The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Inhibition of TGF- β 2 with AP 12009 in Recurrent Malignant Gliomas: From Preclinical to Phase I/II Studies
Abstract
Transforming growth factor-beta2 (TGF-beta2) is known to suppress the immune response to cancer cells and plays a pivotal role in tumor progression by regulating key mechanisms including proliferation, metastasis, and angiogenesis. For targeted protein suppression the TGF-beta2-specific antisense oligodeoxynucleotide AP 12009 was developed. In vitro experiments have been performed to prove specificity and efficacy of the TGF-beta2 inhibitor AP 12009 employing patient-derived malignant glioma cells as well as peripheral blood mononuclear cells (PBMCs) from patients. Clinically, the antisense compound AP 12009 was assessed in three Phase I/II-studies for the treatment of patients with recurrent or refractory malignant (high-grade) glioma WHO grade III or IV. Although the study was not primarily designed as an efficacy evaluation, prolonged survival compared to literature data and response data were observed, which are very rarely seen in this tumor indication. Two patients experienced long-lasting complete tumor remissions. These results implicate targeted TGF-beta2-suppression using AP 12009 as a promising novel approach for malignant gliomas and other highly aggressive, TGF-beta-2-overexpressing tumors.
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Cites
Radiotherapy Plus Concomitant and Adjuvant Temozolomide for Glioblastoma
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Self-citationResponse criteria for phase II studies of supratentorial malignant glioma.
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“…and accurate survival data from the literature that clearly distinguish between AA and GBM are available for temozolomide with 42 to 49 (Chang et al., 2004) weeks for recurrent AA and 31.8 (Yung, 2000, Yung et al., 2000) or 32.0 (Theodosopoulos et al., 2001) weeks for recurrent GBM, respectively.”
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Self-citationTemozolomide in the treatment of recurrent malignant glioma
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Cited by
Targeting the TGFβ signalling pathway in disease
Akhurst, R. J., & Hata, A. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3810 · Cited by 1,466
Targeting TGF-β Signaling in Cancer
Colak, S., & ten Dijke, P. (2017) · Trends in cancer · doi:10.1016/j.trecan.2016.11.008 · Cited by 1,003
Bogdahn, U., Hau, P., Stockhammer, G., Venkataramana, N. K., Mahapatra, A. K., Suri, A., Balasubramaniam, A., Nair, S., Oliushine, V., Parfenov, V., et al. (2011) · Neuro-Oncology · doi:10.1093/neuonc/noq142 · Cited by 433
Self-citationTransforming growth factor‐β in stem cells and tissue homeostasis
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Metadata
- Authors
- Hau, P., Jachimczak, P., Schlingensiepen, R., Schulmeyer, F., Jauch, T., Steinbrecher, A., Brawanski, A., Proescholdt, M., Schlaier, J., Buchroithner, J., Pichler, J., Wurm, G., Mehdorn, M., Strege, R., Schuierer, G., Villarrubia, V., Fellner, F., Jansen, O., Straube, T., Nohria, V., Goldbrunner, M., Kunst, M., Schmaus, S., Stauder, G., Bogdahn, U., & Schlingensiepen, K.-H.
- Venue
- Oligonucleotides
- Publisher
- SAGE Publications
- Published
- 2007-06
- Volume
- 17
- Issue
- 2
- Pages
- 201-212
- ISSN
- 1545-4576 (ISSN-L)
- 1557-8526
- OpenAlex
- W2110994430
- Cited by
- 215
- References
- 5
- FWCI
- 7.62
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Inhibition of TGF- β 2 with AP 12009 in Recurrent Malignant Gliomas: From Preclinical to Phase I/II Studies. https://app.cochat.ai/papers/10.1089/oli.2006.0053
- The paper
- Hau, P., Jachimczak, P., Schlingensiepen, R., Schulmeyer, F., Jauch, T., Steinbrecher, A., Brawanski, A., Proescholdt, M., Schlaier, J., Buchroithner, J., Pichler, J., Wurm, G., Mehdorn, M., Strege, R., Schuierer, G., Villarrubia, V., Fellner, F., Jansen, O., Straube, T., . . . Schlingensiepen, K.-H. (2007). Inhibition of TGF- β 2 with AP 12009 in Recurrent Malignant Gliomas: From Preclinical to Phase I/II Studies. Oligonucleotides. https://doi.org/10.1089/oli.2006.0053
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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