• Title/Summary/Keyword: Acute Leukemia

Search Result 458, Processing Time 0.029 seconds

How to Establish Acute Myeloid Leukemia Xenograft Models Using Immunodeficient Mice

  • Shan, Wu-Lin;Ma, Xiao-Ling
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.12
    • /
    • pp.7057-7063
    • /
    • 2013
  • The discovery of the immunodeficient mice has provided a tool for establishing animal models as hosts for in vivo analysis of AML. Various model systems have been established in the last few decades, and it is essential that murine AML models are developed to exploit more specific, targeted therapeutics. In this review, we concentrate on the models of AML and discuss the development of immunodeficiency models for understanding of leukemogenesis, describe those now available and their values and document the methods used for establishing and identifying AML mice models, as well as factors influencing engraftment of human AML in immunodeficient mice. Thus, the function of this article is to provide clinicians and experimentalists with a chronological, comprehensive appraisal of all AML model systems.

Wild Carrot Oil Extract is Selectively Cytotoxic to Human Acute Myeloid Leukemia Cells

  • Tawil, Mirna;Bekdash, Amira;Mroueh, Mohammad;Daher, Costantine F.;Abi-Habib, Ralph J.
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.16 no.2
    • /
    • pp.761-767
    • /
    • 2015
  • Background: In this study, we used Daucus carota oil extract (DCOE) to target acute myeloid leukemia (AML) cells. All the AML cell lines tested were sensitive to the extract while peripheral mononuclear cells were not. Analysis of mechanism of cell death showed an increase in cells positive for annexinV and for active caspases, indicating that DCOE induces apoptotic cell death in AML. Inhibition of the MAPK pathway decreased sensitivity of AML cells to DCOE, indicating that cytotoxicity may be dependent on its activity. In conclusion, DCOE induces selective apoptosis in AML cells, possibly through a MAPK-dependent mechanism.

Bioinformatics Interpretation of Exome Sequencing: Blood Cancer

  • Kim, Jiwoong;Lee, Yun-Gyeong;Kim, Namshin
    • Genomics & Informatics
    • /
    • v.11 no.1
    • /
    • pp.24-33
    • /
    • 2013
  • We had analyzed 10 exome sequencing data and single nucleotide polymorphism chips for blood cancer provided by the PGM21 (The National Project for Personalized Genomic Medicine) Award program. We had removed sample G06 because the pair is not correct and G10 because of possible contamination. In-house software somatic copy-number and heterozygosity alteration estimation (SCHALE) was used to detect one loss of heterozygosity region in G05. We had discovered 27 functionally important mutations. Network and pathway analyses gave us clues that NPM1, GATA2, and CEBPA were major driver genes. By comparing with previous somatic mutation profiles, we had concluded that the provided data originated from acute myeloid leukemia. Protein structure modeling showed that somatic mutations in IDH2, RASGEF1B, and MSH4 can affect protein structures.

Intraparenchymal Myeloid Sarcoma and Subsequent Spinal Myeloid Sarcoma for Acute Myeloblastic Leukemia

  • Eom, Ki-Seong;Kim, Tae-Young
    • Journal of Korean Neurosurgical Society
    • /
    • v.49 no.3
    • /
    • pp.171-174
    • /
    • 2011
  • Myeloid sarcoma is a solid, extramedullary tumor composed of leukemic myeloblasts or immature myeloid cells. Intraparenchymal myeloid sarcoma without the involvement of the skull or meninges is extremely rare. Here, we present the case of a 49-year-old man who developed intraparenchymal myeloid sarcoma on the left cerebellum after allogeneic bone marrow transplantation (BMT). He received radiotherapy after complete removal of intraparenchymal myeloid sarcoma, but he was diagnosed spinal myeloid sarcoma three month later. Nine months after the operation, new intracranial and spinal myeloid sarcoma were diagnosed and the patient's condition had been worsened rapidly. Although the spinal myeloid sarcoma was not histologically diagnosed, this report provides valuable insights into the clinical course of progression of intraparenchymal myeloid sarcoma.

Gingival Enlargement Occurred in Acute Leukemia (급성 백혈병에 발생한 치은증식증 1례)

  • Cho, Young-Pill;Lee, Nyoun-Jong;Kim, Bong-Hwan
    • The Journal of the Korean dental association
    • /
    • v.17 no.4 s.119
    • /
    • pp.291-296
    • /
    • 1979
  • This patient, 30 year-old korean male, was admitted with complaints of the gingival enlargement and spontaneous bleeding of the gingival tissue with acute leukemia. In reviewing this case, the following points should have been understood; 1. This is a case of the gingivitis, gingival enlargement, gingival bleeding, so the patient showed the masticatory disturbances. 2. The generalized weakness, petechia in skin, anemia, and hepatomegaly on palpation were seen. 3. With the histopathological examination by means of microscopic views, numerous myelocytic cells, of which their shapes were in irregular, were appeared. 4. The prognosis was poor in spite of any other internal treatments.

  • PDF

RUNX1 Mutations in the Leukemic Progression of Severe Congenital Neutropenia

  • Olofsen, Patricia A.;Touw, Ivo P.
    • Molecules and Cells
    • /
    • v.43 no.2
    • /
    • pp.139-144
    • /
    • 2020
  • Somatic RUNX1 mutations are found in approximately 10% of patients with de novo acute myeloid leukemia (AML), but are more common in secondary forms of myelodysplastic syndrome (MDS) or AML. Particularly, this applies to MDS/AML developing from certain types of leukemia-prone inherited bone marrow failure syndromes. How these RUNX1 mutations contribute to the pathobiology of secondary MDS/AML is still unknown. This mini-review focusses on the role of RUNX1 mutations as the most common secondary leukemogenic hit in MDS/AML evolving from severe congenital neutropenia (SCN).

CD26: A Prognostic Marker of Acute Lymphoblastic Leukemia in Children in the Post Remission Induction Phase

  • Mehde, Atheer Awad;Yusof, Faridah;Mehdi, Wesen Adel;Zainulabdeen, Jwan Abdulmohsin
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.16 no.12
    • /
    • pp.5059-5062
    • /
    • 2015
  • Background: ALL is an irredeemable disease due to the resistance to treatment. There are several influences which are involved in such resistance to chemotherapy, including oxidative stress as a result of the generation of reactive oxygen species (ROS) and presence of hypodiploid cells. Cluster of differentiation 26 (CD26), also known as dipeptidyl peptidase-4, is a 110 kDa, multifunctional, membrane-bound glycoprotein. Aim and objectives: The aim of this study was to evaluate the clinical significance of serum CD26 in patients with acute lymphoblastic leukaemia patients in the post remission induction phase, as well as the relationship between CD26 activity and the oxidative stress status. Materials and Methods: CD26, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI), in addition to activity of related enzymes myeloperoxidase, glutathione-s-transferase and xanthine oxidase, were analysed in sixty children with acute lymphoblastic leukaemia in the post remission induction phase. Results: The study showed significant elevation in CD26, TOS and OSI levels in patients with acute lymphoblastic leukaemia in the post remission induction phase in comparison to healthy control samples. In contrast, myeloperoxidase, glutathione-s-transferase and xanthine oxidase activities were decreased significantly. A significant correlation between CD26 concentration and some oxidative stress parameters was evident in ALL patients. Conclusions: Serum levels of CD26 appear to be useful as a new biomarker of oxidative stress in children with acute lymphoblastic leukaemia in the post remission induction phase, and levels of antioxidants must be regularly estimated during the treatment of children with ALL.

Cytogenetic Profile of De Novo B lineage Acute Lymphoblastic Leukemia: Determination of Frequency, Distribution Pattern and Identification of Rare and Novel Chromosomal Aberrations in Indian Patients

  • Bhandari, Prerana;Ahmad, Firoz;Dalvi, Rupa;Koppaka, Neeraja;Kokate, Prajakta;Das, Bibhu Ranjan;Mandava, Swarna
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.16 no.16
    • /
    • pp.7219-7229
    • /
    • 2015
  • Background: Chromosomal aberrations identified in acute lymphoblastic leukemia (ALL) have an important role in disease diagnosis, prognosis and management. Information on karyotype and associated clinical parameters are essential to physicians for planning cancer control interventions in different geographical regions. Materials and Methods: In this study, we present the overall frequency and distribution patterns of chromosomal aberrations in both children and adult de novo B lineage ALL Indian patients using conventional cytogenetics, interphase FISH and multiplex RT-PCR. Results: Among the 215 subjects, cytogenetic results were achieved in 172 (80%) patients; normal karyotype represented 37.2% and abnormal 62.8% with a distribution as follows: 15.3% hypodiploidy; 10.3% hyperdiploidy; 15.8% t(9;22); 9.8% t(1;19); 3.7% t(12;21); 2.8% t(4;11); 2.8% complex karyotypes. Apart from these, we observed several novel, rare and common chromosomal rearrangements. Also, FISH studies using LSI extra-signal dual-color probes revealed additional structural or numerical changes. Conclusions: These results demonstrate cytogenetic heterogeneity of ALL and confirm that the incidence of chromosomal abnormalities varies considerably. To the best of our knowledge, this is one of the largest reported series of cytogenetic investigations in Indian B-lineage ALL cases. In addition, ongoing cytogenetic studies are warranted in larger groups of B-lineage ALL cases to identify newly acquired chromosomal abnormalities that may contribute to disease diagnosis and management.

MDM2 T309G has a Synergistic Effect with P21 ser31arg Single Nucleotide Polymorphisms on the Risk of Acute Myeloid Leukemia

  • Ebid, Gamal T.;Sedhom, Iman A.;El-Gammal, Mosaad M.;Moneer, Manar M.
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.13 no.9
    • /
    • pp.4315-4320
    • /
    • 2012
  • Background: The P53 tumor suppressor gene plays a pivotal role in maintaining cellular homeostasis by preventing the propagation of genome mutations. P53 in its transcriptionally active form is capable of activating distinct target genes that contribute to either apoptosis or growth arrest, like P21. However, the MDM2 gene is a major negative regulator of P53. Single nucleotide polymorphisms (SNP) in codon Arg72Pro of P53 results in impairment of the tumor suppressor activity of the gene. A similar effect is caused by a SNP in codon 31 of P21. In contrast, a SNP in position 309 of MDM2 results in increased expression due to substitution of thymine by guanine. All three polymorphisms have been associated with increased risk of tumorigenesis. Aim of the study: We aimed to study the prevalence of SNPs in the P53 pathway involving the three genes, P53, P21 and MDM2, among acute myeloid leukemia (AML) patients and to compare it to apparently normal healthy controls for assessment of impact on risk. Results: We found that the P21 ser31arg heterozygous polymorphism increases the risk of AML (P value=0.017, OR=2.946, 95% CI=1.216-7.134). Although the MDM2 309G allele was itself without affect, it showed a synergistic effect with P21 ser/arg polymorphism (P value=0.003, OR=6.807, 95% CI=1.909-24.629). However, the MDM2 309T allele abolish risk effect of the P21 polymorphic allele (P value=0.71). There is no significant association of P53 arg72pro polymorphism on the risk of AML. Conclusion: We suggest that SNPs in the P53 pathway, especially the P21 ser31arg polymorphism and combined polymorphisms especially the P21/MDM2 might be genetic susceptibility factors in the pathogenesis of AML.