[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 62 of about 62
1. Niitsu N, Yamamoto-Yamaguchi Y, Kasukabe T, Okabe-Kado J, Umeda M, Honma Y: Antileukemic efficacy of 2-deoxycoformycin in monocytic leukemia cells. Blood; 2000 Aug 15;96(4):1512-6
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antileukemic efficacy of 2-deoxycoformycin in monocytic leukemia cells.
  • However, previous studies have shown that in the presence of 2'-deoxyadenosine (dAd), human monocytoid leukemia cell lines are much more sensitive to dCF with regard to the inhibition of cell proliferation.
  • Thus, dCF might be useful for treating monocytoid leukemia with the aid of dAd analogs.
  • The antiproliferative effects of dCF in combination with dAd or its derivatives were examined on normal and malignant blood and bone marrow cells.
  • In the presence of 10 micromol/L dAd, the concentration of dCF required to inhibit the viability of primary monocytoid leukemia cells was much lower than that required to inhibit normal or non-monocytoid leukemic cells.
  • Athymic nude mice were inoculated with human monocytoid leukemia U937 cells and treated with dCF or a dAd analog or both.
  • Although dCF alone slightly but significantly prolonged the survival of mice inoculated with U937 cells, combined treatment with dCF and AraA markedly prolonged their survival.
  • These data suggest that the combination of dCF and AraA may be useful for the clinical treatment of acute monocytic leukemia. (Blood.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Leukemia, Monocytic, Acute / drug therapy. Pentostatin / pharmacology
  • [MeSH-minor] Animals. Antimetabolites / pharmacology. Antimetabolites / therapeutic use. Cell Survival / drug effects. Humans. Mice. Mice, Nude. U937 Cells. Vidarabine / pharmacology. Vidarabine / therapeutic use

  • Hazardous Substances Data Bank. PENTOSTATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10942399.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites; 395575MZO7 / Pentostatin; FA2DM6879K / Vidarabine
  •  go-up   go-down


2. Ikarashi Y, Kakihara T, Imai C, Tanaka A, Watanabe A, Uchiyama M: Double leukemias simultaneously showing lymphoblastic leukemia of the bone marrow and monocytic leukemia of the central nervous system. Am J Hematol; 2004 Mar;75(3):164-7
MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Double leukemias simultaneously showing lymphoblastic leukemia of the bone marrow and monocytic leukemia of the central nervous system.
  • A 4-year-old girl was diagnosed with acute lymphoblastic leukemia and achieved a complete remission with chemotherapy.
  • Two years after diagnosis, she was found to have acute monocytic leukemia at first relapse in the BM.
  • One month after the second course of induction therapy, lymphoblastic leukemia in the BM and monocytic leukemia in the CNS were found simultaneously.
  • Chromosomal analysis of leukemia cells in the BM and CNS showed distinct results.
  • The mechanism of double leukemias occurring was obscure, although a lineage switch, therapy-related, or de novo leukemia could be considered as possibilities.
  • [MeSH-major] Bone Marrow Neoplasms / pathology. Central Nervous System Neoplasms / pathology. Leukemia, Lymphoid / pathology. Leukemia, Monocytic, Acute / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 14978698.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


3. Demirer S, Ozdemir H, Sencan M, Marakoglu I: Gingival hyperplasia as an early diagnostic oral manifestation in acute monocytic leukemia: a case report. Eur J Dent; 2007 Apr;1(2):111-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gingival hyperplasia as an early diagnostic oral manifestation in acute monocytic leukemia: a case report.
  • Acute Myeloblastic Leukemia (AML) is a malignant disease of bone marrow.
  • Due to its high morbidity rate, early diagnosis and appropriate medical therapy is essential.
  • This case report describes a 17-year-old female who presented rapid gingival overgrowth together with gingival bleeding in only two weeks time.
  • A medical consultation was asked from hematology clinics and after a detailed medical examination Acute Monocytic Leukemia (FAB M5) was rendered.
  • Chemotherapy was the choice of treatment.
  • The patient responded well to chemotherapeutic induction regimen and after two months of medical therapy disease remised and gingival hyperplasia regressed.
  • Also, early medical therapy in acute monocytic leukemia may resolve the gingival hyperplasia that companies the disease progression.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Aust Dent J. 1996 Aug;41(4):235-7 [8870276.001]
  • [Cites] J Nihon Univ Sch Dent. 1997 Jun;39(2):67-70 [9293702.001]
  • [Cites] J Am Dent Assoc. 1988 Dec;117(7):835-7 [3204244.001]
  • [Cites] J Periodontol. 1984 Oct;55(10):585-8 [6387081.001]
  • [Cites] J Am Dent Assoc. 1986 Dec;113(6):899-900 [3466936.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1986 May;61(5):466-70 [3459123.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1983 Jun;55(6):572-9 [6576290.001]
  • [Cites] Int J Oral Surg. 1978 Apr;7(2):119-22 [98458.001]
  • [Cites] J Periodontol. 2002 Jun;73(6):664-8 [12083541.001]
  • [Cites] J Periodontol. 2000 May;71(5 Suppl):876-9 [10875698.001]
  • [Cites] Ann Periodontol. 1999 Dec;4(1):54-64 [10863375.001]
  • [Cites] Mt Sinai J Med. 1998 Oct-Nov;65(5-6):309-15 [9844357.001]
  • [Cites] J Am Acad Dermatol. 2005 Mar;52(3 Pt 1):491-9 [15761428.001]
  • [Cites] J Can Dent Assoc. 2000 Feb;66(2):78-9 [10730004.001]
  • [Cites] J Periodontol. 1988 Dec;59(12):852-5 [3225733.001]
  • (PMID = 19212486.001).
  • [ISSN] 1305-7456
  • [Journal-full-title] European journal of dentistry
  • [ISO-abbreviation] Eur J Dent
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Other-IDs] NLM/ PMC2609944
  • [Keywords] NOTNLM ; Acute monocytic leukemia / Gingival hyperplasia
  •  go-up   go-down


Advertisement
4. Seo YI, Park R, Choi TY, Shin JW, Won JH, Park HS, Lee NS, Cho D: [A case of therapy-related acute monocytic leukemia following low-dose of etoposide treatment for hemophagocytic lymphohistiocytosis]. Korean J Lab Med; 2007 Aug;27(4):244-7
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of therapy-related acute monocytic leukemia following low-dose of etoposide treatment for hemophagocytic lymphohistiocytosis].
  • We report a case of therapy-related acute myeloid leukemia after low-dosed topoisomerase II inhibitor (etoposide) treatment for hemophagocytic lymphohistiocytosis (HLH).
  • Peripheral blood smear and bone marrow study revealed acute monocytic leukemia.
  • [MeSH-major] Etoposide / adverse effects. Leukemia, Monocytic, Acute / chemically induced. Leukemia, Monocytic, Acute / diagnosis. Lymphohistiocytosis, Hemophagocytic / drug therapy

  • Genetic Alliance. consumer health - Hemophagocytic Lymphohistiocytosis (HLH).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18094583.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide
  •  go-up   go-down


5. Ji YY, Zhang WG, Chen YX, Zhao XM, He AL, Liu J, Wang JL, Wang FX, Zhang PY, Zhang WJ: [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):213-8
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism].
  • The aim of this study was to explore the clinical efficiency and side effects of GHA-priming therapy on patients with acute monocytic leukemia, and to analyze its mechanism.
  • 37 patients with refractory, relapse, hypocellular acute monocytic leukemia and elderly patients with AML-M(5) were treated with GHA-priming therapy (G-CSF, homoharringtonine and low dosage of cytarabine).
  • Clinical efficiency, side effects, and therapy-relevant mortality were observed.
  • The expression of MLAA34 on U937 before or after treating with chemotherapy was analyzed by immunohistochemical method.
  • The incidence of granulocyte deficiency was 18.92% (2/37) with median time of 4 days.
  • It is concluded that the GHA priming therapy can be used to treat patients with refractory, relapse, senile and hypocellular acute monocytic leukemia with satisfied response rate and low hematological and non-hematological toxicities.
  • G-CSF can enhance cytotoxicity of drugs such as Ara-C and HHT by promoting G(0) phase cells into the reproductive cycle.
  • GHA and HA therapy can inhibit cell proliferation, induce apoptosis, and the former has a more significant function.
  • GHA priming therapy can down regulate the expression of MLAA 34.
  • MLAA-34 is a novel anti-apoptotic factor of acute monocytic leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20137150.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6FG8041S5B / homoharringtonine
  •  go-up   go-down


6. Sano K, Hayakawa A, Piao JH, Kosaka Y, Nakamura H: Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23). Blood; 2000 Feb 1;95(3):1066-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23).
  • The mixed lineage leukemia (MLL) gene located at chromosome band 11q23 is frequently rearranged in patients with therapy-related acute monocytic leukemia who received topoisomerase II inhibitors.
  • We have identified a novel fusion partner of MLL (FAB M5b) in a patient who developed t-AML 9 years after treatment for acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Adaptor Proteins, Signal Transducing. Leukemia, Monocytic, Acute / genetics. Muscle Proteins. Neoplasms, Second Primary / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. src Homology Domains / genetics
  • [MeSH-minor] Adolescent. Amino Acid Sequence. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Base Sequence. Bone Marrow Transplantation. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. DNA, Complementary / genetics. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein. Nitrosourea Compounds / administration & dosage. Nitrosourea Compounds / adverse effects. Sequence Alignment. Sequence Homology, Nucleic Acid

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. HGNC: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10648423.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / AF3p21-MLL fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / DNA, Complementary; 0 / Muscle Proteins; 0 / NCKIPSD protein, human; 0 / Nitrosourea Compounds; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; RYH2T97J77 / ranimustine; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


7. Al-Tawfiq JA, Al-Khatti AA: Spontaneous remission of acute monocytic leukemia after infection with Clostridium septicum. Int J Lab Hematol; 2007 Oct;29(5):386-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous remission of acute monocytic leukemia after infection with Clostridium septicum.
  • Spontaneous remissions of acute myeloid leukemia (AML) have been reported in association with infection.
  • He was diagnosed with acute monocytic leukemia (AML, FAB M5b) and a perforated bowel.
  • He also had Clostridium septicum bacteremia and thus chemotherapy was deferred.
  • He received supportive therapy and intravenous antibiotics.
  • [MeSH-major] Clostridium Infections / complications. Clostridium septicum / pathogenicity. Intestinal Perforation / complications. Leukemia, Monocytic, Acute / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17824921.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


8. Sakamoto H, Mashima T, Kizaki A, Dan S, Hashimoto Y, Naito M, Tsuruo T: Glyoxalase I is involved in resistance of human leukemia cells to antitumor agent-induced apoptosis. Blood; 2000 May 15;95(10):3214-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glyoxalase I is involved in resistance of human leukemia cells to antitumor agent-induced apoptosis.
  • Abnormality in the machinery of apoptosis is associated with a resistant phenotype of the tumor cell to chemotherapy.
  • To determine the molecular basis of resistance to antitumor agent-induced apoptosis, we performed a complementary DNA (cDNA) subtractive hybridization with messenger RNA (mRNA) from human monocytic leukemia U937 and its variant UK711, which is resistant to apoptosis induced by antitumor agents.
  • The GLO1 enzyme activity was significantly elevated in UK711 and UK110 cells, another drug-resistant mutant, as well as in K562/ADM, adriamycin-resistant leukemia cells, compared with their parental cells.
  • When overexpressed in human Jurkat cells, GLO1 inhibited etoposide- and adriamycin-induced caspase activation and apoptosis, indicating the involvement of GLO1 in apoptosis suppression caused by these drugs.
  • Moreover, cotreatment with S-p-bromobenzylglutathione cyclopentyl diester (BBGC), a cell-permeable inhibitor of GLO1, enhanced etoposide-induced apoptosis in resistant UK711 cells but not in parental U937 cells.
  • Taken together, these results indicate that GLO1 is a resistant factor to antitumor agent-induced apoptosis in human leukemia cells and that the GLO1 inhibitor could be a drug resistance-reversing agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / genetics. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Lactoylglutathione Lyase / genetics. Leukemia / drug therapy. Leukemia / pathology


9. Tamayose K, Sugimoto K, Ando M, Oshimi K: Mononucleosis syndrome and acute monocytic leukemia. Eur J Haematol; 2002 Apr;68(4):236-8
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mononucleosis syndrome and acute monocytic leukemia.
  • The association of infectious mononucleosis and an immunocompromised host such as occurs in acute leukemia is reported.
  • We report a case of acute monocytic leukemia (AMoL) who developed varicella zoster virus (VZV) mononucleosis syndrome in the bone marrow recovery phase after myelosuppression due to high-dose cytarabine.
  • [MeSH-major] Cytarabine / adverse effects. Herpes Zoster / etiology. Herpesvirus 3, Human. Immunosuppressive Agents / adverse effects. Infectious Mononucleosis / etiology. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy

  • MedlinePlus Health Information. consumer health - Infectious Mononucleosis.
  • MedlinePlus Health Information. consumer health - Shingles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12071940.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine
  •  go-up   go-down


10. Kajiwara R, Goto H, Yanagimachi M, Kuroki F, Fujii H, Takahashi H, Yokota S: [Recurrent spontaneous regression of aleukemic leukemia cutis in a girl with acute monocytic leukemia]. Rinsho Ketsueki; 2006 Aug;47(8):764-9
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Recurrent spontaneous regression of aleukemic leukemia cutis in a girl with acute monocytic leukemia].
  • Aleukemic leukemia cutis is a rare form of leukemia manifestation, defined as a skin infiltration of leukemic cells with no evidence of leukemia in the bone marrow.
  • However, the diagnosis could not be made at that time.
  • At 9 and at 13 months old, appearances of exanthema similar to the previous time were combined with systemic fever, abnormal coagulation tests, and the marked increases of atypical lymphocytes in peripheral blood: however, these symptoms resolved spontaneously.
  • Bone marrow aspiration revealed the predominance of monocytic blasts (76.4%), and the patient was diagnosed as having acute monocytic leukemia (M5b) with leukemia cutis.
  • Complete remission was obtained with standard chemotherapy.
  • Six months after the therapy was completed, an extramedullary relapse occurred in the inguinal lymph nodes, which was successfully treated with allogeneic bone marrow transplantation from an HLA-matched unrelated donor, and the patient has been free of disease for two years after the transplantation.
  • [MeSH-major] Leukemia / diagnosis. Leukemia / etiology. Leukemia, Monocytic, Acute / complications. Neoplasm Regression, Spontaneous

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16986716.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


11. Tasaka T, Matsuhashi Y, Uehara E, Tamura T, Kakazu N, Abe T, Nagai M: Secondary acute monocytic leukemia with a translocation t(8;16)(p11;p13): case report and review of the literature. Leuk Lymphoma; 2004 Mar;45(3):621-5
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute monocytic leukemia with a translocation t(8;16)(p11;p13): case report and review of the literature.
  • Acute myeloblastic leukemia cases carrying the translocation t(8;16) (p11;p13) are characterized by the M4 and M5 subtypes, erythrophagocytosis by the blast cells and a poor prognosis, suggesting a new clinical entity.
  • She was diagnosed as having breast cancer and acute monocytic leukemia (M5b).
  • Eleven cases of therapy-related t(8;16) leukemia including the present case have been reported, but prior treatment with paclitaxel and carboplatin-based chemotherapy has never been reported.
  • The relation of histone acetylase and therapy-related leukemia is discussed.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 8. Leukemia, Monocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carboplatin / adverse effects. Cell Transformation, Neoplastic / genetics. Female. Humans. Ovarian Neoplasms / complications. Ovarian Neoplasms / drug therapy. Paclitaxel / adverse effects

  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for acute monocytic leukemia .
  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for monocytic leukemia .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15160929.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
  • [Number-of-references] 26
  •  go-up   go-down


12. Luca DC, Almanaseer IY: Simultaneous presentation of multiple myeloma and acute monocytic leukemia. Arch Pathol Lab Med; 2003 Nov;127(11):1506-8
MedlinePlus Health Information. consumer health - Multiple Myeloma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Simultaneous presentation of multiple myeloma and acute monocytic leukemia.
  • Acute leukemia frequently has been described as a late complication of chemotherapy with alkylating agents in patients treated for multiple myeloma.
  • However, the simultaneous occurrence of multiple myeloma and acute leukemia in the same patient, without previous exposure to chemotherapy, is a rare association.
  • We describe a case of concomitant involvement by multiple myeloma and acute monocytic leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / diagnosis. Multiple Myeloma / diagnosis

  • Genetic Alliance. consumer health - Multiple myeloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14567751.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


13. Hagihara M, Shimakura Y, Tsuchiya T, Ueda Y, Gansuvd B, Munkhbat B, Chargui J, Ando K, Kato S, Hotta T: The efficient generation of CD83 positive immunocompetent dendritic cells from CD14 positive acute myelomonocytic or monocytic leukemia cells in vitro. Leuk Res; 2001 Mar;25(3):249-58
Genetic Alliance. consumer health - Acute Myelomonocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The efficient generation of CD83 positive immunocompetent dendritic cells from CD14 positive acute myelomonocytic or monocytic leukemia cells in vitro.
  • The ability of leukemic cells to differentiate to mature dendritic cells (DCs) was investigated in six acute myelomonocytic or monocytic leukemia cases.
  • Such leukemia derived DCs expressed a sufficient level of costimulatory molecules (CD80 and CD86), and were shown to be monoclonal based on an the X-inactivation analysis.
  • [MeSH-major] Antigens, CD14 / immunology. Cell Differentiation. Dendritic Cells / cytology. Dendritic Cells / immunology. Immunocompetence. Immunoglobulins / biosynthesis. Leukemia, Myeloid / pathology. Membrane Glycoproteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD. Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. Cytokines / pharmacology. Female. Humans. K562 Cells / metabolism. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / immunology. Leukemia, Monocytic, Acute / pathology. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / immunology. Leukemia, Myelomonocytic, Acute / pathology. Lymphocyte Culture Test, Mixed. Male. Middle Aged. T-Lymphocytes, Cytotoxic / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11226522.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / CD83 antigen; 0 / Cytokines; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
  •  go-up   go-down


14. Ashida T, Kawanishi K, Ariyama T, Hamasaki H, Maeda Y, Tsubaki K, Kanamaru A: Successful graft-versus-leukemia effect of second bone marrow transplantation on relapsed leukemia cutis that was refractory to intensive chemotherapy and donor lymphocyte transfusions in a patient with acute monocytic leukemia. Int J Hematol; 2000 Jun;71(4):385-8
MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful graft-versus-leukemia effect of second bone marrow transplantation on relapsed leukemia cutis that was refractory to intensive chemotherapy and donor lymphocyte transfusions in a patient with acute monocytic leukemia.
  • We report a patient with acute monocytic leukemia (AMoL;.
  • M5) who received a second bone marrow transplantation (BMT) with graft-versus-leukemia (GVL) effect on relapsed leukemia cutis, which had been refractory to intensive chemotherapy and donor lymphocyte transfusions (DLTs).
  • A 21-year-old woman was diagnosed with AMoL and achieved complete remission after intensive chemotherapy.
  • Skin tumors developed in her upper extremities, chest, and thigh 11 months after BMT.
  • Leukemia cutis was confirmed by skin biopsy.
  • The patient received several courses of chemotherapy and DLTs for the skin relapse, but the skin tumors persisted.
  • On day 80, grade II acute graft-versus-host disease developed, and the remaining skin tumors were eradicated on day 98, most probably because of GVL effect.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Leukemia, Monocytic, Acute / therapy. Leukemic Infiltration / therapy. Skin / pathology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Graft vs Host Disease. Humans. Lymphocyte Transfusion

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10905060.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


15. Azoulay E, Fieux F, Moreau D, Thiery G, Rousselot P, Parrot A, Le Gall JR, Dombret H, Schlemmer B: Acute monocytic leukemia presenting as acute respiratory failure. Am J Respir Crit Care Med; 2003 May 15;167(10):1329-33
MedlinePlus Health Information. consumer health - Respiratory Failure.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute monocytic leukemia presenting as acute respiratory failure.
  • Acute respiratory failure revealing acute monocytic leukemia is rare.
  • (1) rapidly progressive respiratory distress revealing acute leukemia, (2) monocytic leukemia, and (3) respiratory status deterioration after chemotherapy initiation.
  • The median leukocyte count was 98,250/mm3 (800-529,000), with circulating monocytic cells in all of the patients but one.
  • Bone marrow examination was diagnostic of monocytic leukemia in all patients.
  • Alveolar hemorrhage was the main bronchoalveolar lavage finding, with monocytic cells retrieved from four patients.
  • Respiratory function deteriorated after cancer chemotherapy initiation in all patients.
  • Leukemic pulmonary infiltration as the first manifestation of acute monocytic leukemia should be recognized, and intensive management should be provided in anticipation of the respiratory function deterioration seen consistently after chemotherapy initiation.
  • [MeSH-major] Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / therapy. Respiratory Insufficiency / diagnosis. Respiratory Insufficiency / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols. Cohort Studies. Combined Modality Therapy. Critical Illness. Diagnosis, Differential. Female. Humans. Intensive Care Units. Male. Middle Aged. Respiration, Artificial / methods. Retrospective Studies. Risk Assessment. Severity of Illness Index. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12574074.001).
  • [ISSN] 1073-449X
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Villeneuve P, Kim DT, Xu W, Brandwein J, Chang H: The morphological subcategories of acute monocytic leukemia (M5a and M5b) share similar immunophenotypic and cytogenetic features and clinical outcomes. Leuk Res; 2008 Feb;32(2):269-73
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The morphological subcategories of acute monocytic leukemia (M5a and M5b) share similar immunophenotypic and cytogenetic features and clinical outcomes.
  • Acute monocytic leukemia (M5) is a subtype of acute myeloid leukemia (AML) with two distinct morphologic subcategories, M5a and M5b.
  • We compared the immunophenotype, cytogenetics and clinical outcome of AML M5 with non-M5 AML and also compared M5a with M5b.
  • One hundred and twelve M5 (76 M5a, 36 M5b) and 726 non-M5 cases were identified and treated on protocols at our institution.
  • There were no significant differences in immunophenotype between M5a and M5b.
  • Translocation 11q23 was the sole abnormality in 18.6% of M5 and 3.2% of non-M5 (p<0.001).
  • Trisomy 8 was also more prevalent in M5 (16.9%) than in non-M5 (8.7%; p=0.03).
  • There was no significant difference in karyotypes between M5a and M5b.
  • The complete remission rate was 70% for AML M5 and 57% for non-M5 AML (p=0.03).
  • There was no significant difference in median overall survival or disease free survival for patients with M5 versus non-M5, M5a versus M5b.
  • Our data indicate that the prognosis of AML M5 is similar to non-M5 AML and that M5a and M5b do not differ in immunophenotype, cytogenetics or clinical outcome.
  • [MeSH-major] Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Cytogenetic Analysis. Disease-Free Survival. Female. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged. Prognosis. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17689610.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


17. Martínez-Poventud G, Fradera J, Pérez S, Fernández A, Pacheco E, Acabá L, López-Enriquez A, Román-Díaz A, Castro-Montalvo J, Vélez-García E: Aleukemic leukemia cutis preceding acute monocytic leukemia: a case report. P R Health Sci J; 2008 Sep;27(3):256-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aleukemic leukemia cutis preceding acute monocytic leukemia: a case report.
  • Aleukemic leukemia cutis is an extremely rare clinical presentation in patients who eventually develop acute leukemia, usually of monocytic lineage.
  • We report a case of a 33 years old female with leukemia cutis preceding the onset of acute monocytic leukemia by four months.
  • The patient received induction and consolidation chemotherapy followed by allogeneic bone marrow transplant and has been free of disease for six years.
  • To our knowledge, this is the first documented case in Puerto Rico with the diagnosis of leukemia cutis preceding acute monocytic leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / pathology. Leukemic Infiltration. Skin / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18782972.001).
  • [ISSN] 0738-0658
  • [Journal-full-title] Puerto Rico health sciences journal
  • [ISO-abbreviation] P R Health Sci J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Puerto Rico
  •  go-up   go-down


18. Hasegawa Y, Bai A, Kojima H, Komeno T, Ninomiya H, Nagasawa T: Priming effects of macrophage colony-stimulating factor on monocytic leukemia cells in combination with chemotherapy: induction of programmed cell death in vivo. Leuk Lymphoma; 2000 Feb;36(5-6):589-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Priming effects of macrophage colony-stimulating factor on monocytic leukemia cells in combination with chemotherapy: induction of programmed cell death in vivo.
  • Two elderly patients with chronic myelomonocytic leukemia were treated with cytosine arabinoside (Ara-C) and aclarubicin (ACR) under simultaneous administrations of macrophage colony-stimulating factor (M-CSF) (CAM), and both obtained good responses.
  • Examination of apoptosis using flow cytometry revealed induction of apoptotic death of leukemia cells by CAM in Patient 2, while neither induction of apoptotic death of leukemia cells nor clinical response were seen with CAG (Ara-C, ACR, and granulocyte colony-stimulating factor) given prior to CAM in Patient 1.
  • These findings suggested that chemotherapy combined with simultaneous administration of M-CSF could effectively reduce monocytic leukemia cells by inducing programmed cell death.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Apoptosis / drug effects. Leukemia, Myelomonocytic, Chronic / drug therapy. Leukemia, Myelomonocytic, Chronic / pathology. Macrophage Colony-Stimulating Factor / administration & dosage

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10784404.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 81627-83-0 / Macrophage Colony-Stimulating Factor
  •  go-up   go-down


19. Honma Y, Niitsu N: Vidarabine and 2-deoxycoformycin as antileukemic agents against monocytic leukemia. Leuk Lymphoma; 2000 Sep;39(1-2):57-66
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vidarabine and 2-deoxycoformycin as antileukemic agents against monocytic leukemia.
  • Although 2'-deoxycoformycin (dCF) has been reported in clinical trials to be less effective against myeloid than lymphoid malignancies, it may be useful for treating monocytic leukemia with the aid of 2'-deoxyadenosine (dAd) analogs.
  • In the presence of 10 microM dAd, the concentration of dCF required to inhibit the viability of monocytoid leukemia cells was much lower than that required on normal or non-monocytoid malignant cells in primary culture.
  • Although dCF alone slightly but significantly prolonged the survival of mice inoculated with U937 monocytic leukemia cells, combined treatment with dCF and AraA markedly prolonged the survival.
  • These results suggest that the combination of dCF and AraA may be useful for the clinical treatment of acute monocytic leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / drug therapy. Pentostatin / therapeutic use. Vidarabine / therapeutic use
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Dose-Response Relationship, Drug. Humans

  • Hazardous Substances Data Bank. PENTOSTATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10975384.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites; 395575MZO7 / Pentostatin; FA2DM6879K / Vidarabine
  • [Number-of-references] 47
  •  go-up   go-down


20. Wang YF, Song QS, Zhang YM, Ma DL, Wang Y, Ke XY: [Sensitizing effect of recombinant human PDCD5 protein on chemotherapy of acute monocytic leukemia cell line U937 and its mechanism]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Apr;18(2):277-81

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Sensitizing effect of recombinant human PDCD5 protein on chemotherapy of acute monocytic leukemia cell line U937 and its mechanism].
  • This study was aimed to investigate the sensitizing effect of recombinant human PDCD5 (rhPDCD5) protein on chemotherapy of U937 cell line and its mechanism.
  • RT-PCR was performed to observe the expression level of drug-resistant genes.
  • The results showed that the percentage of apoptotic cells and the activity of caspase-3 remarkably increased in U937 cells treated with rhPDCD5 combined with chemotherapeutic drug; the cell cycle arrest induced by anti-tumor drug was also enhanced when combined with rhPDCD5; meanwhile, the expression levels of drug-resistant genes were down-regulated in jointly treated U937 cells.
  • It is concluded that the chemosensitizing mechanisms of rhPDCD5 are complex. rhPDCD5 may increase the cytotoxicity of anti-tumor drugs by promoting the caspase-3-related apoptosis, influencing cell cycle, decreasing the expression of drug-resistant genes and reversing drug-resistance.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20416151.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / Recombinant Proteins; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


21. Ramos MG, Rabelo FL, Brumatti G, Bueno-da-Silva AE, Amarante-Mendes GP, Alvarez-Leite JI: Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells. Chemotherapy; 2004 Nov;50(5):221-8
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells.
  • Cancer including leukemia is usually treated with chemotherapeutic drugs that can be effective, but frequently problems are encountered that impair the success of the treatment.
  • METHODS: The effect of a combination treatment with butyrate and antineoplastic agents Ara-C, etoposide and vincristine is evaluate on the leukemic cell line THP-1.
  • We also demonstrate that the process of apoptosis induced by butyrate and chemotherapeutic drugs involves the participation of caspases and induced activation of caspase-3, -8 and -9.
  • CONCLUSIONS: We believe that butyrate could be a promising therapeutic agent for the treatment of leukemia in combination with other antineoplastic drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Butyrates / pharmacology. Drug Synergism. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / pathology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Amino Acid Chloromethyl Ketones / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Caspase Inhibitors. Caspases / metabolism. Caspases / therapeutic use. Cell Line, Tumor. Cytarabine / pharmacology. Cytarabine / therapeutic use. DNA Replication / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor / methods. Drug Therapy, Combination. Etoposide / pharmacology. Etoposide / therapeutic use. Humans. Vincristine / pharmacology. Vincristine / therapeutic use

  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15528887.001).
  • [ISSN] 0009-3157
  • [Journal-full-title] Chemotherapy
  • [ISO-abbreviation] Chemotherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents; 0 / Butyrates; 0 / Caspase Inhibitors; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspases
  •  go-up   go-down


22. Morerio C, Rosanda C, Rapella A, Micalizzi C, Panarello C: Is t(10;11)(p11.2;q23) involving MLL and ABI-1 genes associated with congenital acute monocytic leukemia? Cancer Genet Cytogenet; 2002 Nov;139(1):57-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is t(10;11)(p11.2;q23) involving MLL and ABI-1 genes associated with congenital acute monocytic leukemia?
  • Myelocytic types are common, and chromosome band 11q23 rearrangements at the MLL locus are characteristic genetic markers.
  • The fusion of the MLL gene with one of its partners, ABI-1, has recently been described in two infant leukemia patients with monocytic involvement and good clinical outcome.
  • We report a case of congenital monocytic leukemia with the same gene involvement and good response to chemotherapy.
  • [MeSH-major] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cytoskeletal Proteins. DNA-Binding Proteins / genetics. Homeodomain Proteins / genetics. Leukemia, Monocytic, Acute / congenital. Leukemia, Monocytic, Acute / genetics. Proto-Oncogenes. Transcription Factors. Translocation, Genetic
  • [MeSH-minor] Apgar Score. Chromosome Mapping. Female. Histone-Lysine N-Methyltransferase. Humans. Infant, Newborn. Karyotyping. Myeloid-Lymphoid Leukemia Protein

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12547160.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


23. Zhang GS, Peng HL, Dai CW, Gong FJ, Xu YX, Xiao L, Pei MF, Shen JK, Yang JJ: [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof]. Zhonghua Yi Xue Za Zhi; 2005 Dec 28;85(49):3504-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof].
  • OBJECTIVE: To study the clinical features and molecular genetics of acute monocytic leukemia (AML) after orthotopic liver transplantation and significance thereof.
  • METHODS: The clinical manifestations, laboratory findings, development, diagnosis, treatment, and prognosis of the first case of AML after orthotopic liver transplantation in the world, a Chinese, male, aged 46, were observed.
  • The diagnosis of chronic myelomonocytic leukemia was made.
  • Five months after the liver transplantation the disease developed to AML.
  • The patient underwent combined chemotherapy (HA or DA regimens) for 5 courses and showed a partial remission both hematologically and in bone marrow examination at first, however, became resistant to all chemotherapeutic agents.
  • RT-PCR showed absence of wild type FLT3 allele.
  • At last the patient died of infection. (2) A FLT3-ITD mutation of "insertion" type was identified in the BMMCs.
  • CONCLUSION: Orthotopic liver transplantation may be complicated with acute leukemia heterogeneous in clinical features and hematology.
  • [MeSH-major] Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Liver Transplantation / adverse effects. Postoperative Complications

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16686070.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
  •  go-up   go-down


24. Hijiya N, Metzger ML, Pounds S, Schmidt JE, Razzouk BI, Rubnitz JE, Howard SC, Nunez CA, Pui CH, Ribeiro RC: Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):63-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia.
  • BACKGROUND: Life-threatening pulmonary complications that coincide with cell lysis during early chemotherapy and that mimic systemic inflammatory response syndrome (SIRS) have been reported in patients with acute myeloid leukemia (AML).
  • RESULTS: Of 155 patients, 5 (3 with M4eo and 2 with M5) experienced severe pulmonary complications attributed to tumor lysis, met the criteria for severe SIRS, and showed no clear evidence of infection.
  • Severe SIRS was significantly more common in myelomonocytic or monocytic AML (M4/M4eo/M5) than in other subtypes (P = 0.010) and significantly more common in M4eo than in M4/M5 (P = 0.008).
  • Among 112 cases for which information was available, leukocyte reduction was significantly greater in patients with M4/M4eo/M5 than among others during the first 4 days of chemotherapy (P = 0.015).
  • CONCLUSIONS: Patients with M4/M4eo/M5 AML, especially M4eo, experience life-threatening cardiopulmonary complications of tumor lysis that meet the criteria for severe SIRS.
  • [MeSH-major] Cell Death. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / drug therapy. Systemic Inflammatory Response Syndrome / etiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Humans. Male. Retrospective Studies. Risk Factors

  • Genetic Alliance. consumer health - Acute Myelomonocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368547.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


25. Honma Y: A novel therapeutic strategy against monocytic leukemia with deoxyadenosine analogs and adenosine deaminase inhibitors. Leuk Lymphoma; 2001 Sep-Oct;42(5):953-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel therapeutic strategy against monocytic leukemia with deoxyadenosine analogs and adenosine deaminase inhibitors.
  • The adenosine deaminase inhibitor 2'-deoxycoformycin (dCF) significantly inhibits the proliferation of leukemia and lymphoma cells in the presence of either 2'-deoxyadenosine (dAdo) or its analog adenine arabinoside (araA).
  • The concentration of dCF required to induce apoptosis of monocytoid leukemia cells is much lower than that required for myeloid, erythroid, or lymphoma cells. dATP effectively induces caspase-3 activation in cytosol from monocytoid cells, but not in that from non-monocytoid cells, suggesting that dATP-dependent caspase-3 activation is involved in the preferential induction of apoptosis in monocytoid leukemia cells.
  • Athymic nude mice inoculated with human monocytoid leukemia U937 cells show significantly prolonged survival following combined treatment with dCF and araA.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Adenosine Deaminase Inhibitors. Animals. Apoptosis / drug effects. Cell Differentiation / drug effects. Deoxyadenosines / therapeutic use. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11697650.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors
  • [Number-of-references] 75
  •  go-up   go-down


26. Chantrain CF, Sauvage D, Brichard B, Dupont S, Poirel HA, Ameye G, De Weer A, Vandenberghe P, Detaille T, Anslot C, de Cléty SC, Vermylen C: Neonatal acute myeloid leukemia in an infant whose mother was exposed to diethylstilboestrol in utero. Pediatr Blood Cancer; 2009 Aug;53(2):220-2
Hazardous Substances Data Bank. DIETHYLSTILBESTROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neonatal acute myeloid leukemia in an infant whose mother was exposed to diethylstilboestrol in utero.
  • We report on an acute myeloid leukemia in a neonate whose mother was exposed to diethylstilboestrol in utero.
  • The newborn presented with leukemia cutis, hemorrhagic skin lesions, hyperleucocytosis and disseminated intravascular coagulation.
  • A bone marrow examination confirmed the diagnosis of acute monocytic leukemia with a t(11;19) MLL-ELL fusion transcript.
  • Chemotherapy was initiated but the child developed a bilateral pulmonary infection that led to fatal respiratory distress.
  • This case shows acute myeloid leukemia and the third pediatric leukemia reported after maternal diethylstilboestrol exposure.
  • [MeSH-major] Diethylstilbestrol / adverse effects. Estrogens, Non-Steroidal / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Prenatal Exposure Delayed Effects / chemically induced
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. In Situ Hybridization, Fluorescence. Infant, Newborn. Infertility, Female / chemically induced. Male. Mothers. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion. Pedigree. Pregnancy. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19405140.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogens, Non-Steroidal; 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 731DCA35BT / Diethylstilbestrol
  •  go-up   go-down


27. Meng A, Luberto C, Meier P, Bai A, Yang X, Hannun YA, Zhou D: Sphingomyelin synthase as a potential target for D609-induced apoptosis in U937 human monocytic leukemia cells. Exp Cell Res; 2004 Jan 15;292(2):385-92
Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sphingomyelin synthase as a potential target for D609-induced apoptosis in U937 human monocytic leukemia cells.
  • Using U937 human monocytic leukemia cells, we examined the ability of D609 to inhibit sphingomyelin synthase (SMS), since inhibition of SMS may contribute to D609-induced tumor cell cytotoxicity via modulating the cellular levels of ceramide and diacylglycerol (DAG).
  • The results showed that D609 is capable of inducing U937 cell death by apoptosis in a dose- and time-dependent manner.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Bridged Compounds / pharmacology. Leukemia, Monocytic, Acute / drug therapy. Thiones / pharmacology. Transferases (Other Substituted Phosphate Groups) / antagonists & inhibitors
  • [MeSH-minor] Ceramides / metabolism. Ceramides / pharmacology. Cytotoxins / pharmacology. Diglycerides / metabolism. Diglycerides / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Down-Regulation / physiology. Enzyme Inhibitors / pharmacology. Humans. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / metabolism. Reaction Time / drug effects. Reaction Time / physiology. Tetradecanoylphorbol Acetate / pharmacology. U937 Cells. Up-Regulation / drug effects. Up-Regulation / physiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14697345.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL43707
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bridged Compounds; 0 / Ceramides; 0 / Cytotoxins; 0 / Diglycerides; 0 / Enzyme Inhibitors; 0 / Thiones; 038753E78J / N-caproylsphingosine; 83373-60-8 / tricyclodecane-9-yl-xanthogenate; 86390-77-4 / 1-oleoyl-2-acetylglycerol; EC 2.7.11.13 / Protein Kinase C; EC 2.7.8.- / Transferases (Other Substituted Phosphate Groups); EC 2.7.8.- / phosphatidylcholine-ceramide phosphocholine transferase; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


28. Humeniuk-Polaczek R, Marcinkowska E: Impaired nuclear localization of vitamin D receptor in leukemia cells resistant to calcitriol-induced differentiation. J Steroid Biochem Mol Biol; 2004 Apr;88(4-5):361-6
Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired nuclear localization of vitamin D receptor in leukemia cells resistant to calcitriol-induced differentiation.
  • Calcitriol, the hormonal form of vitamin D(3), induces differentiation of monocytic leukemia cell lines in vitro, without inducing cytotoxicity of the cells.
  • Besides this broad in vitro activity, a clinical implementation of calcitriol, or its analogs, as agents for differentiation therapy has been unsuccessful until now.
  • A better understanding of cellular activities of calcitriol necessary for completion of cell differentiation program could help find better solutions for differentiation therapy of myeloid leukemias.
  • In this paper we describe work carried on subline of acute monocytic leukemia, THP-1 resistant to calcitriol induced differentiation.
  • [MeSH-major] Active Transport, Cell Nucleus. Calcitriol / pharmacology. Drug Resistance, Neoplasm. Leukemia / pathology. Receptors, Calcitriol / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line, Tumor. Humans. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / pathology. Monocytes / drug effects. Tetradecanoylphorbol Acetate / pharmacology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15145445.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; FXC9231JVH / Calcitriol; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


29. Takeyama H, Kajiguchi T, Miyata Y, Saito M: [In vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) in acute leukemia]. Gan To Kagaku Ryoho; 2000 Jun;27(6):873-8
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [In vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) in acute leukemia].
  • The in vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) were studied in 24 patients with acute leukemia.
  • Among cases of acute myelogenous leukemia, a positive response to M-CSF (stimulation index > or = 2.5) was seen in 27.3% of the cases, and a significantly higher response rate (81.8%) was seen following G-CSF treatment of leukemia cells in vitro.
  • In cases of acute monocytic leukemia, M-CSF showed a higher stimulating index than that observed for non-monocytic leukemia.
  • G-CSF was administered in 19 cases and M-CSF in 5 cases after chemotherapy, and none of the patients showed leukemia cell proliferation in vivo.
  • There was no correlation between in vitro test results and clinical response of leukemia cells to the CSFs administered.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid, Acute / pathology. Macrophage Colony-Stimulating Factor / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Division / drug effects. Cytarabine / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10897214.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 81627-83-0 / Macrophage Colony-Stimulating Factor; ZRP63D75JW / Idarubicin
  •  go-up   go-down


30. Kounami S, Yoshiyama M, Nakayama K, Hiramatsu C, Aoyagi N, Yoshikawa N: Severe hypercalcemia in a child with acute nonlymphocytic leukemia: the role of parathyroid hormone-related protein and proinflammatory cytokines. Acta Haematol; 2004;112(3):160-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Severe hypercalcemia in a child with acute nonlymphocytic leukemia: the role of parathyroid hormone-related protein and proinflammatory cytokines.
  • Among the hematological malignancies, hypercalcemia has often been reported in lymphoid malignancies such as multiple myeloma and adult T cell leukemia/lymphoma, but it has only rarely been described in acute nonlymphocytic leukemia.
  • We describe here a 14-month-old girl with acute monocytic leukemia complicated by severe hypercalcemia (4.6 mmol/l) at presentation.
  • The patient achieved complete remission with induction chemotherapy, and the levels of PTHrP and the cytokines became normalized.
  • [MeSH-major] Hypercalcemia / etiology. Interleukin-6 / blood. Leukemia, Myeloid, Acute / complications. Parathyroid Hormone-Related Protein / blood

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15345899.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Parathyroid Hormone-Related Protein; 0 / Tumor Necrosis Factor-alpha; 81627-83-0 / Macrophage Colony-Stimulating Factor
  • [Number-of-references] 28
  •  go-up   go-down


31. Athanasiadou A, Saloum R, Gaitatzi M, Anagnostopoulos A, Fassas A: Isolated pentasomy of chromosome 8 in erythroleukemia. Leuk Lymphoma; 2001 Nov-Dec;42(6):1409-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Only 2 such cases, one in acute monocytic leukemia and one in chronic myelomonocytic leukemia have been described in the literature to date.
  • The patient died three days after diagnosis without chemotherapy.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia, Erythroblastic, Acute / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11911427.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


32. Hu XR, He JS, Ye XJ, Zheng WY, Wu WJ, Lin MF: Candida tropicalis arthritis in a patient with acute leukemia. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Oct;16(5):1215-8
MedlinePlus Health Information. consumer health - Yeast Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Candida tropicalis arthritis in a patient with acute leukemia.
  • A case of Candida tropicalis arthritis of knee occurred in a patient with acute monocytic leukemia was reported during the recovery phase of post chemotherapy myelosuppression and agranulocytosis.
  • Itraconazole and amphotericin B were intravenously injected for therapy for 4 - 5 weeks based on the susceptibility test in vitro, which showed better efficacy.
  • But the arthritis relapsed at 4 - 6 weeks after the drug withdrawal.
  • The curative effect was found in patient after treatment with fluconazole injection and articular cavity douching with amphotericin B for 8 weeks.
  • The treatment emphasis showed be placed on the full dosage and full treatment course of antifungal agent.

  • Genetic Alliance. consumer health - Arthritis.
  • MedlinePlus Health Information. consumer health - Infectious Arthritis.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18928631.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antifungal Agents
  •  go-up   go-down


33. Laengle UW, Markstein R, Cazaubon C, Roman D: Antiglaucoma drug GLC756 and its effect on cellular cAMP and tumor necrosis factor alpha release in vitro of activated human monocytic leukemia cells. Jpn J Ophthalmol; 2009 Mar;53(2):159-63
Hazardous Substances Data Bank. BETAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiglaucoma drug GLC756 and its effect on cellular cAMP and tumor necrosis factor alpha release in vitro of activated human monocytic leukemia cells.
  • PURPOSE: GLC756, a putative antiglaucoma drug with dopamine D(2) agonist and D(1) antagonist properties, significantly decreases tumor necrosis factor alpha (TNF-alpha) levels in lipopolysaccharide (LPS)-induced rats.
  • The present study describes the effects of GLC756 on cellular adenosine 3', 5'-cyclic monophosphate (cAMP) in relation to TNF-alpha production on LPS-stimulated human acute monocytic leukemia cells.
  • METHODS: A human peripheral blood acute monocytic leukemia cell line (THP-1) was activated via LPS.
  • CONCLUSION: Intracellular signaling pathway leading to inhibition of the production of the proinflammatory cytokine TNF-alpha after GLC756 treatment might be mediated through the second messenger cAMP.
  • [MeSH-major] Antihypertensive Agents / pharmacology. Cyclic AMP / metabolism. Leukemia, Monocytic, Acute / drug therapy. Quinolines / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Betamethasone / pharmacology. Cell Line, Tumor / drug effects. Enzyme-Linked Immunosorbent Assay. Glucocorticoids / pharmacology. Humans. Lipopolysaccharides / pharmacology. Ophthalmic Solutions / pharmacology. Receptors, Dopamine D1 / antagonists & inhibitors. Receptors, Dopamine D2 / agonists

  • MedlinePlus Health Information. consumer health - Blood Pressure Medicines.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Front Biosci. 1997 Jan 01;2:d12-26 [9159205.001]
  • [Cites] Arthritis Res Ther. 2003;5(6):R317-28 [14680506.001]
  • [Cites] J Neuroimmunol. 2002 Nov;132(1-2):34-40 [12417431.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 1999;135:67-104 [9932481.001]
  • [Cites] Genome Biol. 2006;7(2):R11 [16507166.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2000 Oct;279(4):L615-7 [11000119.001]
  • [Cites] Eur J Ophthalmol. 2006 May-Jun;16(3):401-6 [16761241.001]
  • [Cites] Cell Immunol. 1989 May;120(2):291-300 [2541929.001]
  • [Cites] J Invest Dermatol. 2005 Oct;125(4):783-9 [16185279.001]
  • [Cites] J Immunol. 1995 Nov 15;155(10):4909-16 [7594495.001]
  • [Cites] Neuroreport. 2000 Nov 9;11(16):3565-8 [11095519.001]
  • [Cites] J Pharmacol Exp Ther. 1999 Oct;291(1):258-64 [10490912.001]
  • [Cites] J Immunol. 2002 Oct 1;169(7):3801-10 [12244175.001]
  • [Cites] Trends Pharmacol Sci. 1999 Feb;20(2):66-73 [10101967.001]
  • [Cites] J Neurochem. 2004 Apr;89(2):474-83 [15056290.001]
  • [Cites] Int Immunol. 2005 May;17 (5):599-606 [15802305.001]
  • [Cites] Infect Immun. 1989 Sep;57(9):2837-41 [2547721.001]
  • [Cites] J Ocul Pharmacol. 1992 Winter;8(4):285-94 [1484260.001]
  • [Cites] Crit Care Med. 1997 Nov;25(11):1855-61 [9366770.001]
  • [Cites] Gut. 1998 Apr;42(4):477-84 [9616307.001]
  • [Cites] Jpn J Ophthalmol. 1996;40(2):167-73 [8876383.001]
  • [Cites] Crit Rev Clin Lab Sci. 1999 Aug;36(4):275-328 [10486703.001]
  • [Cites] Eur J Immunol. 1996 Jul;26(7):1580-6 [8766564.001]
  • [Cites] Ophthalmology. 1989 Mar;96(3):327-35 [2710524.001]
  • [Cites] Clin Immunol Immunopathol. 1990 May;55(2):157-70 [2182227.001]
  • [Cites] Placenta. 2005 Sep-Oct;26(8-9):654-60 [16085044.001]
  • [Cites] Int J Immunopharmacol. 1993 Feb;15(2):219-28 [8096834.001]
  • [Cites] Int Ophthalmol. 1996-1997;20(1-3):57-62 [9112165.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 Jan;36(1):247-51 [7822153.001]
  • [Cites] Scand J Immunol. 1991 Jul;34(1):121-5 [1648785.001]
  • [Cites] Arch Ophthalmol. 1994 Nov;112(11):1437-45 [7980133.001]
  • [Cites] Exp Eye Res. 2006 Nov;83(5):1246-51 [16938291.001]
  • [Cites] J Neural Transm (Vienna). 1996;103(1-2):17-30 [9026371.001]
  • [Cites] Ophthalmology. 1995 Sep;102(9):1291-7 [9097765.001]
  • (PMID = 19333701.001).
  • [ISSN] 1613-2246
  • [Journal-full-title] Japanese journal of ophthalmology
  • [ISO-abbreviation] Jpn. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Glucocorticoids; 0 / Lipopolysaccharides; 0 / Ophthalmic Solutions; 0 / Quinolines; 0 / Receptors, Dopamine D1; 0 / Receptors, Dopamine D2; 0 / SDZ GLC 756; 0 / Tumor Necrosis Factor-alpha; 9842X06Q6M / Betamethasone; E0399OZS9N / Cyclic AMP
  •  go-up   go-down


34. Tanaka M, Kanamori H, Yamaji S, Fujimaki K, Tomita N, Fujisawa S, Ishigatsubo Y: Therapy-related CD7+ acute myeloid leukemia with trisomy 8 following acute monocytic leukemia. Anticancer Drugs; 2001 Sep;12(8):681-2
Hazardous Substances Data Bank. MERCAPTOPURINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related CD7+ acute myeloid leukemia with trisomy 8 following acute monocytic leukemia.
  • We report a patient who developed CD7+ therapy-related acute myeloid leukemia (t-AML) with trisomy 8 after chemotherapy for AML.
  • [MeSH-major] Cytarabine / adverse effects. Cytarabine / analogs & derivatives. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Antigens, CD7 / analysis. Biomarkers, Tumor / analysis. Chromosomes, Human, Pair 8 / genetics. Daunorubicin / therapeutic use. Diagnosis, Differential. Female. Humans. Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / drug therapy. Middle Aged. Prednisolone / therapeutic use. Trisomy / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11604555.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Biomarkers, Tumor; 04079A1RDZ / Cytarabine; 9PHQ9Y1OLM / Prednisolone; 9YVR68W306 / enocitabine; E7WED276I5 / 6-Mercaptopurine; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


35. Wu HJ, Chen Y: [Biological characteristics of hyperleukocytic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):450-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biological characteristics of hyperleukocytic acute leukemia].
  • The study was to investigate the biological characteristics of hyperleucocyte acute leukemia (HAL) and its clinical significance.
  • In AML, monocytic leukemia is easier to become into HAL than other leukemias.
  • In ALL, T-lineage antigens of HAL group are more easily expressed than those of NHAL group; the leukemia cells of HAL group are naiver than those of NHAL group, meanwhile the prognosis of HAL is poor.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16800918.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD79; 0 / Antigens, CD8; 0 / Sialic Acid Binding Ig-like Lectin 2
  •  go-up   go-down


36. Jones KH, Liu JJ, Roehm JS, Eckel JJ, Eckel TT, Stickrath CR, Triola CA, Jiang Z, Bartoli GM, Cornwell DG: Gamma-tocopheryl quinone stimulates apoptosis in drug-sensitive and multidrug-resistant cancer cells. Lipids; 2002 Feb;37(2):173-84
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gamma-tocopheryl quinone stimulates apoptosis in drug-sensitive and multidrug-resistant cancer cells.
  • Chemotherapy-induced cell death is linked to apoptosis, and there is increasing evidence that multidrug-resistance in cancer cells may be the result of a decrease in the ability of a cell to initiate apoptosis in response to cytotoxic agents.
  • In previous studies, we synthesized two classes of electrophilic tocopheryl quinones (TQ), nonarylating alpha-TQ and arylating gamma- and delta-TQ, and found that gamma- and delta-TQ, but not alpha-TQ, were highly cytotoxic in human acute lymphoblastic leukemia cells (CEM) and multidrug-resistant (MDR) CEM/VLB100.
  • We have now extended these studies on tumor biology with CEM, HL60 and MDR HL60/MX2 human promyelocytic leukemia, U937 human monocytic leukemia, and ZR-75-1 breast adenocarcinoma cells. gamma-TQ, but not alpha-TQ or tocopherols, showed concentration and incubation time-dependent effects on loss of plasma membrane integrity, diminished viable cell number, and stimulation of apoptosis.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Multiple. Vitamin E / analogs & derivatives. Vitamin E / pharmacology

  • MedlinePlus Health Information. consumer health - Vitamin E.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Toxicol Appl Pharmacol. 1992 Jan;112(1):2-16 [1733045.001]
  • [Cites] Lipids. 1998 Mar;33(3):295-301 [9560804.001]
  • [Cites] Fundam Appl Toxicol. 1997 Jul;38(1):23-37 [9268603.001]
  • [Cites] Cell. 1996 Jul 12;86(1):147-57 [8689682.001]
  • [Cites] Cancer Res. 1993 Sep 15;53(18):4287-96 [8364925.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5570-6 [9850096.001]
  • [Cites] Exp Cell Res. 1998 Feb 1;238(2):389-98 [9473347.001]
  • [Cites] Exp Cell Res. 2000 Feb 25;255(1):125-32 [10666341.001]
  • [Cites] Free Radic Biol Med. 1995 Jun;18(6):963-76 [7628732.001]
  • [Cites] J Lipid Res. 1981 Jul;22(5):763-9 [7288284.001]
  • [Cites] Arch Biochem Biophys. 1996 Sep 15;333(2):482-8 [8809090.001]
  • [Cites] Free Radic Biol Med. 1989;7(4):435-77 [2691341.001]
  • [Cites] Cell Tissue Kinet. 1982 Mar;15(2):225-31 [7039844.001]
  • [Cites] J Bioenerg Biomembr. 1999 Aug;31(4):305-19 [10665521.001]
  • [Cites] Annu Rev Biochem. 1993;62:385-427 [8102521.001]
  • [Cites] Cancer Res. 1993 Aug 15;53(16):3658-61 [8101765.001]
  • [Cites] Cancer Res. 1994 Jan 15;54(2):357-61 [8275468.001]
  • [Cites] Free Radic Biol Med. 1995 Aug;19(2):197-207 [7649491.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9215-20 [10908664.001]
  • [Cites] IARC Sci Publ. 1996;(139):203-19 [8923032.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] J Bioenerg Biomembr. 1999 Aug;31(4):291-304 [10665520.001]
  • [Cites] J Clin Invest. 1986 Mar;77(3):789-96 [3949977.001]
  • [Cites] Cell Death Differ. 1998 Jan;5(1):107-15 [10200451.001]
  • [Cites] J Biol Chem. 1997 Nov 28;272(48):29995-7 [9374472.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):7885-90 [9223282.001]
  • [Cites] Annu Rev Physiol. 1998;60:619-42 [9558479.001]
  • [Cites] Lab Invest. 1980 May;42(5):495-506 [7382425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11494-9 [11005841.001]
  • [Cites] Biochim Biophys Acta. 1970 Dec 1;219(2):361-71 [5497195.001]
  • [Cites] Lipids. 1985 Mar;20(3):151-7 [3921792.001]
  • [Cites] FASEB J. 1995 Oct;9(13):1345-54 [7557025.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):3976-85 [8358726.001]
  • [Cites] Cancer Res. 1989 Aug 15;49(16):4542-9 [2568172.001]
  • [Cites] Toxicol Lett. 1995 Dec;82-83:149-53 [8597043.001]
  • [Cites] Lipids. 1996 Jul;31(7):671-701 [8827691.001]
  • [Cites] J Pharmacol Exp Ther. 1997 Aug;282(2):648-56 [9262326.001]
  • [Cites] Biochemistry. 1996 Feb 6;35(5):1387-96 [8634268.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4616-23 [9788613.001]
  • [Cites] Cell. 2000 Jul 7;102(1):33-42 [10929711.001]
  • [Cites] J Cell Biol. 1992 Nov;119(3):493-501 [1400587.001]
  • [Cites] Cardiovasc Res. 2000 Feb;45(3):549-59 [10728376.001]
  • [Cites] Crit Rev Oncol Hematol. 1998 Sep;28(3):181-205 [9793746.001]
  • [Cites] J Biol Chem. 1994 Dec 2;269(48):30553-60 [7982974.001]
  • [Cites] Cardiovasc Res. 2000 Feb;45(3):528-37 [10728374.001]
  • [Cites] J Bioenerg Biomembr. 1999 Aug;31(4):321-6 [10665522.001]
  • [Cites] Cell. 1994 Aug 26;78(4):539-42 [8069905.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1845-53 [9058703.001]
  • [Cites] Arch Biochem Biophys. 1986 Nov 15;251(1):25-35 [3789732.001]
  • [Cites] Biochim Biophys Acta. 1993 Jul 11;1157(3):313-7 [8323961.001]
  • [Cites] Methods Cell Biol. 1998;57:251-64 [9648109.001]
  • [Cites] Mol Pharmacol. 1997 Aug;52(2):300-5 [9271353.001]
  • [Cites] Free Radic Biol Med. 1994 Jun;16(6):675-84 [8070670.001]
  • [Cites] Brain Res. 1996 Sep 16;733(2):175-83 [8891300.001]
  • (PMID = 11908909.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytochrome c Group; 1406-18-4 / Vitamin E; 7559-04-8 / tocopherylquinone; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; GAN16C9B8O / Glutathione
  •  go-up   go-down


37. Wong KF, Yuen HL, Siu LL, Pang A, Kwong YL: t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia. Hum Pathol; 2008 Nov;39(11):1702-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia.
  • A Chinese girl presented with generalized papular rash and monocytic leukemia 19 days after birth.
  • Spontaneous regression of the leukemia was observed after 2 months, although the t(8;16) translocation persisted cytogenetically.
  • This was followed 7 months later by the development of acute myeloid leukemia with maturation and cytogenetic evolution with extra chromosomes 4 and 8.
  • Molecular study showed that the reciprocal MYST3 and CREBBP gene fusion characteristic of t(8;16) translocation persisted throughout the clinical course, even during spontaneous regression of the neonatal leukemia, and after chemotherapy-induced remission of the subsequent acute myeloid leukemia.
  • The possible role of MYST3 and CREBBP gene fusion in the pathogenesis of the leukemia is discussed.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18657848.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  •  go-up   go-down


38. Park C, Kim GY, Kim GD, Lee WH, Cheong JH, Kim ND, Bae SJ, Jung JH, Choi YH: Suppression of U937 human monocytic leukemia cell growth by dideoxypetrosynol A, a polyacetylene from the sponge Petrosia sp., via induction of Cdk inhibitor p16 and down-regulation of pRB phosphorylation. Oncol Rep; 2006 Jul;16(1):171-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of U937 human monocytic leukemia cell growth by dideoxypetrosynol A, a polyacetylene from the sponge Petrosia sp., via induction of Cdk inhibitor p16 and down-regulation of pRB phosphorylation.
  • The aim of the present study was to further elucidate the possible mechanisms by which dideoxypetrosynol A exerts its anti-proliferative action in cultured human monocytic leukemia U937 cells.
  • [MeSH-major] Alkynes / pharmacology. Fatty Alcohols / pharmacology. Gene Expression Regulation, Neoplastic. Leukemia / drug therapy. Leukemia / pathology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. ACETYLENE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16786142.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Alkynes; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / E2F Transcription Factors; 0 / Fatty Alcohols; 0 / Polymers; 0 / Retinoblastoma Protein; 0 / dideoxypetrosynol A; 25067-58-7 / Polyacetylenes; OC7TV75O83 / Acetylene
  •  go-up   go-down


39. Tokura Y, Shikami M, Miwa H, Watarai M, Sugamura K, Wakabayashi M, Satoh A, Imamura A, Mihara H, Katoh Y, Kita K, Nitta M: Augmented expression of P-gp/multi-drug resistance gene by all-trans retinoic acid in monocytic leukemic cells. Leuk Res; 2002 Jan;26(1):29-36
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Augmented expression of P-gp/multi-drug resistance gene by all-trans retinoic acid in monocytic leukemic cells.
  • P-glycoprotein (P-gp)/multi-drug resistance 1 (MDR1) gene is recognized to be, at least in part, responsible for the refractoriness to chemotherapy of leukemia.
  • Egr1 mRNA was frequently and strongly expressed in monocytic leukemia cells, especially in AML M4 cells.
  • WT1 mRNA was undetectable in t(8;21) AML cells. mRNA expression of MDR1 was frequent in AML M1 and t(8;21) AML cells, in which the expression level was highest in AML M1 and was low in monocytic leukemia (M4 and M5).
  • By liquid culture of leukemia cell lines and fresh AML cells with the addition of all-trans retinoic acid (ATRA), modulation of P-gp/MDR1 and Egr1 was observed and the pattern of modulation was divided into four groups:.
  • (1) blastic AML type, in which distinct expression of P-gp/MDR1 and CD34 was not influenced by ATRA;.
  • (2) t(8;21)AML type, in which P-gp/MDR1 expression was augmented by ATRA, while CD34 was kept high;.
  • (3) AML M3 type, in which P-gp/MDR1 expression was reduced with granulocytic differentiation by ATRA;.
  • (4) monocytic AML type, in which P-gp/MDR1 expression was augmented by ATRA, while CD34 expression decreased, and strong Egr1 expression was downregulated just prior to the augmentation of P-gp/MDR1 expression.
  • Previous reports have suggested that P-gp/MDR1 plays an important role in resistance to chemotherapy, and is recognized as one of the stem cell marker.
  • However, P-gp/MDR1 expression augmented by ATRA, which was observed in monocytic AML, was recognized as a functional molecule of mature monocyte/macrophage, because CD34 expression decreased and CD13 expression increased by ATRA.
  • Finally, expression of P-gp/MDR1 in monocytic leukemia, which was functionally confirmed by Rh123 efflux study, was thought to be closely related to the characteristic modulation of Egr1 expression by ATRA.
  • [MeSH-major] Immediate-Early Proteins. Leukemia, Myeloid, Acute / metabolism. Monocytes / drug effects. P-Glycoprotein / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Cell Differentiation / drug effects. Cell Line. Cell Separation. DNA Primers / chemistry. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Down-Regulation. Drug Resistance, Multiple. Early Growth Response Protein 1. Humans. Immunophenotyping. Karyotyping. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. WT1 Proteins / genetics. WT1 Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11734301.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Immediate-Early Proteins; 0 / P-Glycoprotein; 0 / Transcription Factors; 0 / WT1 Proteins; 5688UTC01R / Tretinoin; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


40. Nishioka C, Ikezoe T, Yang J, Takeshita A, Taniguchi A, Komatsu N, Togitani K, Koeffler HP, Yokoyama A: Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene. Leuk Res; 2008 Jun;32(6):865-72
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene.
  • Activating mutations of this gene occur in nearly 30% of acute myelogenous leukemia (AML) patients.
  • In this study, we found that AZD6244 (ARRY-142886), a novel inhibitor of MEK1/2 kinases, effectively inhibited the proliferation of acute biphenotypic leukemia MV4-11 and acute monocytic leukemia MOLM13 cells.
  • Taken together, concomitant blockade of FLT3 and MEK signaling represents a promising treatment strategy for individuals with leukemia who possess activating mutations of FLT3.
  • [MeSH-major] Apoptosis / drug effects. Indoles / therapeutic use. Leukemia / pathology. MAP Kinase Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mutation / genetics. Pyrroles / therapeutic use. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols. Benzimidazoles / therapeutic use. Cell Proliferation / drug effects. Female. Humans. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17983653.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AZD 6244; 0 / Benzimidazoles; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1
  •  go-up   go-down


41. Egawa K, Yamori T, Nosaka C, Kunimoto S, Takeuchi T, Nos K: Deoxynybomycin is a selective anti-tumor agent inducing apoptosis and inhibiting topoisomerase I. Biol Pharm Bull; 2000 Sep;23(9):1036-40
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Deoxynybomycin selectively inhibited growth of human osteoblastic sarcoma Saos-2, gastric cancer TMK-1, and monocytic leukemia THP-1 cells, but did not affect survival of normal human fibroblasts at doses up to 5 microg/ml.
  • These results suggest that deoxynybomycin may be useful in cancer chemotherapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Topoisomerase I Inhibitors

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10993200.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Quinolones; 0 / Topoisomerase I Inhibitors; 27259-98-9 / deoxynybomycin
  •  go-up   go-down


42. Mashiyama S, Fukawa O, Mitani S, Ito S, Ito K, Asano S, Sai T: [Chronic subdural hematoma associated with malignancy: report of three cases]. No Shinkei Geka; 2000 Feb;28(2):173-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A clinical diagnosis of acute monocytic leukemia was made after the laboratory examination.
  • Remission was achieved by chemotherapy, but she died one year after the operation.
  • A clinical diagnosis of chronic lymphocytic leukemia was made after the laboratory examination.
  • No treatment was given since there were no clinical symptoms of chronic lymphocytic leukemia.
  • Left acute subdural hematoma, which was removed by craniotomy, occurred three days after the second operation.
  • [MeSH-major] Hematoma, Subdural / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Monocytic, Acute / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10666738.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] JAPAN
  •  go-up   go-down


43. Li W, Xi S, Zhang M: [The cytotoxic effect of a low density lipoprotein delivered aclarubicin on leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2001 Dec;22(12):636-8
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The cytotoxic effect of a low density lipoprotein delivered aclarubicin on leukemia cells].
  • OBJECTIVE: To investigate the feasibility and effectiveness of low density lipoprotein (LDL) particles as a carrier of a lipophilic anthracycline drug aclarubicin (ACR) for targeting delivery to an acute monocytic leukemia cell line THP-1.
  • The 3H-TdR incorporation test showed that the complex was more effective in the inhibition of DNA synthesis than that of the free drug.
  • [MeSH-major] Aclarubicin / administration & dosage. Antibiotics, Antineoplastic / administration & dosage. Leukemia / drug therapy. Lipoproteins, LDL / administration & dosage
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. DNA / biosynthesis. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16200711.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Lipoproteins, LDL; 74KXF8I502 / Aclarubicin; 9007-49-2 / DNA
  •  go-up   go-down


44. Xu WL, Jin J, Chen ZM, Lou JY, Yu YB: [Clinical and experimental study of 38 cases with trisomy 8]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2003 Dec;20(6):528-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Thirty-two of 38(84.2%) cases with trisomy 8, and fourteen of 17(82.4%) cases with trisomy 8 as the sole chromosome aberration were myeloid disorders such as myelodysplastic syndrome (MDS), acute myelocytic leukemia (AML), chronic myelocytic leukemia (CML).
  • The incidence of trisomy 8 was higher in myeloid disease than in lymphocytic disease (5% vs 1.3%); the incidence of trisomy 8 was higher in acute monocytic leukemia than in other AML (6.1% vs 2.4%), and the incidence of trisomy 8 in chronic myelomonocytic leukemia( CMML) was higher than that in other myelodysplastic syndrome (MDS) (25% vs 13.2%); 17 cases had trisomy 8 as the sole chromosome aberration, 21 cases had other additional chromosome aberrations.
  • Eleven cases were treated with chemotherapy, among them only 10 cases data were available.
  • Seven cases acquired complete remission but 3 of them were M3, the other 3 cases had no response after two courses of chemotherapy.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia / genetics. Myelodysplastic Syndromes / genetics. Trisomy

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14669224.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


45. Zhang C, Liang MY, Wang SM: [Clinical analysis of bicytopenia and pancytopenia during pregnancy]. Zhonghua Fu Chan Ke Za Zhi; 2009 Jul;44(7):488-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Retrospective chart review was conducted on 24 pregnancies who were found bicytopenia or pancytopenia during pregnancy for the first time.
  • RESULTS: According to the clinical data and laboratory findings, the latter including complete blood cell count, reticulocyte count, peripheral smear, serum folate and vitamin B12 level, autoimmune antibody screening, bone marrow smear and biopsy, thirteen patients were diagnosed as having chronic aplastic anemia (CAA), six as having myelodysplastic syndromes (MDS), two as having megaloblastic anemia (MA), one as having paroxysmal nocturnal hemoglobinuria (PNH), one as having Evan's syndrome and one as having acute leukemia.
  • The patient with acute leukemia died of recurrence six months postpartum.
  • Of the 6 patients with MDS, one achieved partial remission, four no remission, and one transformed into acute monocytic leukemia, then refused chemotherapy and was lost follow-up.
  • [MeSH-major] Anemia, Aplastic / therapy. Blood Transfusion. Pancytopenia / therapy. Pregnancy Complications, Hematologic / diagnosis. Pregnancy Complications, Hematologic / therapy. Pregnancy Outcome
  • [MeSH-minor] Adult. Biopsy, Needle. Bone Marrow / pathology. Bone Marrow Examination. Female. Folic Acid / therapeutic use. Follow-Up Studies. Humans. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Pregnancy. Prognosis. Retrospective Studies. Young Adult


46. Lestringant GG, Masouyé I, El-Hayek M, Girardet C, Révész T, Frossard PM: Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis. Dermatology; 2000;200(2):147-50
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis.
  • We report an unusual case of congenital leukemia with leukemia cutis (LC) and diffuse calcinosis cutis.
  • Bone marrow morphology was consistent with the diagnosis of acute monocytic leukemia of the FAB M5 type.
  • The patient responded to chemotherapy but, following consolidation treatment, developed sepsis and died at 120 days of age.
  • Congenital leukemia is rare and LC is uncommon.
  • Hypercalcemia may be a complication of leukemia, which leads to multiorgan metastatic calcification.
  • Despite the absence of frank hypercalcemia, the presence of bone lesions suggests that the patient's calcinosis cutis was of the metastatic type.
  • [MeSH-major] Calcinosis / congenital. Leukemia, Myeloid / congenital. Skin Neoplasms / congenital
  • [MeSH-minor] Acute Disease. Female. Humans. Infant, Newborn

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 S. Karger AG, Basel.
  • (PMID = 10773706.001).
  • [ISSN] 1018-8665
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


47. Lee YN, Lee HY, Kim JS, Park C, Choi YH, Lee TG, Ryu SH, Kwak JY, Bae YS: The novel phospholipase C activator, m-3M3FBS, induces monocytic leukemia cell apoptosis. Cancer Lett; 2005 May 26;222(2):227-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The novel phospholipase C activator, m-3M3FBS, induces monocytic leukemia cell apoptosis.
  • The results of our study suggest that m-3M3FBS can be developed as a novel anti-leukemic agent.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Monocytic, Acute / pathology. Sulfonamides / pharmacology
  • [MeSH-minor] Cell Survival. Down-Regulation. Humans. Monocytes / drug effects. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Tumor Cells, Cultured. Up-Regulation. bcl-2-Associated X Protein

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15863272.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 2,4,6-trimethyl-N-(meta-3-trifluoromethylphenyl)benzenesulfonamide; 0 / BAX protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sulfonamides; 0 / bcl-2-Associated X Protein
  •  go-up   go-down


48. Rots MG, Pieters R, Jansen G, Kaspers GJ, Van Zantwijk CH, Noordhuis P, Voorn DA, Van Wering ER, Creutzig U, Veerman AJ, Peters GJ: A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia. Eur J Cancer; 2001 Mar;37(4):492-8
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia.
  • Acute myeloid leukaemia (AML) is thought to be methotrexate (MTX)-resistant.
  • However, a small study suggested that acute monocytic leukemia (AML-M5) is sensitive to MTX.
  • We measured MTX accumulation/polyglutamylation in 20 AML-nonM5, 37 AML-M5 and 83 common/preB-acute lymphoblastic leukaemia (c/preB-ALL) samples.
  • Membrane transport was determined in 11 childhood AMLs (including 3 AML-M5) and in 25 c/preB-ALL samples.
  • MTX sensitivity was determined in 23 AML-nonM5, 15 AML-M5 and 63 common/preB-ALL samples using the thymidylate synthase (TS) inhibition assay.
  • Accumulation of long-chain polyglutamates MTX-Glu(4-6) was 3-fold lower for AML-nonM5 compared with c/preB-ALL cells (median 268 versus 889 pmol MTX-Glu(4-6)/10(9) cells; P < or = 0.001); for AML-M5 samples, median accumulation of MTX-Glu(4-6) was 0 pmol/10(9) cells (P < or = 0.001).
  • After short-term MTX exposure, AML-nonM5 was 6-fold more resistant to MTX compared with c/preB-ALL cells (2.16 versus 0.39 microM; P < 0.001), while AML-M5 was 2-fold more resistant (P = 0.02).
  • In both AML-nonM5 and AML-M5 cells, MTX resistance was circumvented by continuous MTX exposure (median TSI(50) values: 0.052 and 0.041 microM, respectively) compared with a c/preB-ALL value of 0.066 microM.
  • In conclusion, AML-M5 is relatively sensitive to MTX compared with other AML-subtypes even though polyglutamylation of MTX is poor.
  • Using continuous exposure, AML-nonM5 and AML-M5 cells were at least as sensitive to MTX as c/preB-ALL cells.
  • This report suggests that MTX might be an overlooked drug in the treatment of childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Leukemia, Monocytic, Acute / drug therapy. Methotrexate / therapeutic use
  • [MeSH-minor] Biological Transport. Child. Drug Resistance, Neoplasm. Humans. Thymidylate Synthase / antagonists & inhibitors. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11267859.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; EC 2.1.1.45 / Thymidylate Synthase; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


49. Guo C, Inghirami G, Ibrahim S, Sen F: Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia. Arch Pathol Lab Med; 2006 Jul;130(7):1075-6
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia.
  • Therapy-related acute myeloid leukemias arise as a result of cytotoxic chemotherapy and/or radiation therapy.
  • The most common types of acute myeloid leukemia arising in this setting are acute myeloid leukemia with maturation, and lesser numbers of acute myelomonocytic leukemia, acute monocytic leukemia, acute erythroleukemia, or acute megakaryocytic leukemia.
  • We present a patient with multiple myeloma who was treated with melphalan and 4 years later developed acute erythroid leukemia.
  • The morphologic diagnosis of pure erythroid leukemia developing in the setting of multiple myeloma may be challenging.
  • [MeSH-major] Epistaxis / complications. Leukemia, Erythroblastic, Acute / complications. Multiple Myeloma / complications. Muscle Weakness / complications
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Humans. Leukemia, Myeloid. Male. Melphalan / adverse effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16831041.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
  •  go-up   go-down


50. Tomonari A, Shirafuji N, Tojo A, Iseki T, Ooi J, Komiya I, Tani K, Asano S: Acute myelogenous leukemia M5b developed during clinical remission of Castleman disease. Int J Hematol; 2003 Apr;77(3):274-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia M5b developed during clinical remission of Castleman disease.
  • We describe the first case of CD associated with acute myelogenous leukemia (AML).
  • His bone marrow aspirate showed that approximately 80% of cells were leukemic, including well-differentiated monocytic cells A diagnosis of AML M5b was made.
  • The patient died of invasive pulmonary aspergillosis after chemotherapy.
  • [MeSH-major] Giant Lymph Node Hyperplasia / complications. Leukemia, Monocytic, Acute / etiology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Bone Marrow / pathology. Fatal Outcome. Humans. Lymph Nodes / pathology. Male. Middle Aged. Prednisolone / therapeutic use. Remission Induction

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Med Pediatr Oncol. 1990;18(2):169-72 [2304424.001]
  • [Cites] J Clin Oncol. 1985 Sep;3(9):1202-16 [4031967.001]
  • [Cites] Am J Surg Pathol. 1990 Jul;14 (7):603-14 [2356921.001]
  • [Cites] Scand J Rheumatol. 1997;26(6):482-4 [9433413.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1276-80 [7632932.001]
  • [Cites] Minerva Chir. 1991 Sep 30;46(18):989-93 [1754099.001]
  • [Cites] Blood. 1989 Sep;74(4):1360-7 [2788466.001]
  • [Cites] Hinyokika Kiyo. 1992 Sep;38(9):1041-4 [1414756.001]
  • [Cites] Am J Clin Pathol. 1990 Jul;94(1):101-4 [2193504.001]
  • [Cites] Ann Pathol. 1994;14(6):384-91 [7857413.001]
  • [Cites] Cancer. 1997 Jan 15;79(2):294-313 [9010103.001]
  • (PMID = 12731671.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9PHQ9Y1OLM / Prednisolone
  •  go-up   go-down


51. Hahn M, Li W, Yu C, Rahmani M, Dent P, Grant S: Rapamycin and UCN-01 synergistically induce apoptosis in human leukemia cells through a process that is regulated by the Raf-1/MEK/ERK, Akt, and JNK signal transduction pathways. Mol Cancer Ther; 2005 Mar;4(3):457-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapamycin and UCN-01 synergistically induce apoptosis in human leukemia cells through a process that is regulated by the Raf-1/MEK/ERK, Akt, and JNK signal transduction pathways.
  • Interactions between the protein kinase C and Chk1 inhibitor UCN-01 and rapamycin in human leukemia cells have been investigated in relation to apoptosis induction.
  • Treatment of U937 monocytic leukemia cells with rapamycin (10 nmol/L) in conjunction with a minimally toxic concentration of UCN-01 (100 nmol/L) for 36 hours resulted in marked potentiation of mitochondrial injury (i.e., loss of mitochondrial membrane potential and cytosolic release of cytochrome c, AIF, and Smac/DIABLO), caspase activation, and apoptosis.
  • Together, these findings indicate that the mammalian target of rapamycin inhibitor potentiates UCN-01 cytotoxicity in a variety of human leukemia cell types and suggest that inhibition of both Raf-1/MEK/ERK and Akt cytoprotective signaling pathways as well as JNK activation contribute to this phenomenon.
  • [MeSH-major] Apoptosis. Extracellular Signal-Regulated MAP Kinases / metabolism. JNK Mitogen-Activated Protein Kinases / metabolism. Leukemia / drug therapy. MAP Kinase Kinase 1 / metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-raf / metabolism. Sirolimus / pharmacology. Staurosporine / analogs & derivatives. Staurosporine / pharmacology
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents / pharmacology. CDC2 Protein Kinase / metabolism. Caspases / metabolism. Cell Line, Tumor. Cyclin D1 / metabolism. Cytochromes c / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Enzyme Activation. Genes, Dominant. Humans. Immunoblotting. Jurkat Cells. MAP Kinase Kinase 4. Phosphorylation. Proto-Oncogene Proteins c-akt. Signal Transduction. Time Factors. U937 Cells


52. Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. Nat Med; 2010 May;16(5):580-5, 1p following 585
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
  • Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.
  • Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.
  • Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.
  • Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1R(high) cells.
  • Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.
  • Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 2002 Nov;17(5):665-76 [12433372.001]
  • [Cites] Blood. 2007 Jul 1;110(1):323-33 [17360941.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):259-71 [12676584.001]
  • [Cites] J Leukoc Biol. 2004 Apr;75(4):612-23 [14726498.001]
  • [Cites] Cancer Res. 1987 Feb 1;47(3):874-80 [2433029.001]
  • [Cites] Nature. 1987 Sep 17-23;329(6136):259-61 [3476856.001]
  • [Cites] Cell. 1987 Nov 20;51(4):663-73 [2824063.001]
  • [Cites] J Clin Invest. 1988 Apr;81(4):1030-5 [2832442.001]
  • [Cites] J Cell Physiol. 1988 Apr;135(1):133-8 [3259234.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):373-81 [8264604.001]
  • [Cites] Mol Cell Biol. 1996 Mar;16(3):1231-40 [8622667.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):33-41 [8782817.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3127-32 [15637141.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1590-600 [15914556.001]
  • [Cites] Cell Cycle. 2005 Jul;4(7):851-3 [15917650.001]
  • [Cites] Oncogene. 2006 Jan 5;25(1):147-51 [16170366.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1175-86 [16651658.001]
  • [Cites] Cancer Res. 2007 Nov 15;67(22):10677-85 [18006809.001]
  • [Cites] Cancer Sci. 2008 Aug;99(8):1523-7 [18754862.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1591-3 [18698081.001]
  • [Cites] Blood. 2009 Jul 9;114(2):299-309 [19339695.001]
  • [Cites] Gene Ther. 2000 Jun;7(12):1063-6 [10871756.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):7184-96 [11742995.001]
  • [Cites] Blood. 2002 Jan 1;99(1):111-20 [11756160.001]
  • [Cites] Genes Dev. 2006 May 15;20(10):1321-30 [16702405.001]
  • [Cites] Mol Cancer Ther. 2006 Nov;5(11):2634-43 [17121910.001]
  • [Cites] Blood. 2007 May 1;109(9):3998-4005 [17227832.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e12 [12582257.001]
  • (PMID = 20418886.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870
  •  go-up   go-down


53. Schmutz C, Cartwright A, Williams H, Haworth O, Williams JH, Filer A, Salmon M, Buckley CD, Middleton J: Monocytes/macrophages express chemokine receptor CCR9 in rheumatoid arthritis and CCL25 stimulates their differentiation. Arthritis Res Ther; 2010;12(4):R161
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Identification of molecules involved in their accumulation and differentiation is important to inform therapeutic strategies.
  • Tumour necrosis factor alpha (TNFα) increased CCR9 expression on human acute monocytic leukemia cell line THP-1 monocytic cells.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation / immunology. Cell Line. Female. Flow Cytometry. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Synovial Membrane / immunology. Synovial Membrane / metabolism. Synovial Membrane / pathology. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology

  • Genetic Alliance. consumer health - Arthritis.
  • Genetic Alliance. consumer health - Rheumatoid arthritis.
  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arthritis Rheum. 2010 Jul;62(7):1921-32 [20506316.001]
  • [Cites] IDrugs. 2010 Jul;13(7):472-81 [20582872.001]
  • [Cites] Eur J Immunol. 2000 Jan;30(1):262-71 [10602049.001]
  • [Cites] J Immunol. 2000 Feb 1;164(3):1293-305 [10640743.001]
  • [Cites] Ann Rheum Dis. 2000 May;59(5):399-400 [10836959.001]
  • [Cites] J Exp Med. 2000 Sep 4;192(5):761-8 [10974041.001]
  • [Cites] J Immunol. 2000 Nov 1;165(9):5069-76 [11046037.001]
  • [Cites] Gastroenterology. 2001 Aug;121(2):246-54 [11487533.001]
  • [Cites] Arthritis Rheum. 2001 Dec;44(12):2750-60 [11762935.001]
  • [Cites] Arthritis Rheum. 2002 Oct;46(10):2578-86 [12384915.001]
  • [Cites] J Clin Invest. 2002 Oct;110(8):1113-21 [12393847.001]
  • [Cites] Microcirculation. 2003 Jun;10(3-4):313-23 [12851648.001]
  • [Cites] Ann Rheum Dis. 2003 Aug;62(8):715-21 [12860725.001]
  • [Cites] Ther Apher Dial. 2003 Feb;7(1):48-59 [12921115.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):963-9 [12963696.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6469-77 [14559839.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Mar;36(3):372-8 [14687914.001]
  • [Cites] Ann Rheum Dis. 1991 Oct;50(10):673-6 [1958087.001]
  • [Cites] Ann Rheum Dis. 1994 May;53(5):315-22 [8017985.001]
  • [Cites] J Rheumatol. 1994 May;21(5):830-5 [7520499.001]
  • [Cites] J Rheumatol. 1994 Sep;21(9):1608-14 [7799336.001]
  • [Cites] J Exp Med. 1995 May 1;181(5):1857-62 [7536797.001]
  • [Cites] Arthritis Rheum. 1996 Jan;39(1):115-24 [8546720.001]
  • [Cites] Immunity. 1997 Aug;7(2):291-301 [9285413.001]
  • [Cites] Drugs Aging. 1998 May;12(5):377-90 [9606615.001]
  • [Cites] Arthritis Rheum. 1998 Nov;41(11):2032-8 [9811059.001]
  • [Cites] J Immunol. 1999 May 15;162(10):5671-5 [10229797.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8743-50 [15623660.001]
  • [Cites] J Immunol. 2005 Feb 1;174(3):1693-700 [15661933.001]
  • [Cites] Arthritis Res Ther. 2005;7(2):R217-29 [15743468.001]
  • [Cites] Arthritis Rheum. 2005 Mar;52(3):710-21 [15751074.001]
  • [Cites] Ann Rheum Dis. 2005 Jun;64(6):834-8 [15576415.001]
  • [Cites] Arthritis Rheum. 2005 Aug;52(8):2331-42 [16052590.001]
  • [Cites] J Immunol. 2005 Aug 15;175(4):2579-88 [16081832.001]
  • [Cites] Rheumatology (Oxford). 2005 Sep;44(9):1140-4 [15927997.001]
  • [Cites] Curr Rheumatol Rep. 2005 Oct;7(5):382-8 [16174489.001]
  • [Cites] J Autoimmun. 2005;25 Suppl:26-8 [16260118.001]
  • [Cites] Cell Immunol. 2005 Jul-Aug;236(1-2):110-4 [16185674.001]
  • [Cites] J Immunol. 2006 Jan 1;176(1):75-84 [16365398.001]
  • [Cites] Arthritis Rheum. 2006 Mar;54(3):765-78 [16508941.001]
  • [Cites] Histol Histopathol. 2007 May;22(5):581-6 [17330813.001]
  • [Cites] Curr Opin Rheumatol. 2007 May;19(3):289-95 [17414958.001]
  • [Cites] Methods. 2007 Nov;43(3):207-17 [17920517.001]
  • [Cites] Annu Rev Pathol. 2006;1:297-329 [18039117.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2008;48:171-97 [17883327.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2008 Nov;28(11):1920-7 [18723831.001]
  • [Cites] Mol Cell Biochem. 2010 Feb;335(1-2):283-9 [19784811.001]
  • [Cites] Expert Opin Investig Drugs. 2010 Mar;19(3):345-55 [20113217.001]
  • [Cites] J Exp Med. 1999 Nov 1;190(9):1241-56 [10544196.001]
  • (PMID = 20738854.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Arthritis Research UK / / 16390; United Kingdom / Arthritis Research UK / / 18547; United Kingdom / Medical Research Council / / G9818340; United Kingdom / Arthritis Research UK / / 20088; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CC chemokine receptor 9; 0 / CCL25 protein, human; 0 / Chemokines, CC; 0 / Receptors, CCR; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2945064
  •  go-up   go-down


54. Barnes BJ, Izydore RA, Hall IH: Cytotoxicity and mode of action of 1-(1-cyclohexenyl) and 1-unsubstituted 3,5-pyrazolidinediones in human Molt4 T cell leukemia. Anticancer Res; 2001 May-Jun;21(3B):1857-68
Hazardous Substances Data Bank. Phenylbutazone .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxicity and mode of action of 1-(1-cyclohexenyl) and 1-unsubstituted 3,5-pyrazolidinediones in human Molt4 T cell leukemia.
  • The 3,5-pyrazolidinediones proved to be potent cytotoxic agents against the growth of a number of murine and human tumor cell lines, e.g. human THP-I monocytic leukemia, Hut-78 lymphoma, MCF-7 breast effusion, A549 lung carcinoma, U87MG glioma, Hela uterine and A431 epidermoid skin cancer.
  • In human Tmolt4 cell leukemia, the agents substantially suppressed DNA and RNA syntheses after 60 min at 100 microM.
  • Suppression of IMPDH activity was due to the inhibition of both the Type I and II isoforms through an uncompetitive mechanism; however, the Type II isoform was preferentially inhibited at lower concentrations of compounds tested (>50-150 microM).
  • Therefore IMPDH Type II activity, which predominates in cancer cells, was selectively inhibited over the Type I isoform (208-312 microM).
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. Phenylbutazone / pharmacology
  • [MeSH-minor] Amidophosphoribosyltransferase / antagonists & inhibitors. Animals. DNA / metabolism. HeLa Cells. Humans. IMP Dehydrogenase / antagonists & inhibitors. Inhibitory Concentration 50. Kinetics. Mice. Models, Chemical. Protein Isoforms. Recombinant Proteins / metabolism. Time Factors. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11497269.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Protein Isoforms; 0 / Recombinant Proteins; 9007-49-2 / DNA; EC 1.1.1.205 / IMP Dehydrogenase; EC 2.4.2.14 / Amidophosphoribosyltransferase; GN5P7K3T8S / Phenylbutazone
  •  go-up   go-down


55. Sturm B, Helminger M, Steinkellner H, Heidari MM, Goldenberg H, Scheiber-Mojdehkar B: Carbamylated erythropoietin increases frataxin independent from the erythropoietin receptor. Eur J Clin Invest; 2010 Jun;40(6):561-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Friedreich's ataxia (FRDA) is a neurodegenerative disorder caused by decreased expression of the mitochondrial protein frataxin.
  • MATERIALS AND METHODS: In our experiments human erythroleukaemic K562 cells (+ EPO-R), human monocytic leukemia THP-1 cells (- EPO-R) and isolated primary lymphocytes from healthy control and FRDA patients were incubated with different concentrations of rhuEPO or CEPO.
  • CONCLUSION: Our results provide a scientific basis for further studies examining the effectiveness of nonerythropoietic derivatives of erythropoietin for the treatment of Friedreich's ataxia patients.
  • [MeSH-major] Erythropoietin / pharmacology. Friedreich Ataxia / drug therapy. Iron-Binding Proteins / analysis. Recombinant Proteins / pharmacology
  • [MeSH-minor] Cell Line. Cells, Cultured. Enzyme-Linked Immunosorbent Assay / methods. Humans. K562 Cells / drug effects. K562 Cells / metabolism. Lymphocytes / drug effects. Lymphocytes / metabolism. Macrophages / drug effects. Macrophages / metabolism

  • MedlinePlus Health Information. consumer health - Friedreich's Ataxia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20456483.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Iron-Binding Proteins; 0 / Recombinant Proteins; 0 / carbamylated erythropoietin; 0 / frataxin; 11096-26-7 / Erythropoietin
  •  go-up   go-down


56. Brown JR, Yang F, Sinha A, Ramakrishnan B, Tor Y, Qasba PK, Esko JD: Deoxygenated disaccharide analogs as specific inhibitors of beta1-4-galactosyltransferase 1 and selectin-mediated tumor metastasis. J Biol Chem; 2009 Feb 20;284(8):4952-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The acetylated form of this compound inhibited sLe(X) formation in U937 monocytic leukemia cells, suggesting that it had inhibitory activity in vivo as well.
  • These data suggest that nonsubstrate disaccharides have therapeutic potential through their ability to bind to glycosyltransferases in vivo and to alter glycan-dependent pathologic processes.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4206-10 [10945631.001]
  • [Cites] J Mol Biol. 2006 Apr 14;357(5):1619-33 [16497331.001]
  • [Cites] Carbohydr Res. 2000 Nov 3;329(2):287-300 [11117312.001]
  • [Cites] J Mol Biol. 2001 Jun 29;310(1):205-18 [11419947.001]
  • [Cites] J Mol Biol. 2002 Apr 26;318(2):491-502 [12051854.001]
  • [Cites] Cell Mol Life Sci. 2002 Jul;59(7):1081-95 [12222957.001]
  • [Cites] Cancer Res. 2003 Jun 1;63(11):2775-81 [12782582.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23352-9 [12686549.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1678-85 [12714507.001]
  • [Cites] Mini Rev Med Chem. 2003 Nov;3(7):679-87 [14529509.001]
  • [Cites] Biochemistry. 2004 Oct 5;43(39):12513-22 [15449940.001]
  • [Cites] Biochem Genet. 1979 Aug;17(7-8):577-83 [540008.001]
  • [Cites] Carbohydr Res. 1980 Mar 15;81(2):239-47 [6769586.001]
  • [Cites] J Biol Chem. 1987 Sep 5;262(25):12189-95 [2957376.001]
  • [Cites] Acta Crystallogr A. 1991 Mar 1;47 ( Pt 2):110-9 [2025413.001]
  • [Cites] J Biol Chem. 1991 Sep 25;266(27):17858-62 [1917926.001]
  • [Cites] Biochem Biophys Res Commun. 1992 Feb 14;182(3):1288-95 [1371678.001]
  • [Cites] Carbohydr Res. 1992 May 14;229(1):C5-9 [1516098.001]
  • [Cites] Oncol Res. 1992;4(11-12):507-15 [1284381.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3323-7 [7724561.001]
  • [Cites] J Biol Chem. 1997 Oct 10;272(41):25608-16 [9325281.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] Bioorg Med Chem Lett. 1998 Dec 1;8(23):3359-64 [9873734.001]
  • [Cites] Clin Cancer Res. 2006 May 1;12(9):2894-901 [16675586.001]
  • [Cites] Glycoconj J. 2006 Nov;23(7-8):525-41 [17006644.001]
  • [Cites] Expert Opin Ther Targets. 2007 Nov;11(11):1473-91 [18028011.001]
  • [Cites] Crit Rev Biochem Mol Biol. 2007 Nov-Dec;42(6):481-515 [18066955.001]
  • [Cites] Cancer Metastasis Rev. 2008 Mar;27(1):19-30 [18180878.001]
  • [Cites] J Med Chem. 1999 Jan 28;42(2):221-8 [9925727.001]
  • [Cites] EMBO J. 1999 Jul 1;18(13):3546-57 [10393171.001]
  • [Cites] J Mol Biol. 2005 Oct 14;353(1):53-67 [16157350.001]
  • [Cites] Bioorg Med Chem. 2000 Sep;8(9):2249-61 [11026538.001]
  • (PMID = 19106107.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112278; United States / NCI NIH HHS / CA / CA46462; United States / NCI NIH HHS / CO / N01-CO-12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Disaccharides; 0 / Enzyme Inhibitors; 0 / Selectins; EC 2.4.1.- / Galactosyltransferases; EC 2.4.1.- / beta1,4-galactosyltransferase, human
  • [Other-IDs] NLM/ PMC2643505
  •  go-up   go-down


57. Feril LB Jr, Tsuda Y, Kondo T, Zhao QL, Ogawa R, Cui ZG, Tsukada K, Riesz P: Ultrasound-induced killing of monocytic U937 cells enhanced by 2,2'-azobis(2-amidinopropane) dihydrochloride. Cancer Sci; 2004 Feb;95(2):181-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrasound-induced killing of monocytic U937 cells enhanced by 2,2'-azobis(2-amidinopropane) dihydrochloride.
  • To determine the effect of 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) on ultrasound (US)-induced cell killing, human monocytic leukemia cells (U937) were incubated at various temperatures (25.0, 37.0 and 40.0 degrees C) for 1 min in air-saturated phosphate-buffered solution (PBS) containing 50 mM AAPH before exposure to nonthermal 1 MHz US for 1 min at an intensity of 2.0 W/cm(2).
  • The results showed that US-induced cell lysis and apoptosis were enhanced in the presence of AAPH regardless of the temperature at the time of sonication.
  • Although free radicals were increased in the combined treatment, this increase did not correlate well with cell killing.
  • These findings suggest the clinical potential of temperature-dependent free radical generators in cancer therapy with therapeutic US.
  • [MeSH-major] Amidines / pharmacology. Apoptosis / drug effects. Sonication. Temperature

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14965370.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amidines; 0 / Free Radicals; 13217-66-8 / 2,2'-azobis(2-amidinopropane)
  •  go-up   go-down


58. Yu C, Rahmani M, Dai Y, Conrad D, Krystal G, Dent P, Grant S: The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process. Cancer Res; 2003 Apr 15;63(8):1822-33
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process.
  • The impact of disruption of the PI3K (phosphatidylinositol 3-kinase) pathway on the response of human leukemia cells to pharmacological cyclin-dependent kinase (CDK) inhibitors has been examined.
  • Exposure of U937 monocytic leukemia cells to minimally toxic concentrations of flavopiridol (FP), roscovitine, or CGP74514A for 3 h in conjunction with the PI3K inhibitor LY294002 (abbreviated LY in the article) resulted in a marked decrease in Akt phosphorylation.
  • Similar interactions were observed in a variety of other leukemia cell types (e.g., HL-60, Jurkat, Raji, and NB4).
  • Inducible expression of constitutively active (myristolated) Akt significantly, albeit partially, attenuated apoptosis in Jurkat leukemia cells treated with either FP alone or the combination of FP and LY.
  • Finally, cotreatment with LY and FP resulted in a dramatic increase in apoptosis in primary leukemic blasts obtained from a patient with acute myeloblastic leukemia.
  • Together, these findings suggest that the PI3K/Akt pathway plays a major role in regulating the apoptotic response of human leukemia cells to pharmacological CDK inhibitors and raise the possibility that combined interruption of CDK- and PI3K-related pathways may represent a novel therapeutic strategy in hematological malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] 2-Aminopurine / analogs & derivatives. 2-Aminopurine / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Chromones / pharmacology. Drug Synergism. Flavonoids / pharmacology. Humans. Morpholines / pharmacology. Piperidines / pharmacology. Proto-Oncogene Proteins c-akt. Purines / pharmacology. Tumor Cells, Cultured


59. Dai Y, Yu C, Singh V, Tang L, Wang Z, McInistry R, Dent P, Grant S: Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells. Cancer Res; 2001 Jul 1;61(13):5106-15
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells.
  • Interactions between the checkpoint abrogator UCN-01 and several pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase (MEK)/MAPK pathway have been examined in a variety of human leukemia cell lines.
  • Exposure of U937 monocytic leukemia cells to a marginally toxic concentration of UCN-01 (e.g., 150 nM) for 18 h resulted in phosphorylation/activation of p42/44 MAPK.
  • Similar interactions were noted in the case of other MEK inhibitors (e.g., PD98059; U0126) as well as in multiple other leukemia cell types (e.g., HL-60, Jurkat, CCRF-CEM, and Raji).
  • Lastly, although UCN-01 +/- PD184352 did not induce p21(CIP1), stable expression of a p21(CIP1) antisense construct significantly increased susceptibility to this drug combination.
  • [MeSH-major] Alkaloids / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. MAP Kinase Signaling System / drug effects. Mitochondria / drug effects. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • [MeSH-minor] Benzamides / administration & dosage. Benzamides / pharmacology. Butadienes / administration & dosage. Butadienes / pharmacology. Caspases / metabolism. Drug Synergism. Enzyme Activation. Flavonoids / administration & dosage. Flavonoids / pharmacology. HL-60 Cells / drug effects. HL-60 Cells / enzymology. Humans. Jurkat Cells / drug effects. Jurkat Cells / enzymology. Nitriles / administration & dosage. Nitriles / pharmacology. Staurosporine / analogs & derivatives. Tumor Cells, Cultured. U937 Cells / drug effects. U937 Cells / enzymology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11431348.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 63753; United States / NCI NIH HHS / CA / CA 77141; United States / NIDDK NIH HHS / DK / DK 52825
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide; 0 / Alkaloids; 0 / Benzamides; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Nitriles; 0 / U 0126; 7BU5H4V94A / 7-hydroxystaurosporine; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.22.- / Caspases; H88EPA0A3N / Staurosporine
  •  go-up   go-down


60. Rand JH, Wu XX, Quinn AS, Chen PP, Hathcock JJ, Taatjes DJ: Hydroxychloroquine directly reduces the binding of antiphospholipid antibody-beta2-glycoprotein I complexes to phospholipid bilayers. Blood; 2008 Sep 1;112(5):1687-95
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment with the antimalarial drug hydroxychloroquine (HCQ) has been associated with reduced risk of thrombosis in the antiphospholipid (aPL) syndrome (APS) and, in an animal model of APS, with reduction of experimentally induced thrombosis.
  • HCQ, at concentrations of 1 mug/mL and greater, significantly reduced the binding of aPL-beta2GPI complexes to phospholipid surfaces and THP-1 (human acute monocytic leukemia cell line) monocytes.
  • The drug also reduced the binding of the individual proteins to bilayers.
  • These results support the possibility that HCQ, or analogous molecules, may offer novel nonanticoagulant therapeutic strategies for treating APS.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arthritis Rheum. 2007 Aug;56(8):2687-97 [17665396.001]
  • [Cites] Arthritis Rheum. 2005 May;52(5):1473-80 [15880829.001]
  • [Cites] Thromb Haemost. 1999 Oct;82(4):1376-7 [10544942.001]
  • [Cites] EMBO J. 1999 Nov 15;18(22):6228-39 [10562535.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3460-6 [10828029.001]
  • [Cites] Thromb Haemost. 2000 Sep;84(3):388-95 [11019960.001]
  • [Cites] Circulation. 2001 Feb 20;103(7):941-6 [11181467.001]
  • [Cites] Circ Res. 2002 Jan 11;90(1):29-37 [11786515.001]
  • [Cites] Thromb Haemost. 2002 Mar;87(3):518-22 [11916085.001]
  • [Cites] Lupus. 2002;11(6):356-61 [12139373.001]
  • [Cites] Rheumatology (Oxford). 2002 Aug;41(8):924-9 [12154210.001]
  • [Cites] Mol Immunol. 2002 Oct;39(5-6):299-311 [12220888.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1827-32 [12393574.001]
  • [Cites] Am J Pathol. 2003 Sep;163(3):1193-200 [12937161.001]
  • [Cites] N Engl J Med. 2003 Sep 18;349(12):1133-8 [13679527.001]
  • [Cites] Drugs. 1975;9(1):19-76 [1092540.001]
  • [Cites] Thromb Res. 1982 Feb 1;25(3):219-27 [6175045.001]
  • [Cites] Prog Clin Biol Res. 1982;89:31-62 [7051035.001]
  • [Cites] Am J Med. 1988 Oct 14;85(4A):53-6 [3177431.001]
  • [Cites] Br J Clin Pharmacol. 1989 Jun;27(6):771-9 [2757893.001]
  • [Cites] J Clin Immunol. 1992 Jan;12(1):27-35 [1372614.001]
  • [Cites] Semin Arthritis Rheum. 1993 Oct;23(2 Suppl 1):82-91 [8278823.001]
  • [Cites] J Immunol. 1995 Jan 15;154(2):954-60 [7814895.001]
  • [Cites] Scand J Rheumatol. 1996;25(4):191-3 [8792794.001]
  • [Cites] Ann Rheum Dis. 2005 Sep;64(9):1321-5 [15731290.001]
  • [Cites] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]
  • [Cites] JAMA. 2006 Mar 1;295(9):1050-7 [16507806.001]
  • [Cites] Nat Clin Pract Rheumatol. 2006 Sep;2(9):458-9 [16951696.001]
  • [Cites] Arthritis Rheum. 2007 May;56(5):1638-47 [17469158.001]
  • [Cites] Ann Rheum Dis. 2007 Jun;66(6):821-4 [17324970.001]
  • [Cites] Curr Rheumatol Rep. 2007 Jun;9(3):198-204 [17531172.001]
  • [Cites] Lupus. 1996 Jun;5 Suppl 1:S11-5 [8803904.001]
  • [Cites] Lupus. 1996 Jun;5 Suppl 1:S23-7 [8803906.001]
  • [Cites] Biochemistry. 1996 Oct 29;35(43):13833-42 [8901526.001]
  • [Cites] N Engl J Med. 1997 Jul 17;337(3):154-60 [9219701.001]
  • [Cites] Biochemistry. 1997 Nov 25;36(47):14384-91 [9398156.001]
  • [Cites] Circulation. 1997 Dec 16;96(12):4380-4 [9416907.001]
  • [Cites] Lupus. 1998;7(2):80-5 [9541091.001]
  • [Cites] Blood. 1998 Sep 1;92(5):1652-60 [9716593.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):102-9 [10233371.001]
  • [Cites] EMBO J. 1999 Oct 1;18(19):5166-74 [10508150.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3598-602 [15315975.001]
  • [Cites] J Thromb Haemost. 2005 May;3(5):848-53 [15869575.001]
  • [Cites] Biochem J. 2005 Aug 1;389(Pt 3):665-73 [15813706.001]
  • (PMID = 18577708.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL061331; United States / NHLBI NIH HHS / HL / HL-61331
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Antigen-Antibody Complex; 0 / Antimalarials; 0 / Lipid Bilayers; 0 / Multiprotein Complexes; 0 / Phospholipids; 0 / beta 2-Glycoprotein I; 4QWG6N8QKH / Hydroxychloroquine
  • [Other-IDs] NLM/ PMC2518879
  •  go-up   go-down


61. Masurier C, Boutin S, Veron P, Bernard J, Danos O, Davoust J: Enhanced lentiviral transduction of monocyte-derived dendritic cells in the presence of conditioned medium from dying monocytes. Hum Gene Ther; 2007 Feb;18(2):161-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This enhanced transduction efficiency requires the presence of MCM during the initial stage of LV transduction and does not affect the phenotype and antigen presentation function of terminally differentiated Mo-DCs.
  • Importantly, we found that MCM derived from a human acute monocytic leukemia cell line, THP-1, was equally effective.
  • [MeSH-major] Culture Media, Conditioned / pharmacology. Dendritic Cells / cytology. Dendritic Cells / drug effects. Lentivirus / genetics. Monocytes / cytology. Monocytes / secretion. Transduction, Genetic / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17326725.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned
  •  go-up   go-down


62. Tasaka T, Nagai M, Matsuhashi Y, Uehara E, Tamura T, Ishida T, Kakazu N, Abe T: Secondary acute monocytic leukemia with a translocation t(8;22)(p11;q13). Haematologica; 2002 May;87(5):ECR19

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute monocytic leukemia with a translocation t(8;22)(p11;q13).
  • [MeSH-major] Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 8. Leukemia, Monocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Acetyltransferases / genetics. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Histone Acetyltransferases. Humans. Male. Middle Aged. Nuclear Proteins / genetics. Trans-Activators / genetics. Waldenstrom Macroglobulinemia / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12010682.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Trans-Activators; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  •  go-up   go-down






Advertisement