Leukaemia, acute promyelocytic

Borden, K. L., et al.. The solution structure of the RING finger domain from the acute promyelocytic leukaemia proto-oncoprotein PML. EmboJ, 1995, 14(7), 1532-41. [Pg.85]

Duprez E, Saurin AJ, Desterro JM, Lallemand-Breitenbach V, Howe K, Boddy MN, Solomon E, de The H, Hay RT, Freemont PS (1999) SUMO-1 modification of the acute promyelocytic leukaemia protein PML implications for nuclear localisation.) Cell Sd 112 381-393... [Pg.147]

Although a mutation in an annexin has never been categorically proven to be the cause of a disease state, they have been implicated in pathologies as diverse as autoimmunity, infection, heart disease, diabetes and cancer. Annexinopathies were first described by Jacob H. Rand to describe the pathological sequelae in two disease states, die overexpression of annexin 2 in a patients with a haemorrhagic form of acute promyelocytic leukaemia, and the under-expression of annexin 5 on placental trophoblasts in the antiphospholipid syndrome. In this chapter we will outline some of the more recent observations in regard to these conditions, and describe the involvement of annexins in some other major causes of human morbidity... [Pg.1]

ANNEXIN 2 IN A HAEMORRHAGIC FORM OF ACUTE PROMYELOCYTIC LEUKAEMIA (APL)... [Pg.4]

Acute promyelocytic leukaemia f2 f8 Haemorrhagic complications consistent with annexin 2 having a role in fibrinolysis (Menell et al., 1999) annexin 8 was found to be expressed at high levels in this leukaemia (Chang et al., 1992). [Pg.17]

Rowley JD, Golomb HM, Dougherty C. 15/17 Translocation, a consistent chromosomal change in acute promyelocytic leukaemia. Lancet 1977 1(8010) 549-550. [Pg.96]

Avvisati G, ten Cate JW, BuUer HR, MandeUi F. Tranexamic acid for control of haemorrhage in acute promyelocytic leukaemia. Laucet 1989 2(8655) 122-4. [Pg.117]

Zompi S, Legrand O, Bouscaiy D, Blanc CM, Picard F, CasadevaU N, Dreyfus F, Marie JP, Viguie F. Therapy-related acute myeloid leukaemia after successful therapy for acute promyelocytic leukaemia with t(15 17) a report of two cases and a review of the literature. Br J Haematol 2000 110(3) 610-13. [Pg.260]

Lehmann S, Paul C. Arsenik effektivt vid akut promyelo-cytleukemi. [Arsenic efficient in acute promyelocytic leukaemia.] Lakartidningen 1999 96(50) 5626-8. [Pg.341]

Brown JE, Olujohungbe A, Chang J, Ryder WD, Morganstern GR, Chopra R, Scarffe JH. All-trans retinoic acid (ATRA) and tranexamic acid a potentially fatal combination in acute promyelocytic leukaemia. Br J Haematol 2000 110(4) 1010-12. [Pg.3479]

Hatake K, Ohtsuki T, Uwai M, Takahashi H, Izumi T, Yoshida M, Kanai N, Saito K, Harigaya K, Miura Y. Tretinoin induces bone marrow collagenous fibrosis in acute promyelocytic leukaemia new adverse, but reversible effect. Br J Haematol 1996 93(3) 646-9. [Pg.3651]

Suzumiya J, Asahara F, Katakami H, Kimuran N, Hisano S, Okumura M, Ohno R. Hypercalcaemia caused by all-trans retinoic acid treatment of acute promyelocytic leukaemia case report. Eur J Haematol 1994 53(2) 126-7. [Pg.3667]

Charles KS, Kanaa M, Winfield DA, Reilly JT. Scrotal ulceration during all-trans retinoic (ATRA) therapy for acute promyelocytic leukaemia. Clin Lab Haematol 2000 22(3) 171. ... [Pg.3667]

Chang SE, Huh J, Choi JH, Sung KJ, Moon KC, Koh JK. Cutaneous relapse in acute promyelocytic leukaemia following treatment with all-trans retinoic acid. Br J Dermatol 1999 141(3) 586-7. [Pg.3668]

Degos, L., Chomienne, C., Daniel, M.T., Berger, R., Dombret, H., Fenaux, P. and Castaigne, S. (1990) Treatment of first relapse in acute promyelocytic leukaemia with all-traus retinoic acid. Lancet, 336, 1440-1441. [Pg.401]

Abbreviations used in this review APL, acute promyelocytic leukaemia CEF, chick embryo fibroblasts CRABP, cellular retinoic acid-binding protein ODC, ornithine decarboxylase RA, retinoic acid RARE, retinoic acid responsive element RAR, retinoic acid receptor RXR, retinoid X receptor TEMPO, 2,2,6,6-tetramethylpiperidine Y-oxide TOC, tracheal organ culture TPA, 12-<2-tetradecanoylphorbol-13-acetate TTNN, 6-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)-2-naphthanoic acid TTNPB, 4-((.Q-2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2- naphthyl)propenyl)benzoic acid. [Pg.2]

The ability of a test compound to induce differentiation of HL-60 cells (derived from a patient with acute promyelocytic leukaemia) is also an important assay of retinoid activity [91-93]. HL-60 cells do not produce superoxide anions upon stimulation by agents like TPA. Differentiated HL-60 cells, however, do produce these anions upon similar stimulation. The presence of these anions can be monitored because of their ability to reduce the yellow nitroblue tetrazolium (NBT) to the water insoluble blue-black formazan. Determination of the concentration (ED50) which results in differentiation of 50% of the cells is the measure of the anti-APL activity of the retinoid. Morphological maturation of the cells can also be checked. [Pg.19]

Isomerization at C-I3 results in diminished activity. For example, the ability of all-trans-RA to induce differentiation of cells obtained from several patients with acute promyelocytic leukaemia, all-trans-RA is 10 times more effective than the 13-cis isomer [98]. [Pg.21]

Therefore, it appears that abnormal expressions of retinoic receptors may be involved in neoplastic progressions, and in some cases, these may completely hinder RA responsiveness. In other cases, as in remission of acute promyelocytic leukaemia, abnormal gene regulation by mutant RARs can be overcome by retinoic acid treatment. [Pg.38]

Combinations of retinoic acid with IFNa, IFN)3, TNF, or G-CSF have been reported to result in synergistic induction of differentiation in the HL-60 acute promyelocytic leukaemia cell Une and the U-937 human histiocytic lymphoma cell line (see references in [232]). Until recently [232,233], combinations of retinoids (natural or synthetic) with other cytokines have not been explored. [Pg.42]

M ndra P, Keeling DH Hood IM, glin TP, Ivfeircus RE Fatal thromboembolism in acute promyelocytic leukaemia treated with a combination of all-trans retinoic acid and aprotinin CUnLabHaematol( 996) 18, 51-2... [Pg.668]

Vanier KL, Mattiussi AJ, Johnston DL. Interaction of all-trans-retinoic acid with fluconazole in acute promyelocytic leukaemia. J Pediatr Hematol Oncol (2003) 25,403-4. [Pg.668]

Schwartz EL, Hallam S, Gallagher RE, Wiemik PH. Inhibition of aU-trans retinoic acid metabolism by fluconazole in vitro and in patients with acute promyelocytic leukaemia. Biochem Pharmacol( 995) 50,923-8. [Pg.668]

Arsenic Syphilis, ulcers, parasitic disease, acute promyelocytic leukaemia [1,14,15]... [Pg.181]

HL-60 cells are a human promyelocytic leukaemia cell line developed by Collins et al. [3], from a patient with acute promyelocytic leukaemia. The HL-60 cells in culture consists predominantly of promyelocytes (approximately 85%) and an smaller per-... [Pg.433]

RARa FUSION PROTEINS IN ACUTE PROMYELOCYTIC LEUKAEMIA... [Pg.311]

Zelent, A. (1994) Translocation of the RARa locus to the PML or PLZF gene in acute promyelocytic leukaemia. Br. J. Haem 86,451-460... [Pg.331]

Grimwade, D. and Solomon, E. (1997) Characterisation of the PMURARa rearrangement associated with t(15 17) acute promyelocytic leukaemia. Curr. Top. Microbiol. Immunol 220,81-112. [Pg.351]

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