Novel therapies for metastatic castrate-resistant prostate cancer
Recent advances in tumor biology have made remarkable achievements in the development of therapy for metastatic castrate-resistant prostate cancer. These advances reflect a growing appreciation for the role of the tumor microenvironment in promoting prostate cancer progression. Prostate cancer is no...
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| Published in: | JNCI : Journal of the National Cancer Institute Vol. 103; no. 22; p. 1665 |
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| Main Authors: | , , , |
| Format: | Journal Article |
| Language: | English |
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United States
16.11.2011
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| ISSN: | 1460-2105, 1460-2105 |
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| Abstract | Recent advances in tumor biology have made remarkable achievements in the development of therapy for metastatic castrate-resistant prostate cancer. These advances reflect a growing appreciation for the role of the tumor microenvironment in promoting prostate cancer progression. Prostate cancer is no longer viewed predominantly as a disease of abnormally proliferating epithelial cells but rather as a disease of complex interactions between prostate cancer epithelial cells (epithelial compartment) and the surrounding tissues (stromal compartment) in which they reside. For example, prostate cancers frequently metastasize to bone, an organ that contains a microenvironment rich in extracellular matrix proteins and stromal cells including hematopoietic cells, osteoblasts, osteoclasts fibroblasts, endothelial cells, adipocytes, immune cells, and mesenchymal stem cells. Multiple signaling pathways provide crosstalk between the epithelial and the stromal compartments to enhance tumor growth, including androgen receptor signaling, tyrosine kinase receptor signaling, and immune surveillance. The rationale to disrupt this "two-compartment" crosstalk has led to the development of drugs that target tumor stromal elements in addition to the cancer epithelial cell. |
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| AbstractList | Recent advances in tumor biology have made remarkable achievements in the development of therapy for metastatic castrate-resistant prostate cancer. These advances reflect a growing appreciation for the role of the tumor microenvironment in promoting prostate cancer progression. Prostate cancer is no longer viewed predominantly as a disease of abnormally proliferating epithelial cells but rather as a disease of complex interactions between prostate cancer epithelial cells (epithelial compartment) and the surrounding tissues (stromal compartment) in which they reside. For example, prostate cancers frequently metastasize to bone, an organ that contains a microenvironment rich in extracellular matrix proteins and stromal cells including hematopoietic cells, osteoblasts, osteoclasts fibroblasts, endothelial cells, adipocytes, immune cells, and mesenchymal stem cells. Multiple signaling pathways provide crosstalk between the epithelial and the stromal compartments to enhance tumor growth, including androgen receptor signaling, tyrosine kinase receptor signaling, and immune surveillance. The rationale to disrupt this "two-compartment" crosstalk has led to the development of drugs that target tumor stromal elements in addition to the cancer epithelial cell.Recent advances in tumor biology have made remarkable achievements in the development of therapy for metastatic castrate-resistant prostate cancer. These advances reflect a growing appreciation for the role of the tumor microenvironment in promoting prostate cancer progression. Prostate cancer is no longer viewed predominantly as a disease of abnormally proliferating epithelial cells but rather as a disease of complex interactions between prostate cancer epithelial cells (epithelial compartment) and the surrounding tissues (stromal compartment) in which they reside. For example, prostate cancers frequently metastasize to bone, an organ that contains a microenvironment rich in extracellular matrix proteins and stromal cells including hematopoietic cells, osteoblasts, osteoclasts fibroblasts, endothelial cells, adipocytes, immune cells, and mesenchymal stem cells. Multiple signaling pathways provide crosstalk between the epithelial and the stromal compartments to enhance tumor growth, including androgen receptor signaling, tyrosine kinase receptor signaling, and immune surveillance. The rationale to disrupt this "two-compartment" crosstalk has led to the development of drugs that target tumor stromal elements in addition to the cancer epithelial cell. Recent advances in tumor biology have made remarkable achievements in the development of therapy for metastatic castrate-resistant prostate cancer. These advances reflect a growing appreciation for the role of the tumor microenvironment in promoting prostate cancer progression. Prostate cancer is no longer viewed predominantly as a disease of abnormally proliferating epithelial cells but rather as a disease of complex interactions between prostate cancer epithelial cells (epithelial compartment) and the surrounding tissues (stromal compartment) in which they reside. For example, prostate cancers frequently metastasize to bone, an organ that contains a microenvironment rich in extracellular matrix proteins and stromal cells including hematopoietic cells, osteoblasts, osteoclasts fibroblasts, endothelial cells, adipocytes, immune cells, and mesenchymal stem cells. Multiple signaling pathways provide crosstalk between the epithelial and the stromal compartments to enhance tumor growth, including androgen receptor signaling, tyrosine kinase receptor signaling, and immune surveillance. The rationale to disrupt this "two-compartment" crosstalk has led to the development of drugs that target tumor stromal elements in addition to the cancer epithelial cell. |
| Author | Dayyani, Farshid Logothetis, Christopher J Gallick, Gary E Corn, Paul G |
| Author_xml | – sequence: 1 givenname: Farshid surname: Dayyani fullname: Dayyani, Farshid organization: Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA – sequence: 2 givenname: Gary E surname: Gallick fullname: Gallick, Gary E – sequence: 3 givenname: Christopher J surname: Logothetis fullname: Logothetis, Christopher J – sequence: 4 givenname: Paul G surname: Corn fullname: Corn, Paul G |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21917607$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Androstenes Androstenols - pharmacology Angiogenesis Inhibitors - pharmacology Anilides - pharmacology Animals Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal, Humanized - pharmacology Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Antineoplastic Agents, Hormonal - pharmacology Atrasentan Bevacizumab Biomarkers, Tumor - blood Bone Remodeling - drug effects Cancer Vaccines - immunology Cancer Vaccines - pharmacology Clinical Trials as Topic Clusterin - pharmacology Dasatinib Denosumab Endothelin-1 - antagonists & inhibitors Humans Immunotherapy - methods Indoles - pharmacology Ipilimumab Male Mice Mice, SCID Molecular Targeted Therapy - methods Orchiectomy Phenylthiohydantoin - analogs & derivatives Phenylthiohydantoin - pharmacology Prostate-Specific Antigen - blood Prostatic Neoplasms - drug therapy Prostatic Neoplasms - immunology Prostatic Neoplasms - pathology Pyridines - pharmacology Pyrimidines - pharmacology Pyrroles - pharmacology Pyrrolidines - pharmacology RANK Ligand - antagonists & inhibitors RANK Ligand - pharmacology Receptor Cross-Talk - drug effects Receptors, Androgen - drug effects Signal Transduction - drug effects Sunitinib Taxoids - pharmacology Thiazoles - pharmacology Tissue Extracts - pharmacology Treatment Failure Tumor Microenvironment - drug effects Xenograft Model Antitumor Assays |
| Title | Novel therapies for metastatic castrate-resistant prostate cancer |
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