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Towards drug discovery for brain tumours: interaction of kinins and tumours at the blood brain barrier interface.
Recent Pat CNS Drug Discov 2011; 6(1):31-40RP

Abstract

Cancers of the brain are intrinsically more complicated to treat than systemic malignancies due to the unique anatomical features of the brain. The blood-brain barrier prevents chemotherapeutic agents from reaching brain neoplasms, and angiogenesis occurs as the metabolic needs of the tumour increase, thus further complicating treatment. The newly formed blood vessels form the blood-tumour barrier and are distinct from the blood-brain barrier in that they are more permeable. Being more permeable, these abnormal blood vessels lead to the formation of peri-tumoural edema, which is the cause of much morbidity and mortality associated with central nervous system neoplasms. While the cause of the increased permeability is unclear, kinins have been implicated in regulating the permeability of normal vasculature. Kinins are also known to exert many inflammatory actions affecting both normal and angiogenic blood vessels, as well as tumour cells. The vasodilatory and vascular permeabilizing effects of kinins, and particularly bradykinin and substance P, have been investigated with regard to delivery of chemotherapeutic agents to neoplastic brain tissue through both vascular barriers. In contrast, kinin receptor antagonists have been found to exert effects on tumour cells that result in decreased angiogenesis, tumour cell motility and growth. Thus, many recent patents describe kinin activity on brain vasculature, which may play an integral role in the development of treatments for malignancies in the central nervous system through amelioration of angiogenesis. In conjunction, patents that discuss the ability of kinins to decrease tumour cell migration and proliferation demonstrate that kinins may offer novel approaches to brain tumour therapy in the future.

Authors+Show Affiliations

Adelaide Centre for Neuroscience Research, and the Discipline of Anatomy and Pathology, University of Adelaide, Adelaide, South Australia.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

21073431

Citation

Harford-Wright, Elizabeth, et al. "Towards Drug Discovery for Brain Tumours: Interaction of Kinins and Tumours at the Blood Brain Barrier Interface." Recent Patents On CNS Drug Discovery, vol. 6, no. 1, 2011, pp. 31-40.
Harford-Wright E, Lewis KM, Vink R. Towards drug discovery for brain tumours: interaction of kinins and tumours at the blood brain barrier interface. Recent Pat CNS Drug Discov. 2011;6(1):31-40.
Harford-Wright, E., Lewis, K. M., & Vink, R. (2011). Towards drug discovery for brain tumours: interaction of kinins and tumours at the blood brain barrier interface. Recent Patents On CNS Drug Discovery, 6(1), pp. 31-40.
Harford-Wright E, Lewis KM, Vink R. Towards Drug Discovery for Brain Tumours: Interaction of Kinins and Tumours at the Blood Brain Barrier Interface. Recent Pat CNS Drug Discov. 2011;6(1):31-40. PubMed PMID: 21073431.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Towards drug discovery for brain tumours: interaction of kinins and tumours at the blood brain barrier interface. AU - Harford-Wright,Elizabeth, AU - Lewis,Kate M, AU - Vink,Robert, PY - 2010/09/12/received PY - 2010/10/27/accepted PY - 2010/11/16/entrez PY - 2010/11/16/pubmed PY - 2011/4/16/medline SP - 31 EP - 40 JF - Recent patents on CNS drug discovery JO - Recent Pat CNS Drug Discov VL - 6 IS - 1 N2 - Cancers of the brain are intrinsically more complicated to treat than systemic malignancies due to the unique anatomical features of the brain. The blood-brain barrier prevents chemotherapeutic agents from reaching brain neoplasms, and angiogenesis occurs as the metabolic needs of the tumour increase, thus further complicating treatment. The newly formed blood vessels form the blood-tumour barrier and are distinct from the blood-brain barrier in that they are more permeable. Being more permeable, these abnormal blood vessels lead to the formation of peri-tumoural edema, which is the cause of much morbidity and mortality associated with central nervous system neoplasms. While the cause of the increased permeability is unclear, kinins have been implicated in regulating the permeability of normal vasculature. Kinins are also known to exert many inflammatory actions affecting both normal and angiogenic blood vessels, as well as tumour cells. The vasodilatory and vascular permeabilizing effects of kinins, and particularly bradykinin and substance P, have been investigated with regard to delivery of chemotherapeutic agents to neoplastic brain tissue through both vascular barriers. In contrast, kinin receptor antagonists have been found to exert effects on tumour cells that result in decreased angiogenesis, tumour cell motility and growth. Thus, many recent patents describe kinin activity on brain vasculature, which may play an integral role in the development of treatments for malignancies in the central nervous system through amelioration of angiogenesis. In conjunction, patents that discuss the ability of kinins to decrease tumour cell migration and proliferation demonstrate that kinins may offer novel approaches to brain tumour therapy in the future. SN - 2212-3954 UR - https://www.unboundmedicine.com/medline/citation/21073431/Towards_drug_discovery_for_brain_tumours:_interaction_of_kinins_and_tumours_at_the_blood_brain_barrier_interface_ L2 - http://www.eurekaselect.com/87276/article DB - PRIME DP - Unbound Medicine ER -