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1. Sanz MA, Grimwade D, Tallman MS, Lowenberg B, Fenaux P, Estey EH, Naoe T, Lengfelder E, Büchner T, Döhner H, Burnett AK, Lo-Coco F: Management of acute promyelocytic leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet. Blood; 2009 Feb 26;113(9):1875-91
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  • [Title] Management of acute promyelocytic leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet.
  • The introduction of all-trans retinoic acid (ATRA) and, more recently, arsenic trioxide (ATO) into the therapy of acute promyelocytic leukemia (APL) has revolutionized the management and outcome of this disease.
  • Cure of APL patients, however, is also dependent on peculiar aspects related to the management and supportive measures that are crucial to counteract life-threatening complications associated with the disease biology and molecularly targeted treatment.
  • The European LeukemiaNet recently appointed an international panel of experts to develop evidence- and expert opinion-based guidelines on the diagnosis and management of APL.
  • Together with providing current indications on genetic diagnosis, modern risk-adapted front-line therapy and salvage treatment, the review contains specific recommendations for the identification and management of most important complications such as the bleeding disorder, APL differentiation syndrome, QT prolongation and other ATRA- and ATO-related toxicities, as well as for molecular assessment of response to treatment.
  • Finally, the approach to special situations is also discussed, including management of APL in children, elderly patients, and pregnant women.
  • [MeSH-major] Health Planning Guidelines. Leukemia, Promyelocytic, Acute / therapy

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  • (PMID = 18812465.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  • [Number-of-references] 148
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2. Tallman MS, Kim HT, Montesinos P, Appelbaum FR, de la Serna J, Bennett JM, Deben G, Bloomfield CD, Gonzalez J, Feusner JH, Gonzalez M, Gallagher R, Miguel JD, Larson RA, Milone G, Paietta E, Rayon C, Rowe JM, Rivas C, Schiffer CA, Vellenga E, Shepherd L, Slack JL, Wiernik PH, Willman CL, Sanz MA: Does microgranular variant morphology of acute promyelocytic leukemia independently predict a less favorable outcome compared with classical M3 APL? A joint study of the North American Intergroup and the PETHEMA Group. Blood; 2010 Dec 16;116(25):5650-9
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  • [Title] Does microgranular variant morphology of acute promyelocytic leukemia independently predict a less favorable outcome compared with classical M3 APL? A joint study of the North American Intergroup and the PETHEMA Group.
  • Few studies have examined the outcome of large numbers of patients with the microgranular variant (M3V) of acute promyelocytic leukemia (APL) in the all-trans retinoic acid era.
  • Here, the outcome of 155 patients treated with all-trans retinoic acid-based therapy on 3 clinical trials, North American Intergroup protocol I0129 and Programa para el Estudio de la Terapéutica en Hemopatía Maligna protocols LPA96 and LPA99, are reported.
  • The incidence of the APL differentiation syndrome was 26%, compared with 25% for classical M3 patients, and the early death rate was 13.6% compared with 8.4% for patients with classical M3 morphology.
  • When outcomes were adjusted for the white blood cell count or the relapse risk score, none of these outcomes were significantly different between patients with M3V and classical M3 APL.

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  • (PMID = 20858857.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / CA12213; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / CA31936; United States / NCI NIH HHS / CA / CA66636; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U10 CA017145; United States / NCI NIH HHS / CA / U10 CA014028; United States / NCI NIH HHS / CA / CA14028; United States / NCI NIH HHS / CA / U10 CA066636; United States / NCI NIH HHS / CA / R01 CA056771; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / N01 CA038926; United States / NCI NIH HHS / CA / U10 CA020319; United States / NCI NIH HHS / CA / U10 CA038926; United States / NCI NIH HHS / CA / U10 CA023318; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA56771
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ PMC3031411
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3. Mandegary A, Mehrabani M: Effects of arsenic trioxide, all-trans-retinoic acid and dexamethasone on NB4 cell line. Daru; 2010;18(4):303-9

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  • BACKGROUND AND THE PURPOSE OF THE STUDY: Experimental and preclinical observations have indicated that combination therapy with all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) may strongly enhance their therapeutic effects in the treatment of acute promyelocytic leukemia (APL).
  • Whilst dexamethasone (Dex) is routinely used for the control of APL- differentiation syndrome, its effect on the pharmacodynamics of ATO is not clear.
  • Therefore, in this study, effects of therapeutic concentrations of ATO, ATRA and Dex and their sequential usages on the proliferation, differentiation and apoptosis in t(15;17)-positive NB4 cells was investigated.
  • Expression of CD11b as an indicator of cell differentiation and the percentage of 7-AAD positive cells as a marker of apoptosis were determined by flow cytometry.
  • CONCLUSION: No improvement or antagonistic effects was observed with the pretreatment/ combination of the ATO and ATRA on the differentiation and apoptosis of the cells.
  • It is possible that concomitant usage of Dex with apoptotic doses of ATO in APL patients counteract therapeutic effects of ATO.

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  • (PMID = 22615633.001).
  • [ISSN] 1560-8115
  • [Journal-full-title] Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences
  • [ISO-abbreviation] Daru
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Other-IDs] NLM/ PMC3304349
  • [Keywords] NOTNLM ; ATO / ATRA / Apoptosis. / Combination therapy / Dexamethasone
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4. Tallman M, Douer D, Gore S, Powell BL, Ravandi F, Rowe J, Ranganathan A, Sanz MA: Treatment of patients with acute promyelocytic leukemia: a consensus statement on risk-adapted approaches to therapy. Clin Lymphoma Myeloma Leuk; 2010 Oct;10 Suppl 3:S122-6
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  • [Title] Treatment of patients with acute promyelocytic leukemia: a consensus statement on risk-adapted approaches to therapy.
  • The integration of all-trans-retinoic acid (ATRA) with anthracycline chemotherapy into up-front regimens for acute promyelocytic leukemia (APL) has produced striking improvements in clinical outcomes, making APL one of the most curable forms of hematologic malignancies in adults.
  • Cure in APL is also largely dependent on timely and effective supportive care measures that counteract such life-threatening emergencies as coagulopathy and APL differentiation syndrome.
  • Multiple European and North American trials have investigated risk-adapted approaches to the treatment of APL and have reported high success rates.
  • A roundtable conference was conducted to discuss risk-adapted therapy for APL and to develop a consensus statement and approach for clinical oncologists.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 21115429.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Consensus Development Conference; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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5. Au WY, Kwong YL: Arsenic trioxide: safety issues and their management. Acta Pharmacol Sin; 2008 Mar;29(3):296-304
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  • Its therapeutic use in leukaemia was described a century ago.
  • Recent rekindling in the interest of As2O3 is due to its high efficacy in acute promyelocytic leukaemia (APL).
  • During induction therapy in APL, a leucocytosis may occasionally occur, which can be associated with fluid accumulation and pulmonary infiltration.
  • The condition is similar to the APL differentiation syndrome during treatment with all-trans retinoic acid, and responds to cytoreductive treatment and corticosteroids.

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  • (PMID = 18298894.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Prodrugs; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 68
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6. Shibakura M, Niiya K, Niiya M, Asaumi N, Yoshida C, Nakata Y, Tanimoto M: Induction of CXC and CC chemokines by all-trans retinoic acid in acute promyelocytic leukemia cells. Leuk Res; 2005 Jul;29(7):755-9
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  • [Title] Induction of CXC and CC chemokines by all-trans retinoic acid in acute promyelocytic leukemia cells.
  • We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA.
  • We, therefore, further investigated the effects of ATRA on the expression of chemokine family in NB4 cells and APL cells prepared from two APL patients.
  • APL cells prepared from two APL patients showed gene expression of chemokines, such as IL-8, MCP-1, MIP-1alpha, and MIP-1beta when stimulated with ATRA in vitro.
  • Furthermore, serum levels of IL-8, MIP-1beta and RANTES were increased during the course of ATRA treatment in both APL patients who developed APL differentiation syndrome.
  • These chemokines are all chemoattractants of particular inflammatory cell types, including neutrophils, monocytes and lymphocytes; therefore, the simultaneous induction of these chemokines after stimulation with ATRA may exacerbate the hyper-inflammation observed in ATRA-induced APL differentiation syndrome.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Base Sequence. Blotting, Northern. Cell Line, Tumor. DNA Primers. Humans. Interleukin-8 / biosynthesis. Leukemia, Promyelocytic, Acute. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15927671.001).
  • [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 / Antineoplastic Agents; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / DNA Primers; 0 / Interleukin-8; 0 / RNA, Messenger; 5688UTC01R / Tretinoin
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7. Emadi A, Gore SD: Arsenic trioxide - An old drug rediscovered. Blood Rev; 2010 Jul-Sep;24(4-5):191-9
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  • Over the last 17 years, clinical trials conducted worldwide have demonstrated the efficacy of arsenic trioxide (As(2)O(3)) in the treatment of relapsed acute promyelocytic leukemia (APL).
  • Recent trials in the US have demonstrated that the addition of As(2)O(3) to standard treatment regimens improves survival outcomes in patients with APL and may allow a reduction in cytotoxic chemotherapy exposure.
  • Adverse events include APL differentiation syndrome, electrocardiographic abnormalities, and mild elevations in liver enzymes.
  • This review highlights trials investigating the role of As(2)O(3) in induction and consolidation for newly diagnosed APL, as well as its role in other hematologic malignancies.

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20471733.001).
  • [ISSN] 1532-1681
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717-05; United States / NCI NIH HHS / CA / CA100904-05; United States / NCI NIH HHS / CA / CA111717-05; United States / NCI NIH HHS / CA / R01 CA100904-05; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / R01 CA100904
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ NIHMS200220; NLM/ PMC2918685
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8. Douer D, Tallman MS: Arsenic trioxide: new clinical experience with an old medication in hematologic malignancies. J Clin Oncol; 2005 Apr 1;23(10):2396-410
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Arsenic trioxide has shown great promise in the treatment of patients with relapsed or refractory acute promyelocytic leukemia (APL).
  • Treatment with arsenic trioxide may be associated with the APL differentiation syndrome, leukocytosis, and electrocardiographic abnormalities.
  • The expanded use of arsenic trioxide in APL for postremission therapy, in conjunction with transplantation, and in patients with newly diagnosed APL is under investigation.
  • The multiple mechanisms of action of arsenic trioxide suggest that it may have antitumor activity in malignancies other than APL and that it may be used in combination with other agents to expand its potential use.

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  • (PMID = 15800332.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 95
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9. Mandegary A, Hosseini R, Ghaffari SH, Alimoghaddam K, Rostami S, Ghavamzadeh A, Ghahremani MH: The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide. Ann Oncol; 2010 Sep;21(9):1884-90
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  • [Title] The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide.
  • BACKGROUND: Promising reports exist regarding the use of arsenic trioxide (ATO) as first-line treatment in acute promyelocytic leukemia (APL).
  • PATIENTS AND METHODS: Newly diagnosed APL patients were involved and received ATO (0.15 mg.kg/day) for 28 days as induction followed by consolidation therapy.
  • Hyperleukocytosis and APL differentiation syndrome (63%), gastrointestinal disorders (30%), liver enzyme elevation and night sweating (50%) were the most prevalent side-effects.
  • However, the increase in ERK1 expression with regard to leukocytosis could translate to a proliferative/differentiation effect.

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  • (PMID = 20164150.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / BAX protein, human; 0 / Oxides; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; S7V92P67HO / arsenic trioxide
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10. Leu L, Mohassel L: Arsenic trioxide as first-line treatment for acute promyelocytic leukemia. Am J Health Syst Pharm; 2009 Nov 1;66(21):1913-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide as first-line treatment for acute promyelocytic leukemia.
  • PURPOSE: The history, clinical pharmacology and toxicities, and role of arsenic trioxide as a first-line agent for treating acute promyelocytic leukemia (APL) are described.
  • SUMMARY: APL is most often characterized by the hallmark reciprocal translocation between chromosomes 15 and 17, leading to the fusion of the promyelocytic gene and retinoic acid receptor alpha.
  • Arsenic trioxide demonstrates a dual, dose-dependent mechanism of action and can induce both partial myeloid differentiation and apoptosis.
  • Toxicities associated with arsenic trioxide include leukocytosis, Q-T interval prolongation, APL differentiation syndrome, and hepatotoxicity.
  • Since 2000, arsenic trioxide has been used as the standard of care for relapsed APL, with remission rates greater than 80% as a single agent.
  • In an attempt to maximize disease-free survival and minimize relapse rates in patients with APL, arsenic trioxide is now being investigated as first-line therapy in the management of APL, with several studies showing promising outcomes.
  • CONCLUSION: Arsenic trioxide, alone or in combination with tretinoin, as first-line therapy in newly diagnosed APL has resulted in high rates of complete remission and molecular remission.
  • Arsenic trioxide combined with tretinoin has shortened the time to achieve complete remission and lengthened disease-free survival, findings that suggest the usefulness of the regimen as first-line treatment for APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 19850784.001).
  • [ISSN] 1535-2900
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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11. Alimoghaddam K, Shariftabrizi A, Tavangar SM, Sanaat Z, Rostami S, Jahani M, Ghavamzadeh A: Anti-leukemic and anti-angiogenesis efficacy of arsenic trioxide in new cases of acute promyelocytic leukemia. Leuk Lymphoma; 2006 Jan;47(1):81-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-leukemic and anti-angiogenesis efficacy of arsenic trioxide in new cases of acute promyelocytic leukemia.
  • Arsenic trioxide is now considered the standard agent in treatment of refractory cases of acute promyelocytic leukemia (APL).
  • This drug is also shown to have anti-angiogenesis effect against APL cells in vitro.
  • This study evaluated clinical efficacy and anti-angiogenesis effect of arsenic trioxide in 17 new cases of APL.
  • Main toxicities included hyper-leukocytosis, hepatic toxicity and APL differentiation syndrome.
  • The results imply that arsenic trioxide is an effective anti-leukemia and anti-angiogenesis agent in new cases of APL.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • [ErratumIn] Leuk Lymphoma. 2006 Apr;47(4):777. Tavangar, Mohammad [corrected to Tavangar, S Mohammad]
  • (PMID = 16321832.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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12. Robertson KA, Colvin ES, Kelley MR, Fishel ML: APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS). J Clin Oncol; 2009 May 20;27(15_suppl):e14613

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS).
  • : e14613 Background: ATRA + chemotherapy has improved the treatment of promyelocytic leukemia(APL).
  • However, 25% of ATRA treated APL patients experience toxicities that comprise the RAS (life-threatening respiratory distress, edema, renal failure, hypotension, coagulopathy and rising blast count).
  • One approach to prevent RAS is to limit blast proliferation and enhance myeloid differentiation.
  • HL60 myeloid leukemia cells are promyeloblasts that respond to ATRA with granulocytic differentiation/growth arrest.
  • Prior studies suggest Ref-1 redox control is integral to ATRA-induced differentiation.
  • Differentiation was evaluated by morphology and expression of CD11b by flow cytometry.
  • 1) APX3330 blockade of Ref-1 redox function resulted in limited cell growth yet a profound increase in differentiation and a moderate increase in apoptosis.
  • 2) dose dependent studies with ATRA showed a similar degree of differentiation in cells treated with 10 μM ATRA to cells treated with APX3330 + 0.01 μM ATRA; allowing HL60 cells + APX3330 to give a similar response to a 1000 fold lower dose of ATRA.
  • APX3330 alone did not induce differentiation and induced only minimal apoptosis but in combination with ATRA, increased the number of cells in G1/G0 phase significantly.
  • CONCLUSIONS: APX3330 + ATRA limits HL60 growth and dramatically enhances terminal granulocytic differentiation.

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  • (PMID = 27964118.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Shigeno K, Naito K, Sahara N, Kobayashi M, Nakamura S, Fujisawa S, Shinjo K, Takeshita A, Ohno R, Ohnishi K: Arsenic trioxide therapy in relapsed or refractory Japanese patients with acute promyelocytic leukemia: updated outcomes of the phase II study and postremission therapies. Int J Hematol; 2005 Oct;82(3):224-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide therapy in relapsed or refractory Japanese patients with acute promyelocytic leukemia: updated outcomes of the phase II study and postremission therapies.
  • Recently, arsenic trioxide (ATO) has been proved to induce complete remission (CR) at a high rate in patients with acute promyelocytic leukemia (APL).
  • We prospectively investigated the safety and efficacy of ATO therapy in patients with relapsed and refractory APL and examined the duration of CR and the postremission therapies.
  • Fifteen patients developed ventricular tachycardia, and 1 of them showed torsades de pointes.
  • Other adverse events were nausea, water retention, APL differentiation syndrome, skin eruption, liver dysfunction, and peripheral neuropathy, all of which were quite tolerable.
  • ATO therapy was remarkably effective for relapsed APL; however, postremission therapies were necessary to maintain a durable remission.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Arsenicals / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / administration & dosage

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  • (PMID = 16207595.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; S7V92P67HO / arsenic trioxide
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14. Fenaux P, Wang ZZ, Degos L: Treatment of acute promyelocytic leukemia by retinoids. Curr Top Microbiol Immunol; 2007;313:101-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute promyelocytic leukemia by retinoids.
  • We review the role of all-trans retinoic acid (ATRA) in the treatment of acute promyelocytic leukemia (APL).
  • The combination of ATRA and conventional anthracycline-ARA-C chemotherapy (CT) has clearly demonstrated its superiority over CT alone (in terms of relapse and survival) in newly diagnosed APL.
  • ATRA syndrome (now generally called APL differentiation syndrome, as it is also seen with arsenic derivatives) remains the major side effect of ATRA treatment.
  • A sizeable proportion of APL patients who relapse after ATRA and CT can be durably salvaged by the same treatment followed by allogeneic or autologous stem cell transplantation, provided the transplant (in the autologous setting) is RT-PCR-negative.
  • However, in relapsing APL arsenic derivatives (mainly arsenic trioxide) are now considered to be the reference treatment.
  • Some of the current issues with ATRA treatment in newly diagnosed APL include whether ATRA has a role during consolidation treatment and whether arabinoside (AraC) is required in addition to anthracyclines in the chemotherapy combined to ATRA.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 17217041.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 132
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15. Dore AI, Santana-Lemos BA, Coser VM, Santos FL, Dalmazzo LF, Lima AS, Jacomo RH, Elias J Jr, Falcão RP, Pereira WV, Rego EM: The association of ICAM-1 Exon 6 (E469K) but not of ICAM-1 Exon 4 (G241R) and PECAM-1 Exon 3 (L125V) polymorphisms with the development of differentiation syndrome in acute promyelocytic leukemia. J Leukoc Biol; 2007 Nov;82(5):1340-3
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  • [Title] The association of ICAM-1 Exon 6 (E469K) but not of ICAM-1 Exon 4 (G241R) and PECAM-1 Exon 3 (L125V) polymorphisms with the development of differentiation syndrome in acute promyelocytic leukemia.
  • The use of all trans-retinoic acid (ATRA) is the basis of treatment of acute promyelocytic leukemia (APL) and represents the paradigm of differentiation therapy.
  • In general, ATRA is well-tolerated but may be associated with a potentially lethal side-effect, referred to as retinoic acid or differentiation syndrome (DS).
  • The cellular and molecular mechanisms of DS are poorly understood and involve changes in the adhesive qualities and cytokine secretion of leukemic cells during ATRA-induced differentiation.
  • As leukocyte extravasation is a key event in DS pathogenesis, we analyzed the association between the polymorphisms at Exon 4 (G241R) and Exon 6 (E469K) of ICAM-1 and Exon 3 (L125V) of PECAM-1 genes with DS development in APL patients treated with ATRA and anthracyclines.
  • DS was diagnosed in 23/127 (18.1%) APL patients at an average of 11.5 days after the start of ATRA.
  • Our results suggest that susceptibility to DS in APL patients may be influenced by genetic variation in adhesion molecule loci.
  • [MeSH-major] Antigens, CD31 / genetics. Exons / genetics. Intercellular Adhesion Molecule-1 / genetics. Leukemia, Promyelocytic, Acute / genetics. Polymorphism, Genetic / genetics
  • [MeSH-minor] Adult. Antineoplastic Agents / adverse effects. Cell Differentiation. Diagnosis, Differential. Female. Humans. Male. Syndrome. Tretinoin / adverse effects

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  • (PMID = 17704297.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antineoplastic Agents; 126547-89-5 / Intercellular Adhesion Molecule-1; 5688UTC01R / Tretinoin
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16. Helwig A, Klemm M, Schüttig R, Röllig C, Wassilew N, Ehninger G, Illmer T: Arsenic-induced APL differentiation in cerebrospinal fluid. Leuk Res; 2007 May;31(5):703-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic-induced APL differentiation in cerebrospinal fluid.
  • Although new approaches have dramatically improved, the treatment of acute promyelocytic leukemia (APL) involvement of the central nervous system (CNS) confers a bad prognosis in the disease.
  • Here, we report a patient who was diagnosed with relapsed APL preferentially involving the CNS.
  • Treatment with arsenic trioxide led to impressive morphological changes in CNS cellularity consistent with the induction of a differentiation syndrome.
  • Since arsenic trioxide could be identified in the CNS, we provide evidence that the drug can cross the blood-brain barrier and can be used for treatment of extramedullary APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Brain Neoplasms / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] Adult. Cell Differentiation. Cerebrospinal Fluid / cytology. Female. Humans. Leukocytes / pathology. Remission Induction. Treatment Outcome

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  • (PMID = 16876245.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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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
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  • [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].
  • [Transliterated title] Koagulopatie a diferenciacní syndrom: hlavní komplikace uvodní lécby akutní promyelocytární leukemie.
  • 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).
  • [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
  • [MeSH-minor] Hemorrhage / etiology. Humans. Syndrome. Thrombocytopenia / etiology

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  • (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
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18. Mathieu J, Giraudier S, Lanotte M, Besançon F: Retinoid-induced activation of NF-kappaB in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells. Oncogene; 2005 Nov 3;24(48):7145-55
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  • [Title] Retinoid-induced activation of NF-kappaB in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells.
  • All-trans retinoic acid (ATRA) significantly improves the survival of patients with acute promyelocytic leukemia (APL) by inducing granulocytic differentiation of leukemia cells.
  • Since an activation of the transcription factor NF-kappaB occurs during ATRA-induced maturation of APL cells, a mechanistic link between these two processes was investigated.
  • Using an in vitro model for APL, we report that ectopic overexpression of a repressor of NF-kappaB activation did not affect granulocytic differentiation.
  • Altogether, our results demonstrate an anti-apoptotic effect of NF-kappaB activation during ATRA-induced differentiation of NB4 cells and identify repression of ROS-mediated JNK activation as a mechanism for this effect.
  • Our observations also suggest that NF-kappaB signalling may contribute to an accumulation of mature APL cells and participate in the development of ATRA syndrome.
  • [MeSH-major] Cell Aging / drug effects. Cell Differentiation / drug effects. Granulocytes / physiology. Leukemia, Promyelocytic, Acute / pathology. NF-kappa B / metabolism. Tretinoin / pharmacology

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  • [Copyright] Oncogene (2005) 24, 7145-7155. doi:10.1038/sj.onc.1208889; published online 25 July 2005.
  • (PMID = 16044154.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11c; 0 / Antioxidants; 0 / NF-kappa B; 0 / Reactive Oxygen Species; 25013-16-5 / Butylated Hydroxyanisole; 5688UTC01R / Tretinoin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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19. Mathieu J, Besançon F: Arsenic trioxide represses NF-kappaB activation and increases apoptosis in ATRA-treated APL cells. Ann N Y Acad Sci; 2006 Dec;1090:203-8
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  • [Title] Arsenic trioxide represses NF-kappaB activation and increases apoptosis in ATRA-treated APL cells.
  • Acute promyelocytic leukemia (APL) is characterized by an arrest of granulopoiesis at the promyelocytic stage.
  • The sensitivity of APL cells to all-trans retinoic acid (ATRA)-induced differentiation has been successfully exploited for treatment of the disease.
  • We previously reported that ATRA-induced NF-kappaB activation in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells.
  • Our results demonstrate a proapoptotic effect of As2O3 in ATRA-treated APL cells and suggest that As2O3 may be helpful in reducing incidence of side effects linked to accumulation of mature cells, like the ATRA syndrome.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Leukemia, Promyelocytic, Acute / pathology. NF-kappa B / metabolism. Oxides / pharmacology. Tretinoin / pharmacology

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  • (PMID = 17384263.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / DNA Probes; 0 / NF-kappa B; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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20. Bi KH, Jiang GS: Relationship between cytokines and leukocytosis in patients with APL induced by all-trans retinoic acid or arsenic trioxide. Cell Mol Immunol; 2006 Dec;3(6):421-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between cytokines and leukocytosis in patients with APL induced by all-trans retinoic acid or arsenic trioxide.
  • Leukocytosis or hyperleukocytosis occurs during ATRA or arsenic trioxide differentiation therapy, which is related to the RA syndrome.
  • The same trend of classification of BM was observed in most of the patients with APL to whom leukocytosis happened.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Cytokines / physiology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Leukocytosis / chemically induced. Oxides / pharmacology. Tretinoin / physiology

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  • (PMID = 17257495.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Cytokines; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 61
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21. Ueda K, Nagai S, Miyashita SI, Kaise T, Ichikawa M, Kumano K, Hangaishi A, Nannya Y, Kurokawa M: Arsenic-induced pericardial and pleural effusion without acute promyelocytic leukemia differentiation syndrome. Leuk Res; 2010 Jan;34(1):e25-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic-induced pericardial and pleural effusion without acute promyelocytic leukemia differentiation syndrome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Pericardial Effusion / chemically induced. Pleural Effusion / chemically induced


22. Luesink M, Pennings JL, Wissink WM, Linssen PC, Muus P, Pfundt R, de Witte TJ, van der Reijden BA, Jansen JH: Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome. Blood; 2009 Dec 24;114(27):5512-21
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  • [Title] Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome.
  • In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA) and/or arsenic trioxide can induce a differentiation syndrome (DS) with massive pulmonary infiltration of differentiating leukemic cells.
  • ATRA stimulation of the APL cell line NB4 induced expression of multiple CC-chemokines (CCLs) and their receptors (> 19-fold), resulting in increased chemokine levels and chemotaxis.
  • In primary leukemia cells derived from APL patients at diagnosis, ATRA induced chemokine production as well.
  • Furthermore, in plasma of an APL patient with DS, we observed chemokine induction, suggesting that chemokines might be important in DS.
  • Dexamethasone, which efficiently reduces pulmonary chemokine production, did not inhibit chemokine induction in APL cells.
  • We propose that differentiation therapy may induce chemokine production in the lung and in APL cells, which both trigger migration of leukemic cells.
  • [MeSH-minor] Anti-Inflammatory Agents / pharmacology. Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism. Chemokine CCL24 / genetics. Chemokine CCL24 / metabolism. Chemokine CCL7 / genetics. Chemokine CCL7 / metabolism. Dexamethasone / pharmacology. Enzyme-Linked Immunosorbent Assay. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Oligonucleotide Array Sequence Analysis. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Syndrome. Tumor Cells, Cultured

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  • [CommentIn] Blood. 2009 Dec 24;114(27):5411-2 [20035042.001]
  • (PMID = 19828696.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE18397
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Arsenicals; 0 / CCL2 protein, human; 0 / CCL24 protein, human; 0 / CCL7 protein, human; 0 / Chemokine CCL2; 0 / Chemokine CCL24; 0 / Chemokine CCL7; 0 / Chemokines; 0 / Oxides; 0 / Receptors, Retinoic Acid; 5688UTC01R / Tretinoin; 7S5I7G3JQL / Dexamethasone; S7V92P67HO / arsenic trioxide
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23. Zhou J, Hu L, Cui Z, Jiang X, Wang G, Krissansen GW, Sun X: Interaction of SDF-1alpha and CXCR4 plays an important role in pulmonary cellular infiltration in differentiation syndrome. Int J Hematol; 2010 Mar;91(2):293-302
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  • [Title] Interaction of SDF-1alpha and CXCR4 plays an important role in pulmonary cellular infiltration in differentiation syndrome.
  • This study aims to investigate the role of stromal cell-derived factor 1alpha (SDF-1alpha) and its receptor CXCR4 in cellular infiltration of the lung in differentiation syndrome (DS).
  • The acute promyelocytic leukemia (APL) NB4 cells and freshly prepared APL cells from the patients were differentiated by all-trans retinoic acid (ATRA).
  • [MeSH-major] Chemokine CXCL12 / metabolism. Leukemia, Promyelocytic, Acute. Lung / pathology. Receptors, CXCR4 / metabolism. Tretinoin / pharmacology
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Adhesion / drug effects. Cell Differentiation / drug effects. Cell Movement / drug effects. Child. Culture Media / pharmacology. Female. Humans. Leukemic Infiltration. Male. Middle Aged. Young Adult

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  • (PMID = 20084476.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antineoplastic Agents; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Culture Media; 0 / Receptors, CXCR4; 5688UTC01R / Tretinoin
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24. Csomós K, Német I, Fésüs L, Balajthy Z: Tissue transglutaminase contributes to the all-trans-retinoic acid-induced differentiation syndrome phenotype in the NB4 model of acute promyelocytic leukemia. Blood; 2010 Nov 11;116(19):3933-43
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  • [Title] Tissue transglutaminase contributes to the all-trans-retinoic acid-induced differentiation syndrome phenotype in the NB4 model of acute promyelocytic leukemia.
  • Treatment of acute promyelocytic leukemia (APL) with all-trans-retinoic acid (ATRA) results in terminal differentiation of leukemic cells toward neutrophil granulocytes.
  • One of the most induced genes in APL NB4 cells is transglutaminase 2 (TG2).
  • The expression of genes related to cell-cycle control also changed, suggesting that TG2 regulates myeloid cell differentiation.
  • CC chemokines CCL2, CCL3, CCL22, CCL24, and cytokines IL1B and IL8 involved in the development of differentiation syndrome are expressed at significantly lower level in TG2-KD NB4 than in wild-type NB4 cells upon ATRA treatment.
  • Based on our results, we propose that reduced expression of TG2 in differentiating APL cells may suppress effector functions of neutrophil granulocytes and attenuate the ATRA-induced inflammatory phenotype of differentiation syndrome.
  • [MeSH-major] GTP-Binding Proteins / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / enzymology. Transglutaminases / metabolism. Tretinoin / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation. Chemokines, CC / biosynthesis. Chemokines, CC / genetics. Gene Expression / drug effects. Gene Expression Profiling. Gene Knockdown Techniques. Granulocytes / drug effects. Granulocytes / enzymology. Granulocytes / immunology. Granulocytes / pathology. Humans. Oligonucleotide Array Sequence Analysis. Phenotype. RNA, Small Interfering / genetics


25. Quenby S, Mountfield S, Cartwright JE, Whitley GS, Chamley L, Vince G: Antiphospholipid antibodies prevent extravillous trophoblast differentiation. Fertil Steril; 2005 Mar;83(3):691-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiphospholipid antibodies prevent extravillous trophoblast differentiation.
  • OBJECTIVE: We investigated the hypothesis that antiphospholipid antibodies (aPL) have a detrimental effect on human extravillous trophoblast (EVT) differentiation into giant multinucleated cells "in vitro."
  • MAIN OUTCOME MEASURE(S): This model was then used to investigate the effect of two different monoclonal aPL to beta2-glycoprotein 1 (IIC5 and ID2), and control mouse IgG antibody on EVT differentiation.
  • The aPL, IIC5, and ID2 significantly inhibited GMC formation, whereas the mouse IgG control had no effect.
  • CONCLUSION(S): Antiphospholipid antibodies can inhibit EVT differentiation and GMC formation "in vitro" suggesting that a failure of trophoblast differentiation and subsequent uteroplacental development may be an underlying pathology in antiphospholipid syndrome-associated pregnancy loss.
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Cell Differentiation / immunology. Cells, Cultured. Female. Giant Cells / cytology. Giant Cells / immunology. Humans. Pregnancy. Pregnancy Complications / immunology. Pregnancy Complications / pathology

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  • (PMID = 15749499.001).
  • [ISSN] 0015-0282
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal
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26. Francis J, Rai R, Sebire NJ, El-Gaddal S, Fernandes MS, Jindal P, Lokugamage A, Regan L, Brosens JJ: Impaired expression of endometrial differentiation markers and complement regulatory proteins in patients with recurrent pregnancy loss associated with antiphospholipid syndrome. Mol Hum Reprod; 2006 Jul;12(7):435-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired expression of endometrial differentiation markers and complement regulatory proteins in patients with recurrent pregnancy loss associated with antiphospholipid syndrome.
  • Antiphospholipid syndrome (APS), characterized by circulating antiphospholipid (aPL) antibodies, is a major cause of early pregnancy failure and placental insufficiency.
  • In this study, we examined whether impaired endometrial differentiation before conception contributes to the high incidence of pregnancy complications in APS.
  • Expression of decidual markers such as prolactin (PRL), tissue factor (TF) and signal transducer and activator of transcription 5 (Stat5), but not insulin-like growth factor-binding protein 1 (IGFBP-1), was significantly lower in samples obtained from aPL(+) patients (n = 24) when compared with aPL(-) group (n = 58) (P < 0.05).
  • However, analysis of transcripts that encode for complement regulatory proteins showed a marked decrease in decay-accelerating factor (DAF/CD55) levels in aPL(+) patients (P = 0.005), which was mimicked at protein level as demonstrated by immunohistochemistry.
  • In summary, patients with RPL have distinct endometrial gene expression profiles depending on the presence or absence of circulating aPL antibodies.
  • In APS, impaired endometrial differentiation and lower DAF/CD55 expression before conception may compromise implantation and predispose to complement-mediated pregnancy failure.
  • [MeSH-major] Abortion, Habitual / genetics. Antigens, Differentiation / genetics. Antiphospholipid Syndrome / genetics. Complement System Proteins / genetics

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  • (PMID = 16735457.001).
  • [ISSN] 1360-9947
  • [Journal-full-title] Molecular human reproduction
  • [ISO-abbreviation] Mol. Hum. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antigens, CD46; 0 / Antigens, CD55; 0 / Antigens, CD59; 0 / Antigens, Differentiation; 0 / Insulin-Like Growth Factor Binding Protein 1; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; 9002-62-4 / Prolactin; 9007-36-7 / Complement System Proteins; 9035-58-9 / Thromboplastin
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27. Cunha De Santis G, Tamarozzi MB, Sousa RB, Moreno SE, Secco D, Garcia AB, Lima AS, Faccioli LH, Falcão RP, Cunha FQ, Rego EM: Adhesion molecules and Differentiation Syndrome: phenotypic and functional analysis of the effect of ATRA, As2O3, phenylbutyrate, and G-CSF in acute promyelocytic leukemia. Haematologica; 2007 Dec;92(12):1615-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adhesion molecules and Differentiation Syndrome: phenotypic and functional analysis of the effect of ATRA, As2O3, phenylbutyrate, and G-CSF in acute promyelocytic leukemia.
  • BACKGROUND AND OBJECTIVES: Differentiation Syndrome (DS) is a treatment complication which can occur in patients treated with acute promyelocytic leukemia (APL) with all transretinoic acid (ATRA) or As(2)O(3), and is characterized by enhanced leukocyte transmigration.
  • DESIGN AND METHODS: APL blasts and NB4 cells were treated with ATRA, As(2)O(3), PB, G-CSF or their association and the expression of adhesion molecules was determined by flow cytometry.
  • RESULTS: In NB4 and APL blasts, ATRA and As(2)O(3) increased CD54 expression, but no synergism was detected.
  • INTERPRETATION AND CONCLUSIONS: The use of As(2)O(3), PB and G-CSF in association with ATRA should not aggravate DS in APL.
  • [MeSH-major] Antigens, CD / biosynthesis. Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Cell Adhesion Molecules / biosynthesis. Cell Differentiation / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Neoplasm Proteins / biosynthesis. Oxides / pharmacology. Phenylbutyrates / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / genetics. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Humans. Mice. Mice, Inbred BALB C. Mice, Knockout. Syndrome. Tumor Cells, Cultured

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  • (PMID = 18055984.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Cell Adhesion Molecules; 0 / Neoplasm Proteins; 0 / Oxides; 0 / Phenylbutyrates; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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28. Montesinos P, Bergua JM, Vellenga E, Rayón C, Parody R, de la Serna J, León A, Esteve J, Milone G, Debén G, Rivas C, González M, Tormo M, Díaz-Mediavilla J, González JD, Negri S, Amutio E, Brunet S, Lowenberg B, Sanz MA: Differentiation syndrome in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline chemotherapy: characteristics, outcome, and prognostic factors. Blood; 2009 Jan 22;113(4):775-83
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  • [Title] Differentiation syndrome in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline chemotherapy: characteristics, outcome, and prognostic factors.
  • Differentiation syndrome (DS) can be a life-threatening complication in patients with acute promyelocytic leukemia (APL) undergoing induction therapy with all-trans retinoic acid (ATRA).
  • We present an analysis of the incidence, characteristics, prognostic factors, and outcome of 739 APL patients treated with ATRA plus idarubicin in 2 consecutive trials (Programa Español de Tratamientos en Hematología [PETHEMA] LPA96 and LPA99).
  • [MeSH-major] Anthracyclines / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Tretinoin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease-Free Survival. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Prognosis. Recurrence. Risk Factors. Syndrome. Time Factors

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  • (PMID = 18945964.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 5688UTC01R / Tretinoin
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29. Jeddi R, Ghédira H, Mnif S, Gouider E, Fenaux P, Meddeb B: High body mass index is an independent predictor of differentiation syndrome in patients with acute promyelocytic leukemia. Leuk Res; 2010 Apr;34(4):545-7
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  • [Title] High body mass index is an independent predictor of differentiation syndrome in patients with acute promyelocytic leukemia.
  • Increased BMI has been correlated to an increased incidence of APL, but not to the occurrence of differentiation syndrome (DS) in APL.
  • We consecutively treated 39 APL patients with ATRA and idarubicin (according to PETHEMA regimen).
  • Eleven of the 36 patients evaluable for DS (30.5%) developed this syndrome (severe in 7 cases, moderate in 4, and fatal in 3 cases) within a median of 12 days (range 3-23) of ATRA onset.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Body Mass Index. Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Female. Humans. Idarubicin / administration & dosage. Idarubicin / adverse effects. Leukocyte Count. Male. Middle Aged. Prognosis. Survival Analysis. Syndrome. Tretinoin / administration & dosage. Tretinoin / adverse effects. Young Adult

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19800119.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; ZRP63D75JW / Idarubicin
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30. Patton GW, Stephens R, Sidorov IA, Xiao X, Lempicki RA, Dimitrov DS, Shoemaker RH, Tudor G: Transcriptomic response to differentiation induction. BMC Bioinformatics; 2006 Feb 17;7:81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptomic response to differentiation induction.
  • METHODS: We applied a transcriptomics analysis tool to elucidate the underlying pathways of leukocyte maturation at the genomic level in an established cellular model of leukemia by examining time-course data in two subclones of U-937 cells.
  • Leukemias such as Acute Promyelocytic Leukemia (APL) are characterized by a block in the hematopoietic stem cell maturation program at a point when expansion of clones which should be destined to mature into terminally-differentiated effector cells get locked into endless proliferation with few cells reaching maturation.
  • Treatment with retinoic acid, depending on the precise genomic abnormality, often releases the responsible promyelocytes from this blockade but clinically can yield adverse sequellae in terms of potentially lethal side effects, referred to as retinoic acid syndrome.
  • Expanded implementation of the techniques and results reported here may better direct future efforts to improve treatment for diseases not restricted to APL.

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  • [Cites] Nucleic Acids Res. 2000 Jan 1;28(1):308-10 [10592257.001]
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  • (PMID = 16503971.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-56000; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC1395336
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31. Metzger J, von Landenberg P, Kehrel M, Buhl A, Lackner KJ, Luppa PB: Biosensor analysis of beta2-glycoprotein I-reactive autoantibodies: evidence for isotype-specific binding and differentiation of pathogenic from infection-induced antibodies. Clin Chem; 2007 Jun;53(6):1137-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biosensor analysis of beta2-glycoprotein I-reactive autoantibodies: evidence for isotype-specific binding and differentiation of pathogenic from infection-induced antibodies.
  • BACKGROUND: For the laboratory diagnosis of the antiphospholipid syndrome (APS) we developed a biosensor with the ability to distinguish between disease-relevant anti-beta2-glycoprotein I (beta2GPI) autoantibodies (anti-beta2GPI) and pathogen-specific beta2GPI cross-reactive antibodies that occur transiently during infections.
  • The amplitudes of the antiphospholipid antibody (APL) responses in the biosensor correlated with the overall IgG and IgM anti-beta2GPI ELISA titers with a correlation coefficient of 0.87.
  • Moreover, we observed immunoglobulin isotype-specific association and dissociation profiles for APL binding of different APS patient sera to the biosensor-immobilized beta2GPI.
  • CONCLUSIONS: The SPR biosensor system enables specific detection of APS-associated beta2GPI-reactive APL and differentiation from beta2GPI cross-reactive antibodies that occur frequently during acute infections.
  • [MeSH-major] Antiphospholipid Syndrome / immunology. Autoantibodies / blood. Biosensing Techniques. Immunoglobulin Isotypes / blood. Lupus Erythematosus, Systemic / immunology. Parvoviridae Infections / immunology. Syphilis / immunology. beta 2-Glycoprotein I / immunology

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  • (PMID = 17434906.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antigens, Bacterial; 0 / Antigens, Viral; 0 / Autoantibodies; 0 / Immunoglobulin Isotypes; 0 / beta 2-Glycoprotein I
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32. Sastre López A, Gago González E, Baños Gallardo M, Gómez-Huertas E, Ortega Suárez F: [All-trans retinoic acid syndrome [corrected] and renal cortical necrosis]. An Med Interna; 2007 Nov;24(11):551-3
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] [All-trans retinoic acid syndrome [corrected] and renal cortical necrosis].
  • We described a patient with acute promyelocytic leukemia (APL) who developed all-trans retinoic acid syndrome (ATRAS).
  • ATRAS presents in patients with APL treated with all-trans retinoic acid (ATRA).
  • It is secondary to ATRA effect on promyelocyte differentiation, which causes systemic inflammatory response syndrome, endothelium damage with increase in capillary permeability, microcirculation obstruction, and tissue infiltration.
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Syndrome

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  • (PMID = 18275266.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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33. Di Simone N, Luigi MP, Marco D, Fiorella DN, Silvia D, Clara DM, Alessandro C: Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature. Ann N Y Acad Sci; 2007 Jun;1108:505-14
Hazardous Substances Data Bank. HEPARIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature.
  • There are several possible mechanisms by which antiphospholipid antibodies (aPL) may have adverse effects on placental functions.
  • Examination of placentas and first-trimester decidua from antiphospholipid syndrome-complicated pregnancies has found little evidence of specific thrombotic placental pathology.
  • It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids.
  • The most important epitope for antiphospholipid syndrome-related aPL resides on beta2-glycoprotein-I (beta2GPI).
  • aPL detected by anti-beta2GPI assays are associated with fetal loss.
  • During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2GPI.
  • It might reduce the binding of aPL, inflammation by inhibiting complement activation, and might facilitate implantation.
  • Further investigations are needed to better understand how aPL induce obstetric complications and to better clarify the functional role of heparin in the human placenta, leading to more successful therapeutic options.
  • [MeSH-major] Antibodies, Antiphospholipid / immunology. Antiphospholipid Syndrome / immunology. Pregnancy Complications / etiology. Trophoblasts / immunology

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  • (PMID = 17894016.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantigens; 0 / beta 2-Glycoprotein I; 9005-49-6 / Heparin
  • [Number-of-references] 55
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34. Gao Y, Camacho LH, Mehta K: Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome. Leuk Res; 2007 Apr;31(4):455-63
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] Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome.
  • All-trans retinoic acid (RA) treatment of patients with acute promyelocytic leukemia (APL) induces complete remission in more than 90% of the cases.
  • Although RA therapy is well tolerated, about 25% of APL patients develop a potentially fatal condition called retinoic acid syndrome (RAS).
  • In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients.
  • Importantly, RA-induced CD38 expression promoted strong attachment of leukemia cells to endothelial cells, and incubation of endothelial cells with either high concentration (100 ng/ml) of IFN-gamma alone or low concentration of IL-1beta and IFN-gamma (10 ng/ml, each) induced strong apoptotic responses as revealed by caspase-8 activation and DNA fragmentation.
  • Our results suggest that these RA-induced events could contribute to the development of RAS pathogenesis in patients with APL.
  • [MeSH-major] Antigens, CD38 / metabolism. Apoptosis / drug effects. Endothelium, Vascular / pathology. Interferon-gamma / pharmacology. Interleukin-1beta / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Tretinoin / pharmacology
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacology. Blast Crisis. Blotting, Western. Cell Adhesion / drug effects. Cell Differentiation. Cells, Cultured. Humans. Lung / blood supply. Nitric Oxide / metabolism. Receptors, Retinoic Acid / metabolism. Respiration Disorders / etiology. Respiration Disorders / metabolism. Respiration Disorders / pathology. Syndrome. Umbilical Veins / cytology

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  • (PMID = 16920192.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA092115; United States / PHS HHS / / P01 PA 55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-1beta; 0 / Receptors, Retinoic Acid; 31C4KY9ESH / Nitric Oxide; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; EC 3.2.2.5 / Antigens, CD38
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35. Ramos-Casals M, Brito-Zerón P, Font J: The overlap of Sjögren's syndrome with other systemic autoimmune diseases. Semin Arthritis Rheum; 2007 Feb;36(4):246-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The overlap of Sjögren's syndrome with other systemic autoimmune diseases.
  • OBJECTIVE: To analyze the main diagnostic problems caused by the overlap between Sjögren's syndrome (SS) and other systemic autoimmune diseases (SAD).
  • Immunologically, antiphospholipid antibodies (aPL) and antineutrophil cytoplasmic antibodies (ANCA) are the most frequent atypical autoantibodies found in primary SS, with a prevalence ranging between 10 and 20%.
  • However, coexisting antiphospholipid syndrome or systemic vasculitis is only detected in around 10% of SS patients with aPL or ANCA.
  • CONCLUSION: The wide variety of clinical and immunological manifestations of patients with primary SS often overlap with other SAD, making the differentiation between primary SS, SS associated with SAD, and SS-like presentations of some other SAD difficult.
  • [MeSH-major] Autoantibodies / blood. Autoimmune Diseases / diagnosis. Sjogren's Syndrome / diagnosis

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  • (PMID = 16996579.001).
  • [ISSN] 0049-0172
  • [Journal-full-title] Seminars in arthritis and rheumatism
  • [ISO-abbreviation] Semin. Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Peptides, Cyclic; 0 / cyclic citrullinated peptide
  • [Number-of-references] 62
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36. Reiterer G, Bunaciu RP, Smith JL, Yen A: Inhibiting the platelet derived growth factor receptor increases signs of retinoic acid syndrome in myeloid differentiated HL-60 cells. FEBS Lett; 2008 Jul 23;582(17):2508-14
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] Inhibiting the platelet derived growth factor receptor increases signs of retinoic acid syndrome in myeloid differentiated HL-60 cells.
  • The standard treatment for acute promyelocytic leukemia (APL) involves differentiation therapy with retinoic acid (RA).
  • Integrin ligand increased differentiation markers CD11b, inducible oxidative metabolism and PDGFR-beta phosphorylation.

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  • (PMID = 18571505.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA033505-24S1; United States / NCI NIH HHS / CA / R01 CA033505-24S1; United States / NCI NIH HHS / CA / R01 CA033505; United States / NCI NIH HHS / CA / CA33505; United States / NCI NIH HHS / CA / CA033505-24; United States / NCI NIH HHS / CA / R01 CA033505-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD18; 0 / Antineoplastic Agents; 0 / Interleukin-8; 0 / Ligands; 0 / Macrophage-1 Antigen; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 0 / Tyrphostins; 126547-89-5 / Intercellular Adhesion Molecule-1; 146535-11-7 / 6,7-dimethoxy-3-phenylquinoxaline; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS59791; NLM/ PMC2585509
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37. Luesink M, Jansen JH: Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia. Br J Haematol; 2010 Nov;151(3):209-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia.
  • In acute promyelocytic leukaemia (APL), differentiation therapy can be complicated by the development of a differentiation syndrome (DS).
  • Several mediators have been identified that may promote migration and extravasation of differentiating APL cells from the bloodstream into the tissue.
  • Adhesion of APL cells to each other and to the endothelium is induced by upregulation of the expression of adhesion molecules and constitutively active β2-integrins during differentiation therapy.
  • Pulmonary chemokine production can trigger transendothelial migration of differentiating APL cells from the bloodstream into the underlying tissue (initiation phase of DS).
  • Massive production of chemokines by infiltrated APL cells can further enhance transendothelial migration of differentiating APL cells, causing an uncontrollable hyperinflammatory reaction in the lung (aggravation phase), which is not efficiently switched-off by corticosteroids.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology. Leukemic Infiltration / pathology. Lung / pathology
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Cell Adhesion / physiology. Cell Differentiation / drug effects. Chemokines / physiology. Humans. Models, Biological. Syndrome

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20735400.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chemokines
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38. de la Serna J, Montesinos P, Vellenga E, Rayón C, Parody R, León A, Esteve J, Bergua JM, Milone G, Debén G, Rivas C, González M, Tormo M, Díaz-Mediavilla J, González JD, Negri S, Amutio E, Brunet S, Lowenberg B, Sanz MA: Causes and prognostic factors of remission induction failure in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and idarubicin. Blood; 2008 Apr 1;111(7):3395-402
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  • [Title] Causes and prognostic factors of remission induction failure in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and idarubicin.
  • An understanding of the prognostic factors associated with the various forms of induction mortality in patients with acute promyelocytic leukemia (APL) has remained remarkably limited.
  • This study reports the incidence, time of occurrence, and prognostic factors of the major categories of induction failure in a series of 732 patients of all ages (range, 2-83 years) with newly diagnosed APL who received all-trans retinoic acid (ATRA) plus idarubicin as induction therapy in 2 consecutive studies of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) Group.
  • Hemorrhage was the most common cause of induction death (5%), followed by infection (2.3%) and differentiation syndrome (1.4%).
  • Multivariate analysis identified specific and distinct pretreatment characteristics to correlate with an increased risk of death caused by hemorrhage (abnormal creatinine level, increased peripheral blast counts, and presence of coagulopathy), infection (age>60 years, male sex, and fever at presentation), and differentiation syndrome (Eastern Cooperative Oncology Group [ECOG] score>1 and low albumin levels), respectively.
  • These data furnish clinically relevant information that might be useful for designing more appropriately risk-adapted treatment protocols aimed at reducing the considerable problem of induction mortality in APL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hemorrhage / mortality. Infection / mortality. Leukemia, Promyelocytic, Acute / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Blast Crisis / blood. Blast Crisis / drug therapy. Blast Crisis / mortality. Child. Child, Preschool. Creatinine / blood. Disease-Free Survival. Female. Humans. Idarubicin / administration & dosage. Idarubicin / adverse effects. Male. Middle Aged. Remission Induction. Risk Factors. Sex Factors. Survival Rate. Syndrome. Treatment Failure. Tretinoin / administration & dosage. Tretinoin / adverse effects

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  • (PMID = 18195095.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; AYI8EX34EU / Creatinine; ZRP63D75JW / Idarubicin
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39. Walker DK, Held-Warmkessel J: Acute promyelocytic leukemia: an overview with implications for oncology nurses. Clin J Oncol Nurs; 2010 Dec;14(6):747-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukemia: an overview with implications for oncology nurses.
  • Acute promyelocytic leukemia (APL), once described as the form of leukemia with the highest mortality, is now the most potentially curable subtype of adult acute myeloid leukemia.
  • A brief review of the history of APL will describe the advances in research and clinical practice and their impact on patient outcomes.
  • Oncology nurses should familiarize themselves with the nuances of APL because of the critical role nurses play in providing support for patients.
  • This article provides an overview of APL, including the epidemiology and pathophysiology that distinguishes APL from other types of acute leukemia.
  • Clinical presentation and diagnostic workup for patients suspected of having APL will be reviewed, as will the treatment course.
  • Nursing implications and management will be provided related to potential treatment complications specific to APL, including coagulopathies, differentiation syndrome, and QT prolongation with the use of arsenic trioxide, as will the side effects and complications that can occur in any patient with leukemia, such as infection, hyperleukocytosis, tumor lysis, and increased intracranial pressure.
  • [MeSH-major] Leukemia, Promyelocytic, Acute. Oncology Nursing / manpower

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  • [ReprintIn] ONS Connect. 2010 Dec;25(12):12-3 [21214084.001]
  • (PMID = 21112852.001).
  • [ISSN] 1538-067X
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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40. Mulla MJ, Brosens JJ, Chamley LW, Giles I, Pericleous C, Rahman A, Joyce SK, Panda B, Paidas MJ, Abrahams VM: Antiphospholipid antibodies induce a pro-inflammatory response in first trimester trophoblast via the TLR4/MyD88 pathway. Am J Reprod Immunol; 2009 Aug;62(2):96-111
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PROBLEM: Women with antiphospholipid antibodies (aPL) are at risk for recurrent miscarriage, pre-eclampsia, and pre-term labor. aPL target the placenta directly by binding to beta(2)-glycoprotein I (beta(2)GPI) expressed on the surface of trophoblast cells.
  • The objective of this study was to determine the effects of aPL on trophoblast function and the mechanisms involved.
  • METHOD OF STUDY: First trimester trophoblast cells were treated with anti-beta(2)GPI monoclonal antibodies and patient-derived aPL, after which cell survival and function was evaluated.
  • Enhanced IL-8, GRO-alpha, and IL-1beta secretion also occurred when trophoblast cells were incubated with antibodies from patients with antiphospholipid syndrome.
  • CONCLUSION: These findings demonstrate that aPL triggers a placental inflammatory response via the TLR-4/MyD88 pathway, which in turn compromises trophoblast survival.
  • Thus, the TLR-4/MyD88 pathway may provide a new therapeutic target to improve pregnancy outcome in antiphospholipid syndrome patients.

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  • (PMID = 19614626.001).
  • [ISSN] 1600-0897
  • [Journal-full-title] American journal of reproductive immunology (New York, N.Y. : 1989)
  • [ISO-abbreviation] Am. J. Reprod. Immunol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD049446-04; United States / NICHD NIH HHS / HD / R01 HD049446; United States / NICHD NIH HHS / HD / R01 HD049446-04; United States / NICHD NIH HHS / HD / R01HD049446
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal; 0 / CXCL1 protein, human; 0 / Chemokine CXCL1; 0 / Cytokines; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; 0 / beta 2-Glycoprotein I; 9005-49-6 / Heparin
  • [Other-IDs] NLM/ NIHMS121593; NLM/ PMC2772057
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41. Tsai WH, Shih CH, Lin CC, Ho CK, Hsu FC, Hsu HC: Monocyte chemotactic protein-1 in the migration of differentiated leukaemic cells toward alveolar epithelial cells. Eur Respir J; 2008 May;31(5):957-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All-trans retinoic acid (ATRA) can induce acute respiratory distress syndrome in patients with acute promyelocytic leukaemia (APL).
  • The current study investigated the role of monocyte chemotactic protein (MCP)-1 in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells.
  • Monocyte chemotactic protein-1 secreted from alveolar epithelial cells plays an important role in the cell-cell interaction involved in the chemotactic transmigration of all-trans retinoic acid-treated acute promyelocytic leukaemia cells toward alveolar epithelial cells.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chemotaxis / drug effects. Epithelial Cells / drug effects. Granulocyte Precursor Cells / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects
  • [MeSH-minor] Cell Differentiation / drug effects. Cells, Cultured. Chemokine CCL2 / drug effects. Coculture Techniques. Humans. Pulmonary Alveoli / cytology. Pulmonary Alveoli / drug effects. Receptors, CCR2

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  • (PMID = 18216048.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCR2 protein, human; 0 / Chemokine CCL2; 0 / Receptors, CCR2; 5688UTC01R / Tretinoin
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42. da Costa Moraes CA, Trompieri NM, Cavalcante Felix FH: Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital. J Pediatr Hematol Oncol; 2008 May;30(5):387-90
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  • [Title] Pediatric acute promyelocytic leukemia: all-transretinoic acid therapy in a Brazilian pediatric hospital.
  • Acute promyelocytic leukemia (APL) is an uncommon form of pediatric acute nonlymphocytic leukemia.
  • It is characterized by clinical (refractory coagulopathy), morphologic (promyelocytic differentiation arrest), and cytogenetic t(15;17) hallmarks.
  • To show the results of APL treatment in our hospital, we reviewed the information about 15 patients less than 18 years old, newly diagnosed with APL between November 2002 and November 2006.
  • Only 1 patient was diagnosed with ATRA syndrome.
  • Preliminary results are encouraging and confirm that ATRA is safe and efficacious as first choice therapy for APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 18458575.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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43. Papanikolaou NA: Rational targeting in acute promyelocytic leukemia. In Vivo; 2010 Jan-Feb;24(1):21-7
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  • [Title] Rational targeting in acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (ARL) is characterized by the nearly homogeneous expression of the fusion oncogenic protein PML-RARalpha and the testis-specific cyclin A1 protein, which are implicated in its pathogenesis.
  • PML-RARalpha binds all-trans retinoic acid with high affinity inducing granulocytic differentiation and remission.
  • Current approaches with high doses of single or combined all-trans retinoic acid and chemotherapeutic agents, though relatively efficacious in the beginning, are highly toxic with severe side-effects (retinoic acid syndrome) and are followed by relapse in a high proportion of patients.
  • Here it is proposed that targeting APL with low levels of all-trans retinoic acid combined with small molecule inhibitors of cyclin-dependent kinases may have the potential to be equally or more efficacious as any of the current single or combined agent approaches, affording reduced toxicity and relapse rates.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 20133971.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 5688UTC01R / Tretinoin; EC 2.7.11.22 / Cyclin-Dependent Kinases
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44. Işık P, Çetin I, Tavil B, Azik F, Kara A, Yarali N, Tunc B: All-transretinoic acid (ATRA) treatment-related pancarditis and severe pulmonary edema in a child with acute promyelocytic leukemia. J Pediatr Hematol Oncol; 2010 Nov;32(8):e346-8
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  • [Title] All-transretinoic acid (ATRA) treatment-related pancarditis and severe pulmonary edema in a child with acute promyelocytic leukemia.
  • Use of all-transretinoic acid (ATRA) with other chemotherapeutic agents in the treatment of acute promyelocytic leukemia (APL) has been shown to cause the differentiation of abnormally granulated specific blast cells into mature granulocytes by acting on the t(15;.
  • The complete remission rate is increased and survival time is prolonged in APL patients who receive chemotherapy plus ATRA, whereas ATRA syndrome and other ATRA-related adverse effects including pseudo tumor cerebri, headache, severe bone pain, mucosal and skin dryness, hypercholesterolemia, and cheilitis may be observed especially during induction phase of the treatment.
  • In this paper, we report a 9-year-old girl with APL who developed pancarditis while receiving the APL-93 treatment protocol.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Myocarditis / chemically induced. Pulmonary Edema / chemically induced. Tretinoin / adverse effects

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  • (PMID = 20881874.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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45. Jeddi R, Ghédira H, Menif S, Ben Neji H, Ben Amor R, Kacem K, Aissaoui L, Bouteraâ W, Abdennebi Y, Raihane BL, Gouider E, Raouf H, Hèla BA, Saad A, Zaher B, Meddeb B: Treatment of acute promyelocytic leukemia with PETHEMA LPA 99 protocol: a Tunisian single center experience. Hematology; 2010 Aug;15(4):204-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute promyelocytic leukemia with PETHEMA LPA 99 protocol: a Tunisian single center experience.
  • Acute promyelocytic leukemia (APL) has now become the most curable of all subtypes of acute myeloid leukemia.
  • From 2004, 39 patients with confirmed APL either by t(15;17) or PML/RARA were treated by the PETHEMA LPA 99 trial.
  • The remaining six patients were considered as failure due to early death: three caused by differentiation syndrome (DS) and three died from central nervous system hemorrhage.
  • Thirty patients are alive in continuous complete remission; two patients died in CR from septic shock and secondary myelodysplastic syndrome respectively; one patient died 47 months after achieving two relapses.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 20670478.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; AYI8EX34EU / Creatinine; ZRP63D75JW / Idarubicin; AIDA protocol
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46. Suzukawa M, Nakazora T, Kawasaki Y, Tominaga T, Shinohara K: Massive ascites associated with all-trans retinoic acid treatment in therapy-related acute promyelocytic leukemia. Intern Med; 2010;49(5):457-60
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  • [Title] Massive ascites associated with all-trans retinoic acid treatment in therapy-related acute promyelocytic leukemia.
  • He was diagnosed with therapy-related acute promyelocytic leukemia (APL), and treated with all trans-retinoic acid (ATRA).
  • He showed the progressive accumulation of ascites with liver damage, without pulmonary symptoms of ATRA differentiation syndrome.
  • [MeSH-major] Ascites / chemically induced. Ascites / diagnosis. Chemoembolization, Therapeutic / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / etiology. Tretinoin / adverse effects. Tretinoin / therapeutic use

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  • (PMID = 20190483.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 3Z8479ZZ5X / Epirubicin; 5688UTC01R / Tretinoin
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47. Di Rocco A, Finolezzi E, Anaclerico B, Calabrese E, Levi A, Trasarti S, Tafuri A: [Therapeutic advances in neoplastic hematology: target therapy anti-CD33]. Clin Ter; 2005 Jul-Aug;156(4):183-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The CD33 antigen is present on 90% of acute myeloid leukemia blasts and is shared on normal hemopoietic cells only on the non stem dillerentiating fraction.
  • Gemtuzumab Ozogamicin (GO) is an engineered humanized antibody anti-CD33 conjugated with a potent intercalating agent, named calicheamicin, which is release only at intracellular level (lower pH), following a selective binding to CD33-positive cells, thus representing a promising approach for target anti-leukemia therapy.
  • GO was approved conditionally by the Federal Drug Administration in May 2000 as a single therapy for first recurrence of Acute Myeloid Leukemia (AML) in a subset of older patients.
  • The strong and homogeneous CD33 expression in Acute Promyelocytic Leukemia (APL), have resulted in an effective treatment of this disease with GO used as salvage treatment, as well as innovative approach for molecular relapsed patients.
  • However, the incidence of veno-occlusive disease, better defined as sinusoidal occlusive syndrome (SOS), must be taken into account as potential complication associated with the GO administration, especially in patients treated with ablative regimens.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Enediynes. Humans. Middle Aged. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16342520.001).
  • [ISSN] 0009-9074
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 27
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48. Tabuchi K: [Acute myeloid leukemia]. Gan To Kagaku Ryoho; 2007 Feb;34(2):156-61
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  • [Title] [Acute myeloid leukemia].
  • The annual incident rate of pediatric acute myeloid leukemia (AML) is now 10 per million in Japan, against 5 to 9 per million in the USA and Europe.
  • APL can be distinguished from other subtypes of AML by virtue of its excellent response and overall outcome as a result of differentiation therapy with ATRA.
  • Children with Down syndrome and AML have been shown to have a superior prognosis to AML therapy compared to other children with AML.
  • A high survival rate of 79% at 3 years was achieved for childhood de novo AML in the AML 99 trial.
  • To evaluate the efficacy and safety of the treatment strategy according to risk stratification based on leukemia cell biology and response to the initial induction therapy in children with AML, the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) has organized multi-center phase II trials in children with newly diagnosed AML.
  • [MeSH-major] Antineoplastic Protocols. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17301520.001).
  • [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
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