T lymphoblastic leukaemia and the central nervous system

Lilleyman, J S; Sugden, P. J.

doi:10.1038/bjc.1981.50

Cited by 14 publications

(4 citation statements)

References 11 publications

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“…It is also worth noting that the Vllth pair of cranial nerves was often affected (50%). This is in agreement with the report of Lillevman and Sugden [20] on a series of children with acute lymphoblastic leukaemia. It appears that the acute Tlymphoblastic leukaemias have a greater tendency to invade the CNS and the facial nerves in particular.…”

Section: Discussionsupporting

confidence: 82%

Lymphoblastic Lymphoma with Convoluted Nuclei

Baldit¹,

Trojani²,

Eghbali³

et al. 1984

Oncology

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A clinically homogeneous population of patients who presented with lymphoblastic lymphoma of convoluted nuclear type was isolated using a histopathological criterion that can easily be applied by trained pathologists. This disease type preferentially affects young male patients, in over half of whom there is initial mediastinal involvement. There is a tendency for the disease to become leukemic and to invade the central nervous system. In spite of heavy chemotherapy and early neuromeningeal prophylaxis, the prognosis is poor.

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Section: Discussionsupporting

confidence: 82%

Lymphoblastic Lymphoma with Convoluted Nuclei

Baldit¹,

Trojani²,

Eghbali³

et al. 1984

Oncology

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“…Indeed, our work shows that the inhibition of ephrin-B1 activity in T-ALL cells through the expression of signaling-deficient and phosphorylation-deficient ephrin-B1 mutants not only affects their repulsive responses but also suppresses the invasive activity of these cells in the Matrigel assay, strongly supporting the significance of ephrin-B1 signaling in the sustaining of T-ALL metastatic behavior. A characteristic feature of pediatric T-ALLs is their ability to rapidly spread into nonhematopoietic organs and relapse at extramedullary sites, including central nervous system, which is typically associated with a worse clinical prognosis (64,(87)(88)(89)(90). Extravasation, or migration of malignant leukocytes from blood into the tissue, is a required step in T-ALL spreading.…”

Section: Discussionmentioning

confidence: 99%

In Human Leukemia Cells Ephrin-B–Induced Invasive Activity Is Supported by Lck and Is Associated with Reassembling of Lipid Raft Signaling Complexes

Jiang

Freywald

Webster

et al. 2008

Molecular Cancer Research

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Proteins of the ephrin-B group operate in nonlymphoid cells through the control of their migration and attachment, and are crucial for the development of the vascular, lymphatic, and nervous systems. Ephrin-B activity is deregulated in various nonlymphoid malignancies; however, their precise role in cancer has only started to be addressed. We show here that ephrin-B1, a member of the ephrin-B group, is expressed in pediatric T-cell leukemias, including leukemia cell line Jurkat. Treatment of Jurkat cells with ephrin-Bstimulating EphB3 enhances ephrin-B1 phosphorylation and induces its relocalization into lipid rafts. These events are mediated by the T lineage -specific kinase, Lck, as ephrin-B1 phosphorylation and lipid raft association are blocked in the Lck-deficient clone of Jurkat, JCAM1.6. Ephrin-B1 also induces colocalization of the CrkL and Rac1 cytoskeleton regulators and initiates in leukemic cells a strong repulsive response. The absence of Lck blocks ephrin-B1 -induced signaling and repulsion, confirming the essential role for Lck in ephrin-B1 -mediated responses. This shows a new role for ephrin-B1 in the regulation of leukemic cells through the Lck-dependent Rac1 colocalization with its signaling partner, CrkL, in lipid rafts. In agreement with its repulsive action, ephrin-B1 seems to support metastatic properties of leukemic cells, as suppression of ephrin-B1 signaling inhibits their invasiveness. Because ephrin-B1 -activating EphB proteins are ubiquitously expressed, our findings suggest that ephrin-B1 is likely to play an important role in the regulation of malignant T lymphocytes through the control of lipid-raftassociated signaling, adhesion, and invasive activity, and therefore may represent a novel target for cancer treatment. (Mol Cancer Res 2008;6(2):291 -305)

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“…The risk factors for CNS relapse despite 'prophylaxis' are similar to those reported for patients treated before prophylaxis was introduced: high white cell counts and low platelet counts (West et al, 1972). There was no evidence of a higher incidence of T cell disease as has.been previously suggested (Lilleyman & Sugden, 1981). In their study, however, when isolated CNS relapse was specifically considered the association with T cell disease was no longer apparent.…”

Section: Discussionmentioning

confidence: 48%

Failed central nervous system prophylaxis in children with acute lymphoblastic leukaemia: treatment and outcome

Pinkerton

Chessells

1984

Br J Haematol

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Summary. Isolated CNS relapse occurred as a first event in 23 (6%) of 354 children with acute lymphoblastic leukaemia (ALL) who shortly after achieving remission had been treated with craniospinal irradiation or cranial irradiation and intrathecal methotrexate. CNS relapse occurred at a median time of 79 weeks from diagnosis and in three cases was asymptomatic, being diagnosed on routine lumbar puncture at completion of maintenance therapy. CNS remission was achieved with weekly intrathecal methotrexate in all but two cases who died in relapse. A second course of radiotherapy was given in 12 cases; at the time of relapse in three and delayed from 14–170 weeks later in nine. Intensified systemic chemotherapy was used in 13 patients and all but three continued on regular maintenance intrathecal methotrexate. Disease free remission following CNS relapse ranged from 9 to 366 weeks (median 76 weeks) with subsequent relapses occurring in the testis, CNS and in particular the bone marrow. Survival after relapse ranged from 11 to 476 weeks (median 92); seven patients are alive; four in continued remission, two with recurrent but controlled CNS disease, and one in remission following bone marrow transplant after subsequent marrow relapse. Recurrent CNS disease was significantly less frequent in patients who were reirradiated. It appears that long‐term survival is possible after isolated CNS relapse but that further intensification of systemic chemotherapy and possibly chemo‐radiotherapy and bone marrow transplant will be required to reduce the high risk of subsequent bone marrow relapse.

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T lymphoblastic leukaemia and the central nervous system

Cited by 14 publications

References 11 publications

Lymphoblastic Lymphoma with Convoluted Nuclei

Lymphoblastic Lymphoma with Convoluted Nuclei

In Human Leukemia Cells Ephrin-B–Induced Invasive Activity Is Supported by Lck and Is Associated with Reassembling of Lipid Raft Signaling Complexes

Failed central nervous system prophylaxis in children with acute lymphoblastic leukaemia: treatment and outcome

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