Search

Your search keyword '"Felding-Habermann, Brunhilde"' showing total 167 results
Start Over Author "Felding-Habermann, Brunhilde"
167 results on '"Felding-Habermann, Brunhilde"'

6. Synthesis of site-specific antibody-drug conjugates using unnatural amino acids

Author

Axup, Jun Y., Bajjuri, Krishna M., Ritland, Melissa, Hutchins, Benjamin M., Kim, Chan Hyuk, Kazane, Stephanie A., Halder, Rajkumar, Forsyth, Jane S., Santidrian, Antonio F., Stafin, Karin, Lu, Yingchun, Tran, Hon, Seller, Aaron J., Biroc, Sandra L., Szydlik, Aga, Pinkstaff, Jason K., Tian, Feng, Sinha, Subhash C., Felding-Habermann, Brunhilde, Smider, Vaughn V., and Schultz, Peter G.

Published
2012

9. Mitochondrial complex I activity and [NAD.sup.+]/NADH balance regulate breast cancer progression

Author

Santidrian, Antonio F., Matsuno-Yagi, Akemi, Ritland, Melissa, Seo, Byoung B., LeBoeuf, Sarah E., Gay, Laurie J., Yagi, Takao, and Felding-Habermann, Brunhilde

Subjects
Gene mutations -- Health aspects, Niacinamide -- Usage -- Health aspects, Breast cancer -- Genetic aspects -- Development and progression -- Research, Mitochondrial DNA -- Physiological aspects -- Research, Health care industry
Abstract

Despite advances in clinical therapy, metastasis remains the leading cause of death in breast cancer patients. Mutations in mitochondrial DNA, including those affecting complex I and oxidative phosphorylation, are found [...]

Published
2013
Full Text
View/download PDF

12. Activation of tumor cell integrin [[alpha].sub.v][[beta].sub.3] controls angiogenesis and metastatic growth in the brain

Author

Lorger, Mihaela, Krueger, Joseph S., ONeal, Melissa, Staflin, Karin, and Felding-Habermann, Brunhilde

Subjects
Integrins -- Physiological aspects, Metastasis -- Physiological aspects, Science and technology
Abstract

The incidence of brain metastasis is rising and poses a severe clinical problem, as we lack effective therapies and knowledge of mechanisms that control metastatic growth in the brain. Here we demonstrate a crucial role for high-affinity tumor cell integrin [[alpha].sub.v][[beta].sub.3] in brain metastatic growth and recruitment of blood vessels. Although [[alpha].sub.v][[beta].sub.3] is frequently up-regulated in primary brain tumors and metastatic lesions of brain homing cancers, we show that it is the [[alpha].sub.v][[beta].sub.3] activation state that is critical for brain lesion growth. Activated, but not non-activated, tumor cell [[alpha].sub.v][[beta].sub.3] supports efficient brain metastatic growth through continuous up-regulation of vascular endothelial growth factor (VEGF) protein under normoxic conditions. In metastatic brain lesions carrying activated [[alpha].sub.v][[beta].sub.3], VEGF expression is controlled at the post-transcriptional level and involves phosphorylation and inhibition of translational respressor 4E-binding protein (4E-BP1). In contrast, tumor cells with non-activated [[alpha].sub.v][[beta].sub.3] depend on hypoxia for VEGF induction, resulting in reduced angiogenesis, tumor cell apoptosis, and inefficient intracranial growth. Importantly, the microenvironment critically influences the effects that activated tumor cell [[alpha].sub.v][[beta].sub.3] exerts on tumor cell growth. Although it strongly promoted intracranial growth, the activation state of the receptor did not influence tumor growth in the mammary fat pad as a primary site. Thus, we identified a mechanism by which metastatic cells thrive in the brain microenvironment and use the high-affinity form of an adhesion receptor to grow and secure host support for proliferation. Targeting this molecular mechanism could prove valuable for the inhibition of brain metastasis. angiogenesis | brain metastasis | integrin activation | 4E-BP1

Published
2009

15. Activated integrin [alpha]v[beta]3 cooperates with metalloproteinase MMP-9 in regulating migration of metastatic breast cancer cells

Author

Rolli, Melanie, Fransvea, Emilia, Pilch, Jan, Saven, Alan, and Felding-Habermann, Brunhilde

Subjects
Breast cancer -- Research, Metastasis -- Research, Science and technology
Abstract

Expression of adhesion receptor integrin [alpha]v[beta]3 in an activated functional form strongly promotes metastasis in human breast cancer cells. Here, we report that [alpha]v[beta]3 cooperates with matrix metalloproteinase type 9 (MMP-9) in breast cancer cell migration. This cooperation is regulated by the activation state of the integrin. Expression of activated [alpha]v[beta]3 in metastatic variants of MDA-MB 435 human breast cancer cells and primary metastatic cells from breast cancer patients strongly enhanced migration toward vitronectin and fibrinogen. This enhancement was mediated by a soluble factor produced by breast cancer cells expressing activated [alpha]v[beta]3. When transferred, this factor also up-regulated [alpha]v[beta]3-dependent migration of breast cancer cells that express the nonactivated integrin. The factor was identified as metalloproteinase MMP-9. Whereas all tested breast cancer cell variants produced latent MMP-9, only those with activated [alpha]v[beta]3 produced the mature form of this metalloproteinase. Recombinant mature MMP-9, but not latent MMP-9 or either form of MMP-2, enhanced [alpha]v[beta]3-dependent breast cancer cell migration. The migratory response was inhibited by tissue inhibitors of metalloproteinase or when MMP-9 was depleted from the inducing supernatants. The results indicate a causal relationship between the expression of activated integrin [alpha]v[beta]3 and production of enzymatically active MMP-9 in metastatic breast cancer cells. These molecules cooperate to enhance breast cancer cell migration toward specific matrix proteins, and this may contribute to the strongly enhanced metastatic capacity of breast cancer cells that express activated [alpha]v[beta]3.

Published
2003

16. Phage-display selection of a human single-chain F (sub v) antibody highly specific for melonoma and breast cancer cells using a chemoenzymatically synthesized G (sub M3) - carbohydrate antigen

Author

Kyung Joo Lee, Mao, Shenlan, Sun, Chengzao, Gao, Changshou, Blixt, Ola, Arrues, Sandra, Hom, Louis G., Kaufmann, Gunnar F., Hoffman, Timothy Z., Coyle, Avery R., Paulson, James, Felding-Habermann, Brunhilde, and Janda, Kim D.

Subjects
Immunotherapy -- Research, Lipid metabolism -- Structure, Chemistry
Abstract

The chemo enzymatic synthesis of two G (sub M3)-derived reagents and their use in the panning of a phage-displayed human single-chain Fv (scFv) antibody library derived from the blood of cancer patients is described. The result is a significant step toward effective immunotherapies for the treatment of cancer.

Published
2002

23. Targeting heat shock proteins on cancer cells: Selection, characterization, and cell-penetrating properties of a peptide GRP78 ligand

Author

Kim, Youngsoo, Lillo, Antonietta M., Steiniger, Sebastian C.J., Liu, Ying, Ballatore, Carlo, Anichini, Andrea, Mortarini, Roberta, Kaufmann, Gunnar F., Zhou, Bin, Felding-Habermann, Brunhilde, and Janda, Kim D.

Subjects
Cancer cells -- Research, Heat shock proteins -- Health aspects, Heat shock proteins -- Research, Protein folding -- Analysis, Cancer -- Care and treatment, Biological sciences, Chemistry
Abstract

A set of cyclic peptide libraries expressed on the pIX coat protein of M13 filamentous phage, which were screened against melanoma cells is prepared and utilized, using whole-cell phage panning method to discover peptides that specifically bind to and are internalized into cancer cells. This showed that cyclic peptide Pep42 is a very important tool in construction of drug conjugates, designed to selectively kill malignant cancer cells.

Published
2006

24. A CXCR4-Targeted Site-Specific Antibody-Drug Conjugate

Author

Kularatne, Sumith A., primary, Deshmukh, Vishal, additional, Ma, Jennifer, additional, Tardif, Virginie, additional, Lim, Reyna K. V., additional, Pugh, Holly M., additional, Sun, Ying, additional, Manibusan, Anthony, additional, Sellers, Aaron J., additional, Barnett, Richard S., additional, Srinagesh, Shailaja, additional, Forsyth, Jane S., additional, Hassenpflug, Wolf, additional, Tian, Feng, additional, Javahishvili, Tsotne, additional, Felding-Habermann, Brunhilde, additional, Lawson, Brian R., additional, Kazane, Stephanie A., additional, and Schultz, Peter G., additional

Published
2014
Full Text
View/download PDF

26. Neural Stem Cell Delivery of Therapeutic Antibodies to Treat Breast Cancer Brain Metastases

Author

SCRIPPS RESEARCH INST LA JOLLA CA, Felding-Habermann, Brunhilde, SCRIPPS RESEARCH INST LA JOLLA CA, and Felding-Habermann, Brunhilde

Abstract

The goal of this study is to develop a new therapeutic approach for clinical inhibition of breast cancer brain metastasis. We have established and validated unique new breast cancer brain metastasis cell models and adapted mouse models to emulate all steps of human breast cancer brain metastasis development and invasive progression. These models are essential new tools for the evaluation of successful new therapies against widespread metastatic brain disease as seen in breast cancer patients. We determined subpopulations of these cells and investigated if cells with a putative stem-like marker profile are responsible for the initiation of brain lesions and successful intracranial metastasis growth. Contrary to current believe, we found that the cells with the putative stem-like marker profile are NOT responsible for highly efficient brain metastatic growth. This finding calls into question approaches that are attempting to target the putative stem cell marker molecules and, if known, their functions. Therefore, our results are valuable for a new outlook guide identification of potential new targets specifically for therapeutic inhibition of brain metastasis in breast cancer. With these advances, and identifying microglial cells as promising host cells for therapeutic use against brain lesions, we have made tangible progress toward new treatment options for breast cancer patients with cerebral metastasis., The original document contains color images.

Published
2010

27. Neural Stem Cell Delivery of Therapeutic Antibodies to Treat Breast Cancer Brain Metastases

Author

SCRIPPS RESEARCH INST LA JOLLA CA, Felding-Habermann, Brunhilde, SCRIPPS RESEARCH INST LA JOLLA CA, and Felding-Habermann, Brunhilde

Abstract

Our goal is to develop a therapeutic approach for clinical inhibition of breast cancer brain metastasis. Our work has identified a new molecular target for treatment of metastatic brain disease in breast cancer patients and provided antibody tools that successfully interrupt breast cancer metastasis in a mouse model. Systemic application of the antibodies does not sufficiently reach brain lesions to interfere with their development and progression. Therefore, we are developing delivery strategies to bring therapeutic antibodies to brain metastatic lesions and inhibit their proliferation. We have established and validated unique new breast cancer brain metastasis cell models and adapted mouse models to emulate all steps of human breast cancer brain metastasis development and invasive progression. These models are essential new tools for the evaluation of successful new therapies against widespread metastatic brain disease as seen in breast cancer patients. By investigating initial as well as late stages of brain metastasis development in the animal model, we have identified host cell responses that can be potentially used as therapeutic targets and for delivery of therapeutic molecules to disseminated breast cancer brain lesions. With these advances, we have made tangible progress toward new treatment options for breast cancer patients with cerebral metastasis.

Published
2009

31. Abstract 5251: CXCL14 as a functional determinant in a novel model of inflammatory, triple negative breast cancer progression

Author

MacDermed, Dhara M., primary, Lorger, Mihaela, additional, O'Sullivan, Deirdre, additional, Ritland, Melissa, additional, Forsyth, Jane, additional, Torkamani, Ali, additional, Murray, Sarah, additional, Steele, Julie, additional, Kroener, Joan, additional, Smider, Vaughn V., additional, and Felding-Habermann, Brunhilde, additional

Published
2011
Full Text
View/download PDF

37. An RNAi Screen Identifies TRRAP as a Regulator of Brain Tumor-Initiating Cell Differentiation

Author

Wurdak, Heiko, primary, Zhu, Shoutian, additional, Romero, Angelica, additional, Lorger, Mihaela, additional, Watson, James, additional, Chiang, Chih-yuan, additional, Zhang, Jay, additional, Natu, Vanita S., additional, Lairson, Luke L., additional, Walker, John R., additional, Trussell, Christopher M., additional, Harsh, Griffith R., additional, Vogel, Hannes, additional, Felding-Habermann, Brunhilde, additional, Orth, Anthony P., additional, Miraglia, Loren J., additional, Rines, Daniel R., additional, Skirboll, Stephen L., additional, and Schultz, Peter G., additional

Published
2010
Full Text
View/download PDF

39. Adhesive Mechanisms in Breast Cancer Metastasis

Author

SCRIPPS RESEARCH INST LA JOLLA CA, Felding-Habermann, Brunhilde, SCRIPPS RESEARCH INST LA JOLLA CA, and Felding-Habermann, Brunhilde

Abstract

Complications from metastatic disease are the primary cause of death in breast cancer. We found that human breast cancer cells can express the adhesion receptor integrin alpha v beta 3 in an activated or a non-activated functional form. Expression of the activated, but not the non-activated receptor supports metastatic dissemination. Mechanisms through which activated integrin alpha v beta 3 promotes metastasis include: binding of soluble ligand, support of tumor cell arrest during blood flow through tumor cell interaction with platelets, and promotion of breast cancer cell migration. Activated integrin alpha v beta 3 promotes breast cancer migration by cooperating with metalloproteinase MMP-9. A model mechanism for this cooperation is proposed. Our new findings support the originally proposed concept, that activation of breast cancer cell integrin alpha v beta 3 supports the metastatic phenotype in the tumor cells. Thus, these studies identify activated alpha v beta 3 as a new functional marker of metastatic breast cancer cells and indicate that activated alpha v beta 3 should be considered as a novel target for the inhibition of breast cancer metastasis., Original contains color plates: All DTIC reproductions will be in black and white.

Published
2001

40. Adhesive Mechanisms in Breast Cancer Metastasis

Author

SCRIPPS RESEARCH INST LA JOLLA CA, Felding-Habermann, Brunhilde, SCRIPPS RESEARCH INST LA JOLLA CA, and Felding-Habermann, Brunhilde

Abstract

The goal of this project is to understand adhesive mechanisms in breast cancer metastasis because this is the primary cause of death. Breast cancer metastasis to bone, lungs, liver and brain involves the blood stream and requires tumor cell arrest within the vasculature. In leukocytes and platelets, arrest within the vasculature depends on integrin activation. We found that breast cancer cells can express integrin alpha v beta 3 in an activated or a non-activated state. Only activated alpha v beta 3 supported breast cancer cell arrest during blood flow. The metastatic activity of breast cancer cells was strongly increased when alpha v beta 3 was activated.

Published
2000

46. Maspin alters the carcinoma proteome

Author

Chen, Emily I., primary, Florens, Laurence, additional, Axelrod, Fumiko T., additional, Monosov, Edward, additional, Barbas, Carlos F., additional, Yates, John R., additional, Felding‐Habermann, Brunhilde, additional, and Smith, Jeffrey W., additional

Published
2005
Full Text
View/download PDF

48. A Human Single-Chain Antibody Specific for Integrin α3β1 Capable of Cell Internalization and Delivery of Antitumor Agents

Author

Lillo, Antonietta M, primary, Sun, Chengzao, additional, Gao, Changshou, additional, Ditzel, Henrik, additional, Parrish, Jay, additional, Gauss, Carla-Marie, additional, Moss, Jason, additional, Felding-Habermann, Brunhilde, additional, Wirsching, Peter, additional, Boger, Dale L, additional, and Janda, Kim D, additional

Published
2004
Full Text
View/download PDF

50. Phage-Display Selection of a Human Single-Chain Fv Antibody Highly Specific for Melanoma and Breast Cancer Cells Using a Chemoenzymatically Synthesized GM3−Carbohydrate Antigen

Author

Lee, Kyung Joo, primary, Mao, Shenlan, additional, Sun, Chengzao, additional, Gao, Changshou, additional, Blixt, Ola, additional, Arrues, Sandra, additional, Hom, Louis G., additional, Kaufmann, Gunnar F., additional, Hoffman, Timothy Z., additional, Coyle, Avery R., additional, Paulson, James, additional, Felding-Habermann, Brunhilde, additional, and Janda, Kim D., additional

Published
2002
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results