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Burkhard Jansen

Researcher at University of British Columbia

Publications -  99
Citations -  6463

Burkhard Jansen is an academic researcher from University of British Columbia. The author has contributed to research in topics: Melanoma & Apoptosis. The author has an hindex of 42, co-authored 95 publications receiving 6216 citations. Previous affiliations of Burkhard Jansen include Idun Pharmaceuticals & Medical University of Vienna.

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Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c

TL;DR: It is shown that in cells transiently transfected with bax, Bax localizes to mitochondria and induces the release of cytochrome c, activation of caspase-3, membrane blebbing, nuclear fragmentation, and cell death, indicating that Bcl-2 can interfere with Bax killing downstream of and independently of cy tochrome c release.
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bcl-2 antisense therapy chemosensitizes human melanoma in SCID mice.

TL;DR: It is demonstrated that bcl-2 antisense oligonucleotide treatment improves the chemo-sensitivity of human melanoma grown in severe combined im-munodeficient (SCID) mice and suggests that reduction of B cl-2 in melanoma may be a novel and rational approach to improve chemosensitivity and treatment outcome.
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Chemosensitisation of malignant melanoma by BCL2 antisense therapy

TL;DR: Systemic administration of augmerosen downregulated the target BCL2 protein in metastatic cancer, combined with standard anticancer therapy, offers a new approach to the treatment of patients with resistant neoplasms.
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Silencing expression of the clusterin/apolipoprotein j gene in human cancer cells using small interfering RNA induces spontaneous apoptosis, reduced growth ability, and cell sensitization to genotoxic and oxidative stress.

TL;DR: It is demonstrated that CLU knockdown in human cancer cells induces significant reduction of cellular growth and higher rates of spontaneous endogenous apoptosis, and siRNA-mediated CLU gene silencing in osteosarcoma and prostate cancer cells proves valuable agents during antitumor therapy or at other pathological conditions where CLU has been implicated.
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Hepatocytes convert to a fibroblastoid phenotype through the cooperation of TGF-β1 and Ha-Ras: steps towards invasiveness

TL;DR: In this article, the authors employed immortalized murine hepatocytes, which display a high degree of differentiation and, expectedly, arrest in the G1 phase under exposure to TGF-β1.