英国癌症研究院

学校简介

英国癌症研究院是英国的一所公立性质院校，位于英国伦敦。英国癌症研究院是世界著名的癌症研究机构，隶属于伦敦大学。英国癌症研究院于1909年做为皇室马斯登医院的一个部门而成立，在2003年加入伦敦大学。连同皇室马斯登医院，英国癌症研究院是欧洲最大的综合癌症研究中心。在2008年的泰晤士报高等教育研究评估报告中，英国癌症研究院表现优秀。英国癌症研究院在北京大学医学部设有中国奖学金项目，英国癌症研究院是世界著名的癌症研究机构。该机构的中国奖学金项目旨在推动中国癌症研究水平，并促进英国癌症研究人员和中国同行之间建立紧密的合作关系。获得该奖学金的中国研究人员将前往英国著名的癌症研究所工作3年。英国癌症研究院可授予学生硕士和博士学位，开设的硕士学位为肿瘤学，开设的博士专业为：医学研究。

The ICR strategic aims

From its foundation in 1909 as a small research department of the Royal Marsden Hospital, the ICR has grown to become one of the world’s foremost independent cancer research organisations.

Our vision:

Is that people may live their lives free from the fear of cancer as a life threatening disease.

Our mission:

Is to relieve human suffering by pursuing excellence in the fight against cancer through:

Research into the causes, prevention, diagnosis and methods of treatment of cancer

Education and advanced training of medical and scientific staff

Treatment and care of the highest quality for cancer patients

Attraction and development of resources to the optimum effect

All that we do is driven by a set of values, which reflect our mission.

Achievements

Chief Executive, Professor Alan Ashworth

The ICR’s record of achievement in understanding the genetic basis of cancer is second to none, and our scientists continue to make significant progress.

Achievements in 2009/10 include:

We performed the first Phase I trial of an oral PARP inhibitor, Olaparib, in patients with cancer. We demonstrated that this treatment is safe and well tolerated, and in a focussed expansion we were the first to show significant activity for this treatment in patients with recurrent BRCA associated ovarian cancer. These trials are the first successful examples of personalised medicine using a synthetic lethality approach that targets a patient’s tumour specific molecular defect.

Genome-wide association studies identified three genetic variants that increase the risk of developing acute lymphoblastic leukaemia (ALL), the most common cancer in children. These results are the first evidence that genetic makeup plays a major role in the risk of ALL and will provide insight into how the disease develops.

Genome-wide association studies have provided insight into the development of brain tumours identifying five genetic variants that can increase the risk of developing Glioma, the most common form of brain cancer.

We have described how Rho GTPases, a key group of proteins, involved in the spread of tumours, are activated. Three-dimensional structural analysis revealed the mechanism through which members of the DOCK family activate Rho GTPases. The results provide a basis for the development of drugs that can target DOCK proteins and block metastasis.

By applying innovative computer modelling to studies of cell movement, ICR researchers have for the first time been able to investigate the timing and duration of key cell-to-cell signalling processes. This approach will be important in understanding how different cell populations communicate with each other during cancer development and progression.

Studies on drugs used to treat Melanoma showed that targeting the BRAF protein should only be undertaken in patients with a faulty version of BRAF. These results underline the importance of personalising treatment to those who are likely to best benefit from BRAF selective inhibitors.

We have discovered that having too many copies of the FGFR1 gene can cause resistance to the widely used drug Tamoxifen and other hormone-based therapy in breast cancer. By identifying the importance of the FGFR1 gene, these findings have revealed a new drug target for treating breast cancer in patients who would otherwise have a poor outcome.

The CR-UK Cancer Therapeutics Unit has developed GDC-0941 – a new drug which inhibits the PI3 kinase pathway – that reduces the most common form of brain tumour by 98% in laboratory tests. As a result, Phase I clinical trials are now being conducted in the UK and USA. 

We have found that in bowel cancer cells carrying the inherited mutation of either MLH1 or MSH2 genes (which prevent cells from repairing damaged DNA), blocking the action of another type of DNA repair protein stops the cells repairing DNA damage. Targeting cells already carrying one of these mutations with a drug that blocks this second part of DNA repair could be an effective personalised treatment for bowel cancers caused by these mutations.

Results from clinical trials in early breast cancer have found that the effectiveness and patient-reported chronic side-effects of radiotherapy, are not any worse when given as

a lower total dose, delivered in fewer, larger treatments compared with the standard of a higher total dose delivered over a longer time. As a result, radiotherapy treatments

can be changed so that women spend less time in hospital and the cost to the NHS is reduced.