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B. C. Trauth

Researcher at German Cancer Research Center

Publications -  8
Citations -  3133

B. C. Trauth is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Apoptosis & Antigen. The author has an hindex of 6, co-authored 8 publications receiving 3099 citations.

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Monoclonal antibody-mediated tumor regression by induction of apoptosis

TL;DR: Histological thin sections of the regressing tumor showed that anti-APO-1 was able to induce apoptosis in vivo, suggesting induction of apoptosis as a consequence of a signal mediated through cell surface molecules like APO- 1 may be a useful therapeutic approach in treatment of malignancy.
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Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen.

TL;DR: The APO-1 antigen was expressed upon transfection of APo-1 cDNA into BL60-P7 Burkitt's lymphoma cells and conferred sensitivity towards anti-APO- 1-induced apoptosis to the transfectants.
Journal Article

Induction of apoptosis by monoclonal antibody anti-APO-1 class switch variants is dependent on cross-linking of APO-1 cell surface antigens.

TL;DR: The data show that selective targeting of apoptosis to tumors may be an efficient antitumor mechanism and suggests that cross-linking of APO-1 on the tumor cell surface may also be required for tumor regression by apoptosis in vivo.
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Expression of the APO-1 antigen in Burkitt lymphoma cell lines correlates with a shift towards a lymphoblastoid phenotype.

TL;DR: The sensitivity of lymphoblastoid cell lines to anti-APO-1-mediated apoptosis may open a new therapeutic approach for the treatment of EBV- induced lymphoproliferative lesions in immunocompromised individuals, because these are composed of cells with a lymphobstonoid phenotype.
Book Chapter

Apoptosis in the Apo-1 system

TL;DR: This research attacked the mode of action of E.P.C.H.’s “cell reprograming” by focusing on the “spatially-based” component of the immune response to cancer.