Institution
St. Jude Children's Research Hospital
Healthcare•Memphis, Tennessee, United States•
About: St. Jude Children's Research Hospital is a healthcare organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Virus. The organization has 9344 authors who have published 19233 publications receiving 1233399 citations. The organization is also known as: St. Jude Children's Hospital & St. Jude Hospital.
Papers published on a yearly basis
Papers
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TL;DR: A perfect genetic linkage is reported between Etc-1 and Mtv-9 and it is shown that EtC-1 is also involved in the I–E-dependent deletion of T cells bearing Vβ5.1 and Vβ11 domains.
Abstract: A special class of self-antigens (endogenous superantigens) is capable of deleting many murine T cells on the basis of their expression of particular T-cell receptor V beta gene segments. In mice that endogenously express these antigens, tolerance is mediated in part by the clonal deletion of the relevant V beta-bearing T cells. The deletion of I-E-reactive V beta 5.2-bearing T cells is dependent on the coexpression of an I-E tolerogenic coligand (Etc)14 and the gene for one of these coligands, Etc-1, maps to chromosome 12, near the mouse mammary tumour viral integrant, Mtv-9. Here we report a perfect genetic linkage between Etc-1 and Mtv-9 and show that Etc-1 is also involved in the I-E-dependent deletion of T cells bearing V beta 5.1 and V beta 11 domains. We also demonstrate that Mtv-9 transcripts are present in B cells expressing Etc-1 and suggest that the coligand recognized by roughly 15% of all T lymphocytes is encoded by the Mtv-9 genome.
266 citations
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TL;DR: It is demonstrated that the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl-ketone (z-VAD-fmk) prevented hippocampal neuronal cell death and white blood cell influx into the cerebrospinal fluid compartment in experimental pneumococcal meningitis.
Abstract: Half of the survivors of bacterial meningitis experience motor deficits, seizures, hearing loss or cognitive impairment, despite adequate bacterial killing by antibiotics. We demonstrate that the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl-ketone (z-VAD-fmk) prevented hippocampal neuronal cell death and white blood cell influx into the cerebrospinal fluid compartment in experimental pneumococcal meningitis. Hippocampal neuronal death was due to apoptosis derived from the inflammatory response in the cerebrospinal fluid. Apoptosis was induced in vitro in human neurons by inflamed cerebrospinal fluid and was blocked by z-VAD-fmk. As apoptosis drives neuronal loss in pneumococcal meningitis, caspase inhibitors might provide a new therapeutic option directed specifically at reducing brain damage.
266 citations
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TL;DR: Early intensive triple intrathecal therapy, together with more effective systemic therapy, including consolidation and reinduction treatment, resulted in a very low rate of isolated central nervous system (CNS) relapse rate, despite the reduced use of cranial irradiation.
Abstract: We analyzed the long-term outcome of 1011 patients treated in five successive clinical trials (Total Therapy Studies 11, 12, 13A, 13B, and 14) between 1984 and 1999. The event-free survival improved significantly (P=0.003) from the first two trials conducted in the 1980s to the three more recent trials conducted in the 1990s. Approximately 75% of patients treated in the 1980s and 80% in the 1990s were cured. Early intensive triple intrathecal therapy, together with more effective systemic therapy, including consolidation and reinduction treatment (Studies 13A and 13B) as well as dexamethasone (Study 13B), resulted in a very low rate of isolated central nervous system (CNS) relapse rate (<2%), despite the reduced use of cranial irradiation. Factors consistently associated with treatment outcome were age, leukocyte count, immunophenotype, DNA index, and minimal residual disease level after remission induction treatment. Owing to concerns about therapy-related secondary myeloid leukemia and brain tumors, in our current trials we reserve the use of etoposide for patients with refractory or relapsed leukemia undergoing hematopoietic stem cell transplantation, and cranial irradiation for those with CNS relapse. The next main challenge is to further increase cure rates while improving quality of life for all patients.
266 citations
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University of California, San Francisco1, University of Freiburg2, St. Jude Children's Research Hospital3, Boston Children's Hospital4, University of Texas MD Anderson Cancer Center5, University of Arkansas at Little Rock6, Aarhus University Hospital7, Children's Oncology Group8, University of Pavia9, Charles University in Prague10
TL;DR: The exclusivity of CBL mutations with respect to other Ras pathway-associated mutations indicates that CBL may have a role in deregulating this key pathway in JMML.
265 citations
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TL;DR: The recent advances in understanding of these regulatory processes in MAPK signaling with a focus on their impacts on immune function are discussed.
265 citations
Authors
Showing all 9410 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard A. Flavell | 231 | 1328 | 205119 |
David Baltimore | 203 | 876 | 162955 |
John C. Reed | 190 | 891 | 164382 |
Joan Massagué | 189 | 408 | 149951 |
Stuart H. Orkin | 186 | 715 | 112182 |
Douglas R. Green | 182 | 661 | 145944 |
Richard K. Wilson | 173 | 463 | 260000 |
Todd R. Golub | 164 | 422 | 201457 |
Robert G. Webster | 158 | 843 | 90776 |
Elaine R. Mardis | 156 | 485 | 226700 |
David Cella | 156 | 1258 | 106402 |
Rafi Ahmed | 146 | 633 | 93190 |
Ching-Hon Pui | 145 | 805 | 72146 |
Yoshihiro Kawaoka | 139 | 883 | 75087 |
Seth M. Steinberg | 137 | 936 | 80148 |