Brain tumour detection and treatment
While the blood brain barrier is essential for protecting the brain against the invasion of unwanted molecules, it also blocks the passage of diagnostic and therapeutic agents, presenting a limitation to the early detection, diagnosis and treatment of brain metastases.
A research team from Oxford University have shown in a preclinical model that the use of a cytokine adjunct can facilitate the detection of brain metastases as small as 100µm in diameter. This equates to a clinical diagnosis several months earlier than currently possible and potentiates the selective delivery of high molecular weight therapeutic agents such as antibodies and radiosensitisers to otherwise untreatable early tumours.
Metastatic spread to the brain
Brain metastasis (BM) is one of the greatest hurdles in cancer therapy. 20-40% of all cancer patients will suffer metastatic spread of the primary cancer to the brain. Unfortunately, the challenge in diagnosing and quantitating BM at a sufficiently early stage presents a major limitation in the treatment and management of cancer patients. Clinical diagnosis of BM is limited to larger, late-stage metastases and early detection of microtumours <5mm remains impossible.
Oxford researchers have shown that the cytokine tumour necrosis factor-alpha (TNFa) may act as an adjunct to selectively and transiently permeabilise the intact blood brain barrier, to potentiate delivery of high molecular weight drugs and imaging agents to early brain metastases. The group have recently demonstrated delivery of the anti-breast cancer antibody Herceptin® to discrete brain metastases. Importantly, this approach offers a treatment option to otherwise inaccessible and untreatable brain tumours.
The work at the University of Oxford has demonstrated that:
low dose cytokines can be used as an adjunct therapy to temporarily and reversibly increase blood-brain barrier permeability and improve delivery of imaging and therapeutic agents
cytokines selectively permeabilise the blood-brain barrier at tumour sites only – TNFR1 is mechanistically implicated by specific expression of TNFR1 in the brain vasculature of metastatic lesions
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