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Malcolm K. Brenner

Researcher at Center for Cell and Gene Therapy

Publications -  632
Citations -  50064

Malcolm K. Brenner is an academic researcher from Center for Cell and Gene Therapy. The author has contributed to research in topics: Antigen & Cytotoxic T cell. The author has an hindex of 109, co-authored 606 publications receiving 45233 citations. Previous affiliations of Malcolm K. Brenner include St. Jude Children's Research Hospital & Northwick Park Hospital.

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A comparison of double β-lactam combinations with netilmicin/ureidopenicillin regimens in the empirical therapy of febrile neutropenic patients

TL;DR: Results indicate that ceftazidime plus a ureidopenicillin would be adequate empirical therapy in situations where the concomitant use of nephrotoxic agents precludes the use of aminoglycoside containing combinations.
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Standardization of T-cell depletion in HLA matched bone marrow transplantation.

TL;DR: New specifications for the use of Ficoll‐Metrizoate, the method used to calculate T‐lymphocyte depletion and the details of attempts to improve T‐depletion are reported.
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Gene-Marking studies of hematopoietic cells

TL;DR: With continuing advances in gene-marking technology, the value of the information provided by these studies increases, thereby ensuring their continued relevance to the field of gene transfer.
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Clonal Dynamics In Vivo of Virus Integration Sites of T Cells Expressing a Safety Switch.

TL;DR: It is proposed that suboptimal iC9 transgene expression is responsible for the incomplete elimination ofiC9-T cells and illustrated here by simple model how cis-modulatory influences of local genome context and T-cell receptor activation status at time of CID treatment contribute to stochastic sparing of iC 9- T cells.
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Expression of the human immunodeficiency virus type 1 primer binding sequence inhibits HIV-1 replication

TL;DR: It is proposed that the LTR-driven vector transcript containing 18 nucleotides identical to the HIV-1 PBS may act like an RNA decoy to titrate viral proteins such as reverse transcriptase and nucleocapsid away from genuine viral transcripts, thus compromising virus replication.