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Results

Clinical PhD Programme in Cancer Research 30 Nov 2016

The Institute of Cancer Research (ICR), a degree-awarding, independent college of the University of London, proposes to host a Clinical PhD Programme in Cancer Research. The Clinical Fellows appointed to this Programme will be embedded in the highly successful translational research culture of the ICR, and our hospital partner the Royal Marsden Hospital (RM). Clinical Fellows will directly contribute to delivering practice-changing research and will be an integral part of the flow of ideas in both directions between the laboratory and the clinic. The Clinical Fellows will participate in, and learn from, research teams working as parts of global consortia on projects as diverse as understanding cell division, MR-guided radiotherapy, novel drug discovery and development; genome damage and stability and big data approaches. We will continue to maximise opportunities to support the career development of Clinical Fellows on this Programme; build on existing good practice in supporting clinical academics, strengthen the provision of training tools, workshops and mentorship opportunities; and facilitate communication and the establishment of collaborative relationships between ICR and RM clinical researchers at different career stages. The ultimate goal of the Programme is to train, develop and support future international leaders in clinical cancer research.

Amount: £2,565,000
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Epigenetic analysis of the LSP1-rs3817198 breast cancer risk locus 31 May 2018

rs3817198 at 11p15.5 is associated with estrogen receptor-positive breast cancer risk. This locus shows a parent of origin effect and effect modification by parity. Fine-scale mapping of this region identified seven possible single nucleotide polymorphisms (SNPs), all within 11kb of the 5’ end of Lymphocyte Specific Protein (LSP1), any of which could be causally associated with risk. Four of these map within a region that shows differential methylation and one of them (rs686722) co-localises precisely with a CpG methylated site. We hypothesise that rs686722 influences breast cancer risk because both the allele (C/T) and the methylation of the "C" affect expression of LSP1. The mechanism by which LSP1 could influence breast cancer risk is not clear; one possibility is via an effect on the motility of lymphocytes within the breast stroma. For this project we will use lymphocyte DNA from women participating in the Generations Study and CEPH individuals. The key goals are to investigate the methylation of rs686722 with regard to the parental origin of a woman's C allele and her parity. We will also use lymphoblastoid cell lines from heterozygous CEPH individuals to test for allele specific expression of LSP1.

Amount: £0
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Investigating functional pathway dependencies in mutation EGFR lung cancer 27 Apr 2017

EGFR inhibitors (EGFRi) are successfully used to treat non-small cell lung cancer (NSCLC), however, 10-20% of patients with EGFR mutations initially fail to respond to first-line EGFRi treatment. The mechanisms underlying intrinsic resistance to EGFRi in NSCLC patients are unclear. This project will investigate the signalling pathways essential for the survival of EGFRi-resistant NSCLC. Targeted siRNA screens have been performed in the laboratory using unique established and patient-derived cell line models which model intrinsic EGFRi resistance. The key goals of this 8 week project will be to validate preliminary RNAi screening data using an orthogonal approach. An inducible CRISPR interference (CRISPRi) system will be developed to validate the cytotoxic response observed upon knockdown of specific genes in combination with EGFRi treatment. An advantage of CRISPRi is that it is scalable, providing flexibility to examine the global signalling alterations arising from lethal interactions. CRISPRi will facilitate large-scale molecular profiling techniques including RNA-Seq and mass spectrometry based proteomics. This will provide the groundwork to ultimately define the bypass signalling pathways driving intrinsic resistance in mutant EGFR lung cancer. With this knowledge, novel therapeutic strategies can be developed as effective salvage treatments for lung cancer patients who do not respond to EGFRi treatment.

Amount: £0
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Unravelling the genetics of testicular cancer 01 Apr 2016

Genome wide association studies (GWAS) have enabled great progress in our understanding of testicular germ cell tumour (TGCT), with 25 risk variants identified to date which increase cancer risk. Mapping a risk variant to its gene target is a non-trivial task, given the complex nature of gene regulation and possibility of long range regulatory effects. A systems level approach is required, with multiple regulatory data-sets combined to gain an integrated functional viewpoint. To this end, we propose using GWAS region fine-mapping, expression quantitative trait loci analysis and transcription factor binding analyses. The clinical benefits of this are two-fold. Firstly, there is potential for diagnostic utility, in particular testing healthy individuals to identify those at high risk. These individuals could then benefit from enhanced screening protocols with the ultimate aim of early detection/cancer prevention. Secondly these genetic variants offer rich biological insight into the mechanisms of cancer development, providing new opportunities for drug development. This second benefit is rapidly becoming a major focus, as genetic evidence is becoming increasingly important for drug target identification and validation.

Amount: £2,000
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Functional genomic screens to determine initiating and maintenance events in human medulloblastoma 18 May 2016

Medulloblastoma (MB) is the most common malignant brain tumour in children. Four molecular subgroups have been identified through large-scale genomic studies, and approximately one-third of patients have the sonic hedgehog (SHH) subtype. Mutations in the SHH-receptor Patched (PTCH) are found in 25% of this sub-type. Mouse models have provided critical insight into mechanisms of MB initiation. However, the experimental tumours do not reflect the mutational complexity of the human disease. The co-operative events that initiate transformation of pre-malignant cells to MB in humans is unknown. Recent advances in stem cell technology have led to novel in vitro systems representing hindbrain precursors. Stable, long-term neuro-epithelial stem (NES) cells with hindbrain identity and potency for cerebellar cells have been generated during my time in Austin Smith’s lab from human pluripotent stem cells and directly from the human hindbrain. These cells represent a candidate cell of origin for MB, and my preliminary studies in collaboration with William Weiss show that NES cells harbouring germ-line mutations in PTCH generate medulloblastoma in xenografts. My goal for this fellowship is to use PTCH+/- NES cells in combination with genome-editing tools to discover genes that co-operate with PTCH to initiate and maintain MB in the human context.

Amount: £239,643
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Open access publishing costs 2014/15. 15 Sep 2014

Not available

Amount: £63,573
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Identification of PARP inhibitors for cancer therapy 15 Sep 2014

While effective treatments for many forms of cancer exist, therapies that are tailored for patients with niche forms of the disease, such as triple negative breast cancer are currently unavailable. The Trust has awarded £3.9 million over three years to Prof. Alan Ashworth, FRS, Dr. Christopher Lord, Prof. Caroline Springer and Prof. Laurence Pearl, FRS, for the development of orally available small molecules that could target specific cancer subtypes. Researchers led by Prof Alan Ashworth and Dr Christopher Lord have pioneered the exploitation of novel therapeutic approaches such as synthetic lethality and the use of PARP inhibitors in cancer treatment. PARP (Poly ADP-Ribose Polymerase) enzymes modify proteins and control cell function by catalyzing the addition of poly (ADP-ribose) polymers onto substrates. With funding from the Trust, Ashworth, Lord, Springer and Pearl, in collaboration with Domainex, will develop novel small molecule inhibitors that target additional PARP superfamily members. These inhibitors will be assessed in specific tumour models and then progressed into clinical candidates that could be ultimately assessed in drug trials that target cancer subtypes for which there is significant unmet clinical need.

Amount: £1,459,846
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Mechanism based drug descovery. 24 Jun 2013

The interactions of small molecules and proteins are highly dependent on their shape complementarity and electronics. Exploration of the shapes of protein binding sites through in silico analysis and relation of these to the shapes of exemplified ligand space could enable us to tune the shapes of the molecules in screening libraries to specific drug discovery targets. This analysis could also allow us to identify protein binding site shapes for which hit molecules are scarce and by giving attention to this, could be used to generate hits for targets that are considered 'undruggable'. Initially, conformational analysis of the bound shapes of endogenous ligands will be conducted in order to learn from nature's balance between protein binding site space and ligand space.

Amount: £160,623
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Mechanism-based Drug Discovery. 24 Jun 2013

The Hsp70 proteins are a family of molecular chaperones required for correct protein folding in response to cellular stress. Hsp70 is up-regulated in numerous cancer types,and both RNAi silencing and pharmacological inhibition has been shown to induce cell death in transf ormed cells. As a result,extensive efforts have been made to develop an Hsp70 inhibitor. Several inhibitors have been reported,however all possess poor drug-like properties and for most their mechanism of action remains poorly understood. The aim of this study is to characterise these inhibitors,by their comparison using a suite of biochemical and biophysical assays. Dependent on the outcome of these studies, selected compounds will be further investigated using structural studies.

Amount: £160,623
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Understanding the structure and mechanism of macromolecular machines that regulate chromatin dynamics 10 May 2011

Eukaryotic genomes are packaged into nucleosomes in which the DNA is wrapped around histone octamers, that in turn form higher order structures (chromatin) withinwhich the nucleosomes are packed together. While this arrangement of the genetic material adds a level of organisation and stability, it also creates problems for processes that need to access DNA such as transcription, replication and repair. For example, the DNAdamage response involves a whole slew of changes to chromatin that are orchestrated during DNA repair. This has made the regulation of chromatin structure and dynamics a central focus for understanding a wide range of fundamental biological processes that involve the genetic material. As we learn more about chromatin regulation it is becoming clear how much morethere is to understand, particularly at a molecular and mechanistic level. How do proteins slide nucleosomes around so that proteins can access the DNA? How are nucleosomes assembled and disassembled? How is damage detected within nucleosomes ? What signals recruit remodellers to nucleosomes that are damaged? As we begin to unveil these processes, we are discovering fascinating and intricate, multi-subunit proteinmachines that carry out these complex tasks in a coordinated fashion. Although the sheer complexity and size of many of the protein machines that deal with chromatin can appear daunting, we need to be able to understand these processes at a molecular level to trulyunderstand how things work, how they go wrong and how we might interfere with them in a specific manner to control disease.

Amount: £2,218,192
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

The development of tankyrase inhibitors for use in breast cancer therapy. 28 May 2013

We propose to develop orally-bioavailable small molecule drugs that inhibit tankyrase 1 - a novel target for breast cancer therapy. Our data indicate that such drugs could be used in a synthetic lethality approach to treat cancer. A tankyrase 1 inhibitor would confront several tumour-specific characteristics and would be useful for treatment of specific breast cancer subtypes with a poor prognosis, where few treatment options exist. As part of this drug research programme, we will build on our existing in-house and proprietary knowledge to generate novel, patented candidate drugs that will be used in first in class Phase 1 clinical trials at The Royal Marsden Hospital. The programme we propose will include: 1) the further development of our existing prototype tankyrase 1 inhibitors, which we have identified following pre-selection of a compound set using an in silico based screen, 2) the delineation of a proprietary crystal structure of the active form of tankyrase 1 to guide the design of inhibitors, 3) a comprehensive medicinal chemistry programme, 4) the use of cellular assay systems and in vivo therapeutic efficacy assessments to aid the development of inhibitors and companion biomarkers and 5) high-throughput genetic and drug synergy screens that will identify companion biomarkers and direct the design of clinical trials. This programme will be underpinned by: (i) the unique in-depth knowledge of breast cancer, synthetic lethality and tankyrase 1 biology of the research team led by the Principal Applicant, (ii) the strong track-record of key members of the project team in drug research, and (iii) the strengths in structural biology and drug development available within the host Institute.

Amount: £100,000
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

The development of tankyrase inhibitors for use in breast cancer therapy. 06 Nov 2009

We propose to develop orally-bioavailable small molecule drugs that inhibit tankyrase 1 - a novel target for breast cancer therapy. Our data indicate that such drugs could be used in a synthetic lethality approach to treat cancer. A tankyrase 1 inhibitor would confront several tumour-specific characteristics and would be useful for treatment of specific breast cancer subtypes with a poor prognosis, where few treatment options exist. As part of this drug research programme, we will build on our existing in-house and proprietary knowledge to generate novel, patented candidate drugs that will be used in first in class Phase 1 clinical trials at The Royal Marsden Hospital. The programme we propose will include: 1) the further development of our existing prototype tankyrase 1 inhibitors, which we have identified following pre-selection of a compound set using an in silico based screen, 2) the delineation of a proprietary crystal structure of the active form of tankyrase 1 to guide the design of inhibitors, 3) a comprehensive medicinal chemistry programme, 4) the use of cellular assay systems and in vivo therapeutic efficacy assessments to aid the development of inhibitors and companion biomarkers and 5) high-throughput genetic and drug synergy screens that will identify companion biomarkers and direct the design of clinical trials. This programme will be underpinned by: (i) the unique in-depth knowledge of breast cancer, synthetic lethality and tankyrase 1 biology of the research team led by the Principal Applicant, (ii) the strong track-record of key members of the project team in drug research, and (iii) the strengths in structural biology and drug development available within the host Institute.

Amount: £1,465,153
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Inhibitors of Lysyl Oxidase for the Prevention and Treatment of Invasive and Metastatic Cancer 30 Jul 2010

Inhibitors of Lysyl Oxidase for the Prevention and Treatment of Invasive and Metastatic CancerThe enzyme lysyl oxidase (LOX) regulates cross-linking of structural proteins in the extracellular matrix.LOX also plays a role in stimulating the metastatic spread of cancer through the body. Its expression is increased in hypoxic cancers and is correlated with tumour metastasis and decreased patient survival. In model systems its inhibition significantly decreases cancer metastasis and increases survival. Since metastasis is responsible for over 90 per cent of cancer deaths these data validate LOX as an important therapeutic target in cancer. Professor Caroline Springer and Professor Richard Marais from the Institute of Cancer Research have been awarded Seeding Drug Discovery funding to develop drugs that target LOX. They are applying a medicinal chemistry drug discovery approach underpinned by a strong programme in LOX biology with the aim of producing orally available, small molecular weight drugs that inhibit LOX activity for cancer treatment.See our video: BRAF and cancer: collaborative drug discovery

Amount: £818,674
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Biomedical Vacation Scholarship 14 Jun 2010

Not available

Amount: £1,520
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Synthesis of cancer targeting compounds derived from a fragment-based approach. 08 Jun 2009

In the initial phase of this project, the PhD student will synthesise selected fragment type molecules, which mimic the observed5 interaction of TLE1 with the small peptide sequences. These specific fragments will supplement the fragment library, which is routinely used at the I CR. Within the structure based drug design team (SBDD} and the section of structure biology these specific fragments as well as the ICR fragment collection will be screened for binding to TLE1. Fragments with sufficient affinity for TLE1 will be co-crystalized. The PhD student will use these co-crystal structures to design and synthesise more complex and potent inhibitors of TLE1 binding thus completing the first round of testing, crystallography and synthesis. Additional iterative rounds will lead to inhibitors with further improved properties. The overall goal is to obtain inhibitors suitable for investigating the role of TLE1 in a cellular setting and potentially in in vivo models.

Amount: £152,502
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research