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Peter Möller

Researcher at Heidelberg University

Publications -  136
Citations -  8547

Peter Möller is an academic researcher from Heidelberg University. The author has contributed to research in topics: Antigen & B cell. The author has an hindex of 42, co-authored 136 publications receiving 8424 citations. Previous affiliations of Peter Möller include University of Würzburg & University of Ulm.

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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.
Journal Article

Constitutive and induced expression of APO-1, a new member of the nerve growth factor/tumor necrosis factor receptor superfamily, in normal and neoplastic cells.

TL;DR: Tissue distribution, in vitro expression, and reaction upon cytokine-induced activation suggest that APO-1 might not only transmit apoptotic signals but might play a more general role in growth control.
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T Cell Awareness of Paternal Alloantigens During Pregnancy

TL;DR: During pregnancy a semiallogeneic fetus survives despite the presence of maternal T cells specific for paternally inherited histocompatibility antigens, and during pregnancy maternal T Cells acquire a transient state of tolerance specific for paternal alloantigens.
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Estimation of surface area and length with the orientator.

TL;DR: The orientator is an unbiased, design‐based approach to the quantitative study of anisotropic structures such as muscle, myocardium, bone and cartilage, and generation of isotropic sections for second‐order stereology (three‐dimensional pattern analysis).
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Expression of APO-1 (CD95), a member of the NGF/TNF receptor superfamily, in normal and neoplastic colon epithelium.

TL;DR: It is concluded that neoplastic transformation of colon epithelium often leads to a loss of the physiologic, high level of surface APO‐I by giving rise either to a stable lack of APo‐I or to an IFN‐γ/TNF‐α‐sensitive phenotype of inducible APO'I expression.