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M Geppert (1990)
Glucocorticoid therapy obscures the diagnosis of cerebral lymphomaActa Neuropathol, 80
CM Bamberger, HM Schulte, GP Chrousos (1996)
Molecular determinants of glucocorticoid receptor function and tissue sensitivity to glucocorticoidsEndocr Rev, 17
B Pirotte (1997)
Glucocorticoid-induced long-term remission in primary cerebral lymphoma: case report and review of the literatureJ Neuro-Oncol, 32
S Geley, BL Hartman, K Kapelari, A Egle, A Villunger, D Heidacher, R Greil, B Auer, R Kofler (1997)
The interleukin-1_-converting enzyme inhibitorCrmAprevents APO-1/Fas-but not glucocorticoid-induced poly(ADP-ribose) polymerase cleavage and apoptosis in lymphoblastic leukemia cellsFEBS Lett, 402
T Miyashita (1992)
Cancer Res, 52
U Herrlinger, M Schabet, M Eichhorn, D Petersen, EH Grote, R Meyermann, J Dichgans (1996)
Prolonged corticosteroidinduced remission in primary central nervous system lymphoma: report of a case and review of the literatureEur Neurol, 36
U Herrlinger (1996)
Prolonged Corticosteroid-lnduced Remission in Primary Central Nervous System Lymphoma: Report of a Case and Review of the LiteratureEur Neurol, 36
CM Bamberger (1996)
Molecular Determinants of Glucocorticoid Receptor Function and Tissue Sensitivity to GlucocorticoidsEndocr Rev, 17
SA Memon, MB Moreno, D Petrak, CM Zacharchuk (1995)
Bcl-2 blocks glucocorticoid-but not Fas-or activationinduced apoptosis in a T cell hybridomaJ Immunol, 155
S Geley (1997)
The interleukin 1β-converting enzyme inhibitor CrmA prevents Apo1/Fas- but not glucocorticoid-induced poly(ADP-ribose) polymerase cleavage and apoptosis in lymphoblastic leukemia cellsFEBS Lett, 402
KA Jellinger (1995)
Primary central nervous system lymphomas?New pathological developmentsJ Neuro-Oncol, 24
KA Jellinger, W Paulus (1995)
Primary central nervous system lymphomas-new pathological developmentsJ Neuro-Oncol, 24
SW Lowe, EM Schmitt, SW Smith, BA Osborne, T Jacks (1993)
p53 is required for radiation-induced apoptosis in mouse thymocytesNature, 362
M Geppert, CB Ostertag, G Seitz, M Kiessling (1990)
Glucocorticoid therapy obscures the diagnosis of cerebral lymphomaActa Neuropathol, 80
LM DeAngelis (1990)
Primary CNS lymphoma: Combined treatment with chemotherapy and radiotherapyNeurology, 40
SA Memon (1995)
Bcl-2 blocks glucocorticoid- but not Fas- or activation-induced apoptosis in a T cell hybridoma.J Immunol, 155
T Miyashita, JC Reed (1992)
Bcl-2 gene transfer increases relative resistance of S49.1 and WEHI7.2 lymphoid cells to cell death and DNA fragmentation induced by glucocorticoids and multiple chemotherapeutic drugsCancer Res, 52
M Wisniewska, M Stanczyk, B Grzelakowska-Sztabert, B Kamiska (1997)
Nuclear factor of activated T cells (NFAT) is a possible target for dexamethasone in thymocyte apoptosisCell Biol Int, 21
AH Wyllie (1980)
Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activationNature, 284
AH Wyllie (1980)
Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activationNature, 284
B Pirotte, M Levivier, S Goldman, JM Brucher, J Brotchi, J Hildebrand (1997)
Glucocorticoid-induced long-term remission in primary cerebral lymphoma: case report and reviewof the literatureJ Neuro-Oncol, 32
KGC Smith (1996)
CrmA expression in T lymphocytes of transgenic mice inhibits CD95 (Fas/APO-1)-transduced apoptosis, but does not cause lymphadenopathy or autoimmune disease.EMBO J, 15
SW Lowe (1993)
p53 is required for radiation-induced apoptosis in mouse thymocytesNature, 362
M Wisniewska (1997)
NUCLEAR FACTOR OF ACTIVATED T CELLS (NFAT) IS A POSSIBLE TARGET FOR DEXAMETHASONE IN THYMOCYTE APOPTOSISCell Biol Int, 21
LM DeAngelis, J Yahalom, MH Heinemann, C Cirrincione, HT Thaler, G Krol (1990)
Primary CNS lymphoma: combined treatment with chemotherapy and radiotherapyNeurology, 40
A Helmberg, N Auphan, C Caelles, M Karin (1995)
Glucocorticoid-induced apoptosis of human leukemic cells is caused by the repressive function of the glucocorticoid receptorEMBO J, 14
A Helmberg (1995)
Glucocorticoid-induced apoptosis of human leukemic cells is caused by the repressive function of the glucocorticoid receptor.EMBO J, 14
KGC Smith, A Strasser, DL Vaux (1996)
CrmaA expression in T lymphocytes of transgenic mice inhibits CD95 (Fas/ APO-1)-transduced apoptosis but does not cause lymphadenopathy or autoimmune diseaseEMBO J, 15
Glucocorticoid therapy may result in the rapid resolution of cerebral mass lesions in patients with primary CNS lymphoma. Since glucocorticoids will obscure the histological diagnosis of primary CNS lymphoma upon biopsy, steroids should be withheld if primary CNS lymphoma is a likely diagnosis by neuroradiological criteria. The lympholytic effect of glucocorticoids is mediated by cytoplasmic steroid receptors which are translocated to the nucleus and signal apoptosis. Glucocorticoid-induced apoptosis of lymphoid cells does not require wild-type p53 activity, seems not to depend on caspase activation, but is attenuated by the bcl-2 protooncogene product. Long-term glucocorticoid therapy of primary CNS lymphoma is not recommended because relapse is probably inevitable and because of the prominent side effects of long-term glucocorticoid treatment. Further, long-term glucocorticoid treatment is contraindicated in immunocompromised patients with primary CNS lymphoma.
Journal of Neuro-Oncology – Springer Journals
Published: Oct 14, 2004
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