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Ibrahim, Rian, Nada Idrees, and Nasir Younis. "Epidemiology of leukemia among children in Nineveh Province, Iraq." Rawal Medical Journal 48, no. 1 (2023): 1. http://dx.doi.org/10.5455/rmj20221101110317.

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Objective: To determine the prevalence of leukemia among children during 2018-2021 in Mosul city. Methodology: This retrospective study was conducted on leukemia patients in Oncology Center at Ibn Al-Atheer Hospital from 10th January to 30th April 2022. Data were collected from patients’ records. Results: Out of 153 patients, 99 (64.8%) were males and 54 (35.2%) females. The disease was found in children of school age more than in the rest of the ages and more males and those belonging to urban areas were affected. Acute lymphatic leukemia was commonest form found. Conclusion: The prevalence o
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Sampat, Nakul Y., Arvind Govind Valand, Rakshak Dinesh Prajapati, Pervaiz Ahmed Khan, and Pradeep Wagh. "Incidental association: Acute myeloid leukemia and filariasis - A case report." IP Journal of Diagnostic Pathology and Oncology 8, no. 4 (2023): 222–24. http://dx.doi.org/10.18231/j.jdpo.2023.052.

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Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation of myeloid cells in the bone marrow. Symptoms include fatigue, frequent infections, easy bruising or bleeding, and shortness of breath. Filariasis is a parasitic infection caused by filarial worms (a nematode) transmitted through mosquito bites from infected individuals, leading to chronic lymphatic dysfunction, lymphedema, hydrocele, and elephantiasis. Here, we present the case of a 38-year-old male who was diagnosed with acute myeloid leukemia without maturation (M1) and an incidental findi
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Nel, J. S., and Carta I. Falkson. "Granulocyte-Macrophage-Colony-Stimulating Factor Support in Patients with Acute Non-Lymphatic Leukemia." Oncology 53, no. 6 (1996): 482–87. http://dx.doi.org/10.1159/000227624.

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Slater, L. M., P. Sweet, M. Stupecky, and S. Gupta. "Cyclosporin A reverses vincristine and daunorubicin resistance in acute lymphatic leukemia in vitro." Journal of Clinical Investigation 77, no. 4 (1986): 1405–8. http://dx.doi.org/10.1172/jci112450.

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Ichihara, Hideaki, Junichi Ueno, Masayo Umebayashi, Yoko Matsumoto, and Ryuichi Ueoka. "Chemotherapy with hybrid liposomes for acute lymphatic leukemia leading to apoptosis in vivo." International Journal of Pharmaceutics 406, no. 1-2 (2011): 173–78. http://dx.doi.org/10.1016/j.ijpharm.2010.12.041.

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Veyalkin, I. V., and A. A. Cheshik. "RISK OF HEMOBLASTOSIS IN THE POPULATION AFFECTED BY THE CHERNOBYL DISASTER." Journal of the Grodno State Medical University 19, no. 6 (2021): 686–90. http://dx.doi.org/10.25298/2221-8785-2021-19-6-686-690.

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Background. Until now, there are disputes about the role of the Chernobyl disaster in the formation of an excess incidence of malignant neoplasms of the blood in the affected population. Aim. To study the peculiarities of the formation of the incidence of malignant neoplasms of the blood and lymphatic system in people of Belarus exposed to radiation as a result of the Chernobyl accident. Material and methods. Retrospective radiation-epidemiological risk analysis based on the State register of persons exposed to radiation as a result of the Chernobyl disaster. Results. The excess incidence of l
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Cesano, A., R. O'Connor, B. Lange, J. Finan, G. Rovera, and D. Santoli. "Homing and progression patterns of childhood acute lymphoblastic leukemias in severe combined immunodeficiency mice." Blood 77, no. 11 (1991): 2463–74. http://dx.doi.org/10.1182/blood.v77.11.2463.2463.

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Abstract The aim of this study was to analyze the homing and progression patterns of childhood acute lymphoblastic leukemias (ALL) in mice with severe combined immunodeficiency (SCID). Upon intraperitoneal (IP) transfer, cells from relapse samples of three children with T-lineage ALL spread hematogenously and infiltrated the non-lymphoid and/or lymphoid organs with a pattern reminiscent of the human clinical disease. These mice either died or were killed in extremis at a mean of 9 weeks. Moreover, cell lines established in vitro from two of these samples manifested identical homing and progres
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Cesano, A., R. O'Connor, B. Lange, J. Finan, G. Rovera, and D. Santoli. "Homing and progression patterns of childhood acute lymphoblastic leukemias in severe combined immunodeficiency mice." Blood 77, no. 11 (1991): 2463–74. http://dx.doi.org/10.1182/blood.v77.11.2463.bloodjournal77112463.

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The aim of this study was to analyze the homing and progression patterns of childhood acute lymphoblastic leukemias (ALL) in mice with severe combined immunodeficiency (SCID). Upon intraperitoneal (IP) transfer, cells from relapse samples of three children with T-lineage ALL spread hematogenously and infiltrated the non-lymphoid and/or lymphoid organs with a pattern reminiscent of the human clinical disease. These mice either died or were killed in extremis at a mean of 9 weeks. Moreover, cell lines established in vitro from two of these samples manifested identical homing and progression in t
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Pfeiffer, Matthias M., Michael Schumm, Klaus Dietz, Tobias Feuchtinger, Rupert Handgretinger, and Peter J. Lang. "Quantitative HLA Class I Expression and KIR-Mismatch between NK-Cell-Donor and Patient Predict NK Cell Mediated Lysis of Leukemic Cells from Children with Acute Lymphatic Leukemia." Blood 108, no. 11 (2006): 5205. http://dx.doi.org/10.1182/blood.v108.11.5205.5205.

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Abstract Relapses represent a major problem after transplantations in children with ALL. Natural Killer (NK) cells have been shown to exert remarkable Graft versus Leukemia effects after mismatched stem cell transplantation in myeloic leukemia, whereas the efficacy against lymphatic leukemia is still unclear. We therefore measured intensity of HLA class I expression on leukemic blasts by quantitative FACS analysis and investigated the impact of quantitative HLA class I expression, of several adhesion molecules and of KIR-mismatch on NK cell mediated lysis of the leukemic blasts from 21 pediatr
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