Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D03343 (MDS)
 2,225 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 34-year old female was admitted to our clinic because of fever and general fatigue on March 26, 1987. On admission, peripheral blood (PB) revealed pancytopenia. Bone marrow smears revealed 9. 0% of promyelocytic cells with or without Auer rods. Diagnosis of RAEB in transformation was made. Chromosome study of the bone marrow cells showed t(15; 17) in 3 out of 20 cells analysed. After 3 months, the leukemic cells were observed in PB and increased in number. Then the patient showed bleeding tendency and fibrin degradation products (FDP) increased up to 40 micrograms/ml. And the leukemic cells were over 30% in PB at the end of July, 1987. The diagnosis of APL with DIC was made. To our knowledge, this is the first case of APL with a history of MDS with t(15; 17).
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PMID:[Acute promyelocytic leukemia with a history of RAEB in transformation and the 15/17 translocation]. 271 1

We have presented a working hypothesis showing the possible interrelations between proliferative, aproliferative and autoimmune disorders that may follow infection with lymphotropic herpesviruses. Aproliferative disorders in this context may also indicate immune or hematopoietic deficiency. Although this hypothesis can currently be best documented with the lymphotropic viruses (herpesviruses as well as similarly HTLV and HIV), the model may apply as well--with certain variations--to other viral infections such as with hepatitis virus B or C with acute or chronic infectious diseases, post-infectious arthritis, aplastic anemia, and other autoimmune liver diseases, as well as neoplastic diseases (hepatocellular carcinoma, chronic lymphocytic leukemia). The working hypothesis as depicted in Figure 2 permits a preview of which combinations of symptoms may occur in an individual disease independent of its initial classification and what clinical testing should be done respectively, and it also permits certain prognostic considerations. The above-mentioned transitions or combinations of various disease patterns have been repeatedly described in the medical literature (to refer to only a few examples: APL and MPD, HD and MDS, SLE and aplastic anemia, SLE and Kikuchi's disease; 23, 80-83). Finally the hypothesis can ideally serve as the basis for future planning of clinical research.
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PMID:A unifying concept of viral immunopathogenesis of proliferative and aproliferative diseases (working hypothesis). 789 76

Cytogenetic analysis was performed in 86 cases of hematologic malignancy, using conventional cytogenetic analysis and fluorescence in situ hybridization (FISH) analysis at two university hospitals in Korea between 1993 and 1995. In addition to well-known anomalies, some unusual abnormalities were found, such as t(17;22), trisomy 9 combined with t(14;17), (2;7) and Philadelphia chromosome in CML; t(1;12), t(11;22), t(9;17), and t(12;21) in AML; trisomy 11 in MDS; t(2;9) and complex t(8;8;13;14) in ALL. The results of FISH analysis in interphase nuclei using a translocation probe for CML and APL showed more than 85% positive cells in CML, and 75% positive cells in APL.
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PMID:Cytogenetic and fluorescence in situ hybridization analyses of hematologic malignancies in Korea. 946 Apr 92

The oral antitumor drugs against hematological malignancies are summarized. Sobuzoxane, a topoisomerase II inhibitor, is useful for the treatment of lymphoma, especially adult T cell leukemia/lymphoma. Sobuzoxane has an effect to protect against doxorubicin cardiotoxicity. Cytarabine ocfosfate, a derivative of cytosine arabinoside, is a useful agent against acute leukemia and MDS, especially RAEB, RAEB in T, CMMoL. The JALSG AML 92 study for APL with all-trans retinoic acid resulted in a 89% CR rate in 196 and 64% 4-year DFS in CR cases. Hydroxycarbamide is can control the WBC in CML. This agent is also effective for other myeloproliferative disorders, such as acute leukemia and MDS. Oral administration of 50 mg etoposide daily showed a good outcome in old patients with malignant lymphoma. For old patients and those with refractory hematological malignancies, oral administration of these agents can offer a new form of palliative therapy to allow them to remain at home while maintaining a high quality of life.
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PMID:[Oral antitumor drugs for hematological malignancies]. 1006 91

An 87-year old female presented with unsteady gait and occasional subcutaneous hematomas. Blood examination findings revealed pancytopenia and mild coagulopathy. Both the histopathological evaluation of bone marrow smears and bone marrow biopsy revealed a hypocellular bone marrow. However, APL cells were observed and PML-RARA fusion gene was detected. On the basis of these findings, the patient was diagnosed with hypoplastic acute promyelocytic leukemia. She received ATRA treatment and achieved complete remission (CR) 29 days from the commencement of therapy. After the first CR, she received two courses of ATO as a consolidation therapy. Following the latter treatments, she maintained CR, but a hypoplastic bone marrow was still observed. Hypoplastic AML is defined as AML with a low bone marrow cellularity. It is clinically important to distinguish it from aplastic anemia and hypoplastic MDS. It has been suggested that both cytogenetic and morphological diagnosis are imperative to the differential diagnosis of hypocellular bone marrow.
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PMID:[Hypoplastic acute promyelocytic leukemia with continuous hypocellular bone marrow after remission]. 2974 1

Although molecular targeted therapies have recently displayed therapeutic effects in acute myeloid leukemia (AML), limited response and acquired resistance remain common problems. Numerous studies have associated autophagy, an essential degradation process involved in the cellular response to stress, with the development and therapeutic response of cancers including AML. Thus, we review studies on the role of autophagy in AML development and summarize the linkage between autophagy and several recurrent genetic abnormalities in AML, highlighting the potential of capitalizing on autophagy modulation in targeted therapy for AML. Abbreviations: AML: acute myeloid leukemia; AMPK: AMP-activated protein kinase; APL: acute promyelocytic leukemia; ATG: autophagy related; ATM: ATM serine/threonine kinase; ATO: arsenic trioxide; ATRA: all trans retinoic acid; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; BET proteins, bromodomain and extra-terminal domain family; CMA: chaperone-mediated autophagy; CQ: chloroquine; DNMT, DNA methyltransferase; DOT1L: DOT1 like histone lysine methyltransferase; FLT3: fms related receptor tyrosine kinase 3; FIS1: fission, mitochondrial 1; HCQ: hydroxychloroquine; HSC: hematopoietic stem cell; IDH: isocitrate dehydrogenase; ITD: internal tandem duplication; KMT2A/MLL: lysine methyltransferase 2A; LSC: leukemia stem cell; MDS: myelodysplastic syndromes; MTORC1: mechanistic target of rapamycin kinase complex 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; NPM1: nucleophosmin 1; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PML: PML nuclear body scaffold; ROS: reactive oxygen species; RB1CC1/FIP200: RB1 inducible coiled-coil 1; SAHA: vorinostat; SQSTM1: sequestosome 1; TET2: tet methylcytosine dioxygenase 2; TKD: tyrosine kinase domain; TKI: tyrosine kinase inhibitor; TP53/p53: tumor protein p53; ULK1: unc-51 like autophagy activating kinase 1; VPA: valproic acid; WDFY3/ALFY: WD repeat and FYVE domain containing 3.
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PMID:The role of autophagy in targeted therapy for acute myeloid leukemia. 3291 24