[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 23 of about 23
1. Han SB, Lim J, Kim Y, Kim HJ, Han K: A variant acute promyelocytic leukemia with t(11;17) (q23;q12); ZBTB16-RARA showing typical morphology of classical acute promyelocytic leukemia. Korean J Hematol; 2010 Jun;45(2):133-5
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] A variant acute promyelocytic leukemia with t(11;17) (q23;q12); ZBTB16-RARA showing typical morphology of classical acute promyelocytic leukemia.
  • A subgroup of acute leukemia with morphology resembling acute promyelocytic leukemia (APL) shows variant translocations involving RARA and has a different morphology from that of classical APL.
  • The variant APL with t(11;17)(q23;q12); ZBTB16-RARA subgroup has been reported to have leukemic cells with regular nuclei, many granules, absence of Auer rods, an increased number of Pelgeroid neutrophils, strong myeloperoxidase (MPO) activity, and all-trans-retinoic-acid (ATRA) resistance.
  • Here, we report a case of variant APL with t(11;17)(q23;q12); ZBTB16-RARA showing typical morphological features of classical APL, including numerous Auer rods and faggot cells.
  • The diagnosis was confirmed by cytogenetic and molecular studies.
  • To distinguish variant APL cases from classical APL cases, regardless of whether morphologically the findings are consistent with those of classical APL, combining morphologic, immunophenotypic, cytogenetic, and molecular studies before chemotherapy is very important.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21120193.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983015
  • [Keywords] NOTNLM ; APL / PLZF / ZBTB16-RARA / t(11;17)
  •  go-up   go-down


2. Hamada M, Nishio K, Doe M, Usuki Y, Tanaka T: Farnesylpyridinium, an analog of isoprenoid farnesol, induces apoptosis but suppresses apoptotic body formation in human promyelocytic leukemia cells. FEBS Lett; 2002 Mar 13;514(2-3):250-4
Hazardous Substances Data Bank. FARNESOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Farnesylpyridinium, an analog of isoprenoid farnesol, induces apoptosis but suppresses apoptotic body formation in human promyelocytic leukemia cells.
  • 1-Farnesylpyridinium (FPy), an analog of isoprenoid farnesol, initially induced morphological changes similar to those of typical apoptosis in human leukemia HL-60 cells but FPy-treated cells were characterized by the absolute absence of final apoptotic events such as fragmentation into apoptotic bodies.
  • At concentrations too low to induce apoptosis, FPy could suppress the induction of apoptotic body formation in HL-60 cells by typical inducers of apoptosis such as actinomycin D or anisomycin.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Cytochalasin B / analogs & derivatives. Farnesol / analogs & derivatives. Inclusion Bodies / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Pyridinium Compounds / pharmacology. Sesquiterpenes / pharmacology
  • [MeSH-minor] Actin Cytoskeleton / drug effects. Actin Cytoskeleton / metabolism. Caspase Inhibitors. Cysteine Proteinase Inhibitors / pharmacology. DNA / metabolism. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. HL-60 Cells. Humans. Mitochondria / drug effects. Mitochondria / physiology. Nucleic Acid Synthesis Inhibitors / pharmacology. Protein Synthesis Inhibitors / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTOCHALASIN B .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11943160.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Protein Synthesis Inhibitors; 0 / Pyridinium Compounds; 0 / Sesquiterpenes; 0 / farnesylpyridinium; 39156-67-7 / dihydrocytochalasin B; 3CHI920QS7 / Cytochalasin B; 4602-84-0 / Farnesol; 9007-49-2 / DNA
  •  go-up   go-down


3. Avvisati G, Petti MC, Lo-Coco F, Vegna ML, Amadori S, Baccarani M, Cantore N, Di Bona E, Ferrara F, Fioritoni G, Gallo E, Invernizzi R, Lazzarino M, Liso V, Mariani G, Ricciuti F, Selleri C, Sica S, Veneri D, Mandelli F, GIMEMA (Gruppo Italiano Malattie Ematologische dell'Adulto) Italian Cooperative Group: Induction therapy with idarubicin alone significantly influences event-free survival duration in patients with newly diagnosed hypergranular acute promyelocytic leukemia: final results of the GIMEMA randomized study LAP 0389 with 7 years of minimal follow-up. Blood; 2002 Nov 1;100(9):3141-6
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] Induction therapy with idarubicin alone significantly influences event-free survival duration in patients with newly diagnosed hypergranular acute promyelocytic leukemia: final results of the GIMEMA randomized study LAP 0389 with 7 years of minimal follow-up.
  • Shortly before the all-trans retinoic acid (ATRA) era, the GIMEMA cooperative group initiated a randomized study comparing idarubicin (IDA) alone with IDA plus arabinosylcytosine (Ara-C) as induction treatment in patients with newly diagnosed hypergranular acute promyelocytic leukemia (APL).
  • Of the 257 patients evaluable for induction treatment, 131 were randomized to receive IDA alone (arm A) and 126 to receive IDA + Ara-C (arm B).
  • Treatment in arm A consisted of 10 mg/m(2) IDA daily for 6 consecutive days, whereas in arm B it consisted of 12 mg/m(2) IDA daily for 4 days combined with 200 mg/m(2) Ara-C daily in continuous infusion for 7 days.
  • Once in complete remission (CR), patients received 3 consolidation courses of standard chemotherapy, and those still in CR at the end of the consolidation were randomized to receive or not receive 1 mg/kg 6-mercaptopurine daily and intramuscular injections of 0.25 mg/kg methotrexate weekly for 2 years.
  • Multivariate analysis revealed that EFS was favorably influenced by induction treatment with IDA alone (P =.0352) and unfavorably influenced by white blood cell (WBC) counts greater than 3000/microL (P =.0001) and increasing age (P =.0251).
  • These results indicate that anthracycline monochemotherapy with IDA favorably influences the EFS of patients with newly diagnosed hypergranular APL.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Idarubicin / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects. Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Cytarabine / administration & dosage. Cytarabine / adverse effects. Disease-Free Survival. Drug-Induced Liver Injury / etiology. Female. Follow-Up Studies. Hemorrhage / chemically induced. Humans. Infection / etiology. Leukocyte Count. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Middle Aged. Remission Induction. Treatment Outcome. Vomiting / chemically induced

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cancer Treat Rev. 2003 Apr;29(2):143-6 [12670460.001]
  • (PMID = 12384411.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 04079A1RDZ / Cytarabine; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate; ZRP63D75JW / Idarubicin
  •  go-up   go-down


Advertisement
4. Liu J, Hu WX, He LF, Ye M, Li Y: Effects of lycorine on HL-60 cells via arresting cell cycle and inducing apoptosis. FEBS Lett; 2004 Dec 17;578(3):245-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • HL-60 cells exhibited typical apoptotic morphological changes, apoptotic DNA "ladder" pattern, and sub-G1 peak in cell phase distribution, showing apoptosis of HL-60 cells.
  • Our finding suggests that lycorine can suppress leukemia growth and reduce cell survival via arresting cell cycle and inducing apoptosis of tumor cells.
  • [MeSH-major] Amaryllidaceae Alkaloids / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Phenanthridines / pharmacology
  • [MeSH-minor] Blotting, Western. Caspases / analysis. Caspases / drug effects. Caspases / metabolism. Cell Survival. Colorimetry. Cytotoxicity Tests, Immunologic. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Flow Cytometry. G2 Phase / drug effects. HL-60 Cells. Humans. Inhibitory Concentration 50. Leukemia, Promyelocytic, Acute / drug therapy. Microscopy, Fluorescence. Proto-Oncogene Proteins c-bcl-2 / analysis. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. bcl-2-Associated X Protein

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15589827.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amaryllidaceae Alkaloids; 0 / Antineoplastic Agents, Phytogenic; 0 / BAX protein, human; 0 / Phenanthridines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspases; I9Q105R5BU / lycorine
  •  go-up   go-down


5. Tanaka Y, Komatsu H, Ishii K, Nakamura F, Hayashi T, Sawada H, Ono Y, Imanaka T: [Successful treatment of relapsed and refractory acute promyelocytic leukemia with arsenic trioxide (As2O3)]. Rinsho Ketsueki; 2000 Apr;41(4):354-7
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful treatment of relapsed and refractory acute promyelocytic leukemia with arsenic trioxide (As2O3)].
  • It has been shown that arsenic trioxide (As2O3) may induce hematologic remissions in patients with acute promyelocytic leukemia (APL) refractory to all-trans retinoic acid (ATRA).
  • We reported on a patient with ATRA and drug-resistant APL that was successfully treated with As2O3.
  • The patient had been given a diagnosis of typical APL and was treated with ATRA and chemotherapy for 12 months.
  • He achieved complete remission (CR), but leukemia relapsed with 43% APL cells in the bone marrow in the 16th month of treatment.
  • These results demonstrated the therapeutic efficacy of As2O3 in treating ATRA and drug-resistant APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasm Recurrence, Local. Oxides / therapeutic use
  • [MeSH-minor] Adult. Drug Resistance, Neoplasm. Humans. Idarubicin / therapeutic use. Male. Pleural Effusion / chemically induced. Pleural Effusion / drug therapy. Remission Induction. Treatment Outcome. Tretinoin / pharmacology

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10846468.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide; ZRP63D75JW / Idarubicin
  •  go-up   go-down


6. Elezović I, Colović M, Tomin D, Bosković D: Pregnancy after treatment of secondary acute promyelocytic leukemia following Hodgkin's disease: a case report. Med Oncol; 2000 Aug;17(3):222-4
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pregnancy after treatment of secondary acute promyelocytic leukemia following Hodgkin's disease: a case report.
  • The authors report a case of therapy-related acute promyelocytic leukemia (t-APL), with typical cytogenetic translocation t(15;17), which appeared following chemotherapy (ABVD), and radiotherapy for Hodgkin's disease (IIB).
  • After treatment with all-trans retinoic acid (Vesanoid(R) 45 mg/m2 daily) complete remission of t-APL was achieved.
  • Then only one course of chemotherapy '3+7' (doxorubicin 45 mg/m2 1-3 d, cytosar 200 mg/m2 1-7d) was applied and the patient interrupted further treatment in July 1994.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hodgkin Disease / drug therapy. Leukemia, Promyelocytic, Acute / chemically induced. Neoplasms, Second Primary / drug therapy
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Bleomycin / administration & dosage. Dacarbazine / administration & dosage. Doxorubicin / administration & dosage. Female. Humans. Pregnancy. Pregnancy Outcome. Treatment Outcome. Tretinoin / therapeutic use. Vinblastine / administration & dosage

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Genetic Alliance. consumer health - Pregnancy.
  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • Hazardous Substances Data Bank. BLEOMYCIN .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1996 Sep;94(4):699-701 [8826895.001]
  • [Cites] J Clin Pathol. 1994 Jun;47(6):565-6 [8063946.001]
  • [Cites] Cancer. 1995 Dec 1;76(11):2237-41 [8635026.001]
  • [Cites] Ann Oncol. 1995 Oct;6(8):777-9 [8589014.001]
  • [Cites] Haematologica. 1998 Sep;83(9):812-23 [9825578.001]
  • [Cites] Obstet Gynecol. 1997 May;89(5 Pt 2):826-8 [9166337.001]
  • [Cites] Blood. 1994 Aug 15;84(4):1209-15 [8049435.001]
  • [Cites] Am J Hematol. 1999 Apr;60(4):300-4 [10203104.001]
  • [Cites] Med Oncol. 1997 Jun;14(2):65-72 [9330265.001]
  • [Cites] Cancer Treat Rep. 1983 Jun;67(6):603-4 [6190561.001]
  • [Cites] Leukemia. 1996 Jan;10(1):178-82 [8558926.001]
  • [Cites] Rinsho Ketsueki. 1997 Sep;38(9):770-5 [9364869.001]
  • (PMID = 10962534.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11056-06-7 / Bleomycin; 5688UTC01R / Tretinoin; 5V9KLZ54CY / Vinblastine; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; ABVD protocol
  •  go-up   go-down


7. Schwarz J, Kacírková P, Marková J, Mikulenková D, Marinov I, Ballingová I, Michalová K: [Urgent states in hematology: acute promyelocytic leukemia--principles of diagnosis]. Vnitr Lek; 2008 Jul-Aug;54(7-8):728-44
MedlinePlus Health Information. consumer health - Blood Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Urgent states in hematology: acute promyelocytic leukemia--principles of diagnosis].
  • A review of diagnosis of acute promyelocytic leukemia (APL) is presented.
  • In Czechia, we have, in some instances, noted an unacceptably long time from the first symptoms to diagnosis and to administration of the highly specific differentiation therapy with tretinoin (ATRA) along with anthracycline chemotherapy.
  • In the following more detailed review of diagnostic measures, much attention is given to APL morphology, which is the first clue leading to diagnosis.
  • The finding of the typical hypergranular FAB M3 morphology and of cells with bundles of Auer rods ("faggot cells"), along with the HLA-DR, CD33+ immunophenotype, is highly (but not absolutely) specific for APL.
  • Given that morphology of APL cases, as defined according to WHO criteria (95% of which carry the PML/RARalpha fusion gene), admits extremely divergent morphological pictures ofthe variant forms, we recommend these investigations to be performed in every case of de novo acute myeloid leukemia.
  • [MeSH-major] Hematologic Diseases / diagnosis. Leukemia, Promyelocytic, Acute / diagnosis

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18780572.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 90
  •  go-up   go-down


8. Argani P, Laé M, Ballard ET, Amin M, Manivel C, Hutchinson B, Reuter VE, Ladanyi M: Translocation carcinomas of the kidney after chemotherapy in childhood. J Clin Oncol; 2006 Apr 1;24(10):1529-34
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation carcinomas of the kidney after chemotherapy in childhood.
  • PATIENTS AND METHODS: We describe the clinical, pathologic, cytogenetic, and molecular data on six translocation RCCs that arose in five young patients who had received chemotherapy.
  • RESULTS: The ages at time of diagnosis of the RCC ranged from 6 to 22 years.
  • Histologically, these tumors showed typical features previously described for translocation RCCs.
  • The intervals between chemotherapy and the diagnosis of RCC ranged from 4 to 13 years.
  • The indications for the antecedent chemotherapy were varied and included acute promyelocytic leukemia, acute myeloid leukemia with t(9;11), bilateral Wilms' tumor, systemic lupus erythematosus, and conditioning regimen of bone marrow transplant for Hurler's syndrome.
  • Hence, among 39 genetically confirmed translocation RCCs in our personal experience, six (15%) have arisen in patients who had received cytotoxic chemotherapy.
  • CONCLUSION: Cytotoxic chemotherapy may predispose to the development of renal translocation carcinomas.

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16575003.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA95785
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Neoplasm Proteins; 0 / TFE3 protein, human; 0 / TFEB protein, human
  •  go-up   go-down


9. Lobe I, Rigal-Huguet F, Vekhoff A, Desablens B, Bordessoule D, Mounier C, Ferrant A, Sanz M, Fey M, Chomienne C, Chevret S, Degos L, Fenaux P, European APL group experience: Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience. Leukemia; 2003 Aug;17(8):1600-4
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] Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience.
  • With improved treatment of acute promyelocytic leukemia (APL) by all trans retinoic acid (ATRA) combined to anthracycline-aracytin chemotherapy (CT), a larger number of those patients may be at risk of late complications.
  • Recently, the Rome group reported five cases of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML, non-APL) occurring during the course of 77 APL patients (6.5%) in complete remission (CR).
  • With a median follow-up of 51 months, 6 patients (0.97%) developed MDS, 13-74 months after the diagnosis of APL.
  • In all six cases, t(15;17) and PML-RARalpha rearrangement were absent at the time of MDS diagnosis, and karyotype mainly showed complex cytogenetic abnormalities involving chromosomes 5 and/or 7, typical of MDS observed after treatment with alkylating agents, although none of the six patients had received such agents for the treatment of APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / complications. Myelodysplastic Syndromes / etiology
  • [MeSH-minor] Adolescent. Adult. Aged. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Cytarabine / therapeutic use. Cytogenetic Analysis. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Remission Induction. Retrospective Studies. Tretinoin / therapeutic use


10. Mochiduki Y, Muramoto S: [Therapy-related acute promyelocytic leukemia with a t(9;22)(q34;q11) and t(15;17)(q22;q11 to approximately 12) subclone]. Rinsho Ketsueki; 2005 Nov;46(11):1218-22
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] [Therapy-related acute promyelocytic leukemia with a t(9;22)(q34;q11) and t(15;17)(q22;q11 to approximately 12) subclone].
  • The translocation (15;17) is a typical marker of acute promyelocytic leukemia, whereas t(9;22) is predominantly associated with chronic myelogenous leukemia, and seldom with acute myelogenous leukemia.
  • We present a case of therapy-related acute promyelocytic leukemia (t-APL) with a subclone accompanied by karyotype 46, XX, t(9; 22)(q34;q11), t(15 ;17)(q22;11 to approximately 12) at onset.
  • In June 2000, having developed t-APL, she was referred to our department.
  • The patient attained CR following treatment with chemotherapy containing all-trans retinoic acid.
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cyclophosphamide / adverse effects. Doxorubicin / adverse effects. Etoposide / adverse effects. Female. Humans. Karyotyping. Prednisolone / adverse effects. Remission Induction. Tretinoin / therapeutic use. Vincristine / adverse effects

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16440807.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
  •  go-up   go-down


11. Mori A, Wada H, Okada M, Takatsuka H, Tamura A, Fujimori Y, Okamoto T, Takemoto Y, Kanamaru A, Kakishita E: Acute promyelocytic leukemia with marrow fibrosis at initial presentation: possible involvement of transforming growth factor-beta(1). Acta Haematol; 2000;103(4):220-3
Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukemia with marrow fibrosis at initial presentation: possible involvement of transforming growth factor-beta(1).
  • Although the occurrence of marrow fibrosis in acute myeloid leukemia has been described, there have been no reports of acute promyelocytic leukemia (APL) associated with marrow fibrosis.
  • He had the typical manifestations of APL, except for marrow fibrosis.
  • Complete remission was achieved by treatment with all-trans retinoic acid plus chemotherapy, and his marrow fibrosis gradually improved concomitantly with the decrease in leukemic cells.
  • An overexpression of transforming growth factor-beta(1) was noted in his leukemic cells at initial presentation, whereas no increase in expression was observed at the time of relapse when he no longer had marrow fibrosis.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / complications. Primary Myelofibrosis / etiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • [CommentIn] Acta Haematol. 2002;108(2):111-2 [12187033.001]
  • (PMID = 11014898.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Recombinant Fusion Proteins; 0 / Transforming Growth Factor beta; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  •  go-up   go-down


12. Specchia G, Storlazzi CT, Cuneo A, Surace C, Mestice A, Pannunzio A, Rocchi M, Liso V: Acute promyelocytic leukemia with additional chromosome abnormalities in a renal transplant case. Ann Hematol; 2001 Apr;80(4):246-50
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukemia with additional chromosome abnormalities in a renal transplant case.
  • Some cases of acute myeloid leukemia following organ transplant (PT-AML) have been published in the literature.
  • We report the second case of acute promyelocytic leukemia (APL), which developed post-transplant and immunosuppressive treatment, in a 50-year-old male who had undergone a renal transplant.
  • At diagnosis he presented typical t(15;17)(q12;q13) with additional abnormalities, including +8,t(13;22)(q12;q13) and an abnormal chromosome 1 which was better characterized by fluorescence in situ hybridization (FISH).
  • He obtained cytological, karyotypic and molecular complete remission (CR) with induction treatment according to the all-trans retinoic acid + idarubican (AIDA) protocol; after 12 months, he relapsed (molecular relapse) and achieved molecular remission with all-trans retinoic acid (ATRA) plus mitoxantrone and cytosine arabinoside.
  • He is alive 3.3 years after diagnosis of APL.
  • Cyclosporin A (CsA) was given during all cycles of chemotherapy.
  • We did not observe any severe infections or kidney failure during treatments.
  • [MeSH-major] Chromosome Aberrations. Immunosuppressive Agents / adverse effects. Kidney Transplantation / adverse effects. Leukemia, Promyelocytic, Acute / etiology. Leukemia, Promyelocytic, Acute / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 13. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 22. Cytarabine / therapeutic use. Humans. Idarubicin / therapeutic use. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mitoxantrone / therapeutic use. Polycystic Kidney Diseases / surgery. Recurrence. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Tretinoin / therapeutic use

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Kidney Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11401094.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
  •  go-up   go-down


13. Miyazaki K, Kikukawa M, Kiuchi A, Shin K, Iwamoto T, Ohyashiki K: Complex translocations derived stepwise from standard t(15;17) in a patient with variant acute promyelocytic leukemia. Cancer Genet Cytogenet; 2007 Jul 15;176(2):127-30
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex translocations derived stepwise from standard t(15;17) in a patient with variant acute promyelocytic leukemia.
  • We report the case of an elderly man with an acute promyelocytic leukemia variant carrying complex variant translocations.
  • The Q-banded karyotype and spectral karyotyping method revealed a typical t(15;17), and two complex rearrangements caused by stepwise translocation derived from a typical t(15;17).
  • The patient received induction chemotherapy using all-trans retinoic acid and achieved complete remission.
  • To our knowledge, a case with complex rearrangements, caused by apparent stepwise translocation, at diagnosis, has not been reported previously.
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Humans. Male. Oncogene Proteins, Fusion / genetics. Tretinoin / therapeutic use

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17656255.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
  •  go-up   go-down


14. Chen B, Xu X, Ji M, Lin G: Myeloid/NK cell acute leukemia. Int J Hematol; 2009 Apr;89(3):365-7
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] Myeloid/NK cell acute leukemia.
  • Myeloid/NK cell leukemia is distinct entity, being different from the myeloid/NK cell precursor acute leukemia and blastic NK cell lymphoma/leukemia in morphology and immunotypes.
  • We reported a typical case with presentation, immunology and cytogenetic results.
  • The morphology of leukemia cells in bone marrow was similar to that of acute promyelocytic leukemia.
  • The leukemia cells express CD13, CD33, CD15, and CD56, not expressing CD34, HLA-DR and CD16.
  • The patients were given chemotherapy as acute myeloid leukemia, and got complete remission.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Antigens, CD / immunology. Antigens, CD / metabolism. Antineoplastic Agents / therapeutic use. Humans. Male. Middle Aged. Physical Examination

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Haematologica. 2000 Mar;85(3):322-4 [10702827.001]
  • [Cites] Blood. 1994 Jul 1;84(1):244-55 [7517211.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2417-28 [9310493.001]
  • (PMID = 19326059.001).
  • [ISSN] 1865-3774
  • [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 / Antigens, CD; 0 / Antineoplastic Agents
  •  go-up   go-down


15. Qiu H, Wang W, Cen J, Pan J, Wang Y, Fu J, Chen Z: [Study on the differentiation and apoptosis of promyelocytic leukemia cells induced by tributyrin]. Zhonghua Xue Ye Xue Za Zhi; 2000 Feb;21(2):77-80
Hazardous Substances Data Bank. TRIBUTYRIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study on the differentiation and apoptosis of promyelocytic leukemia cells induced by tributyrin].
  • Treated with 1 mmol/L TB for 24 hours NB4 and MR2 cells exhibited a morphological characteristic of apoptosis and typical DNA ladder on gel electrophoresis.
  • CONCLUSION: TB exerts synergetic effect on ATRA-induced differentiation and induces apoptosis in promyelocytic leukemic cells.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Triglycerides / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Tretinoin / pharmacology

  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11876963.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Triglycerides; 5688UTC01R / Tretinoin; S05LZ624MF / tributyrin
  •  go-up   go-down


16. Okoshi Y, Akiyama H, Kono N, Matsumura T, Mizuchi D, Mori S, Ohashi K, Sakamaki H: Effect of additional chromosomal abnormalities in acute promyelocytic leukemia treated with all-trans-retinoic acid: a report of 17 patients. Int J Hematol; 2001 Jun;73(4):496-501
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of additional chromosomal abnormalities in acute promyelocytic leukemia treated with all-trans-retinoic acid: a report of 17 patients.
  • Seventeen cases of acute promyelocytic leukemia (APL) treated with all-trans-retinoic acid (ATRA) and combination chemotherapy at Tokyo Metropolitan Komagome Hospital between 1992 and 1999 were reviewed, and divided into 2 karyotype-based cytogenetic groups.
  • One group comprised 7 patients with either the typical t(15;17) alone or a normal karyotype, and the other group comprised 10 patients with additional karyotypic abnormalities.
  • No patient had received prior chemotherapy or irradiation, and no cases were complicated by a history of myelodysplastic syndrome before the diagnosis of APL.
  • The analysis did not reveal any significant effect of additional chromosomal abnormalities on the prognosis of APL patients undergoing treatment with ATRA.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Cytogenetic Analysis. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Rinsho Ketsueki. 1989 Jan;30(1):67-71 [2716201.001]
  • [Cites] Cancer Genet Cytogenet. 1988 Jun;32(2):287-92 [3163267.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1786-95 [9164186.001]
  • [Cites] Genes Chromosomes Cancer. 1991 Sep;3(5):332-7 [1797083.001]
  • [Cites] Br J Haematol. 1997 Feb;96(2):314-21 [9029019.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1192-200 [10438706.001]
  • [Cites] Blood. 1997 Aug 1;90(3):1014-21 [9242531.001]
  • [Cites] Blood. 1996 Aug 15;88(4):1390-8 [8695858.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1430-5 [1517786.001]
  • [Cites] EMBO J. 1992 Apr;11(4):1397-407 [1314166.001]
  • [Cites] Br J Haematol. 1996 Sep;94(3):493-500 [8790148.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1264-9 [8394752.001]
  • [Cites] Blood. 1995 Mar 1;85(5):1202-6 [7858250.001]
  • [Cites] Br J Haematol. 1994 Jan;86(1):231-2 [8011541.001]
  • (PMID = 11503965.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  •  go-up   go-down


17. Korístek Z, Zák P: [Coagulopathy and differentiation syndrome: the main complications of the initial treatment of acute promyelocytic leukemia]. Vnitr Lek; 2008 Jul-Aug;54(7-8):745-50
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Coagulopathy and differentiation syndrome: the main complications of the initial treatment of acute promyelocytic leukemia].
  • Two main causes of early mortality of acute promyelocytic leukemia (APL) are rewieved, unique type ofcoagulopathy typical for APL and differentiation syndrome sometimes complicating treatment of APL with all-trans retinoic acid (ATRA) or arsenic trioxide (ATO).
  • The information covers analysis of the patophysiologies of both conditions and also recommendations considering treatments and preventive measures.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Disseminated Intravascular Coagulation / etiology. Leukemia, Promyelocytic, Acute / drug therapy. Leukocytosis / chemically induced. Oxides / adverse effects. Respiratory Insufficiency / chemically induced. Tretinoin / adverse effects

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Respiratory Failure.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18780573.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 43
  •  go-up   go-down


18. Kurian S, Hogan TF, Bleigh OC, Dowdy YG, Merghoub T, Pandolfi PP, Wenger SL: Atypical t(15;17)(q13;q12) in a patient with all-trans retinoic acid refractory secondary acute promyelocytic leukemia: a case report and review of the literature. Cancer Genet Cytogenet; 2002 Oct 15;138(2):143-8
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical t(15;17)(q13;q12) in a patient with all-trans retinoic acid refractory secondary acute promyelocytic leukemia: a case report and review of the literature.
  • A 69-year-old woman developed microgranular acute promyelocytic leukemia (APL-M3) 10 months after receiving adjuvant cyclophosphamide, doxorubicin, and paclitaxel for breast cancer.
  • Replicate bone marrow aspirate karyotypes contained a translocation between the long arms of chromosomes 15 and 17, but not at breakpoints typical for APL.
  • Although the patient received induction chemotherapy and a several month trial of all-trans retinoic acid (ATRA), there was no clinical improvement or hematological remission.
  • We suspect that this patient developed postchemotherapy secondary APL with an atypical t(15;17), which rendered her leukemic cells unresponsive to ATRA therapy.
  • [MeSH-major] Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Drug Resistance, Neoplasm. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Aged. Bone Marrow / pathology. Breast Neoplasms / complications. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Chromosome Breakage / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Cancer Genet Cytogenet. 2003 May;143(1):92
  • (PMID = 12505260.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
  • [Number-of-references] 38
  •  go-up   go-down


19. La Fianza A, Bonfichi M, Gorone MS, Gallotti A, Torretta L: Unusual abdominal findings of all-trans-retinoic acid syndrome: role of diagnostic imaging. Clin Imaging; 2007 Jul-Aug;31(4):276-8
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The standard therapy for patients affected by acute promyelocytic leukemia is based on all-trans-retinoic acid (ATRA), whose rare complication is a syndrome known as retinoic acid syndrome.
  • We describe for the first time the computed tomography findings of a case of ATRA syndrome with typical pulmonary findings, along with the involvement of the upper abdomen organs (liver and spleen) as a further complication of the pathology.
  • [MeSH-major] Abdomen / pathology. Abdomen / ultrasonography. Leukemia, Promyelocytic, Acute / complications. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects. Tretinoin / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Fatal Outcome. Humans. Male. Syndrome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17599624.001).
  • [ISSN] 0899-7071
  • [Journal-full-title] Clinical imaging
  • [ISO-abbreviation] Clin Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  •  go-up   go-down


20. Zhong L, Chen F, Han J, Shao N, Ouyang R: Effects of red orpiment on cell morphology and expression of PML mRNA and protein in NB4 and HL-60 cells. Chin Med J (Engl); 2003 Jan;116(1):148-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To investigate the effects of red orpiment on cell morphology, expression of promyelocytic leukemia (PML) mRNA and its protein localization in NB4 and HL-60 cell lines.
  • RESULTS: The typical apoptosis was found in NB4 and HL-60 cells after treatment with red orpiment.
  • The expression of promyelocytic leukemia (PML) mRNA was not changed in the treated cells.
  • CONCLUSION: Red orpiment inhibits the proliferation of leukemia cells by inducing them to undergo apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Medicine, Chinese Traditional. Neoplasm Proteins / genetics. Nuclear Proteins. Transcription Factors / genetics
  • [MeSH-minor] Apoptosis / drug effects. HL-60 Cells. Humans. RNA, Messenger / analysis. Tumor Cells, Cultured. Tumor Suppressor Proteins

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12667410.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  •  go-up   go-down


21. Han B, Zhou G, Zhang Q, Zhang J, Wang X, Tang W, Kakudo K: Effect of arsenic trioxide (ATO) on human lung carcinoma PG cell line: ATO induced apoptosis of PG cells and decreased expression of Bcl-2, Pgp. J Exp Ther Oncol; 2004 Dec;4(4):335-42
Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Arsenic trioxide (ATO) has been established to be an effective agent for treating newly diagnosed and relapsed acute promyelocytic leukemia (APL) patients.
  • We found ATO significantly inhibited the proliferation of PG cells in a dose- and time-dependent manner.
  • ATO-induced apoptosis of PG cells was confirmed by the observance of typical morphological changes and detected by the analysis of flow cytometry (FCM).
  • [MeSH-major] Apoptosis. Arsenicals / pharmacology. Carcinoma / drug therapy. Carcinoma / metabolism. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Oxides / pharmacology. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Proliferation. Cell Survival. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Immunohistochemistry. In Vitro Techniques. Microscopy, Electron, Scanning. Microscopy, Electron, Transmission. Microscopy, Phase-Contrast. Time Factors

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15844663.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


22. Niu YP, Wu LM, Jiang YL, Wang WX, Li LD: Beta-escin, a natural triterpenoid saponin from Chinese horse chestnut seeds, depresses HL-60 human leukaemia cell proliferation and induces apoptosis. J Pharm Pharmacol; 2008 Sep;60(9):1213-20
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] Beta-escin, a natural triterpenoid saponin from Chinese horse chestnut seeds, depresses HL-60 human leukaemia cell proliferation and induces apoptosis.
  • Beta-escin, a natural triterpenoid saponin isolated from the seed of the horse chestnut, is known to generate a wide variety of biochemical and pharmacological effects.
  • The purpose of the present study was to examine the apoptotic and antiproliferative activity of beta-escin in HL-60 human acute myeloid leukaemia cells.
  • The results showed that beta-escin caused a significant inhibition of HL-60 cell proliferation in a dose- and time-dependent manner.
  • Typical DNA ladders, DNA with a unit length of about 180 bp, were detected in cells treated with beta-escin (30-50 microg mL(-1)) for 48 h by agarose gel electrophoresis.
  • Taken together, the results demonstrate that beta-escin is a potent natural inhibitor of cell proliferation and inducer of apoptosis in HL-60 acute myeloid leukaemia cells.
  • The results indicate that beta-escin may be a useful candidate agent for exploring potential antileukaemic drugs.
  • [MeSH-major] Aesculus / chemistry. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Escin / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Proliferation / drug effects. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. G1 Phase / drug effects. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / drug therapy. S Phase / drug effects. Seeds. Time Factors

  • 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
  • [RetractionIn] Jones DS. J Pharm Pharmacol. 2009 May;61(5):685 [19406009.001]
  • (PMID = 18718126.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6805-41-0 / Escin
  •  go-up   go-down


23. Zhang XH, Xia LH, Liu ZP, Wei WN, Hu Y, Song SJ: [Experimental study on activating antileukemic T cells by vaccination with dendritic cells pulsed with survivin]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2003 Feb;11(1):66-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The expression of survivin on acute leukemic cells were detected by cofocal microscopy and immunoprecipitation-Western blot.
  • DCs from peripheral blood mononuclear cells were successfully induced, with typical DC morphologic characteristic.
  • In conclusion, survivin antigen expressed in the cytoplasm of leukemic cells, leukemic vaccination with DCs pulsed with survivin antigen in vitro inhibited the proliferation of leukemic cells, that may be a pathway for therapy of leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12667293.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / BIRC5 protein, human; 0 / Cancer Vaccines; 0 / HLA-DR Antigens; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
  •  go-up   go-down






Advertisement