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Cancer Drug Resist 2018;1:266-302 I http://dx.doi.org/10.20517/cdr.2018.18 Page 299

factor (HER2). The majority of aggressive (invasive and metastatic) breast cancers are negative for the ER
receptor (ER-) including the triple negative and basal subtypes (ER-, PR-, HER2-). Due to this, traditional
treatments such as hormonal replacement therapy are not suitable. Using bioinformatics, R scripting, and
datasets from 1,485 Caucasian samples (1,437 tumours and 48 normal tissues) with 21,000 genes from the
publicly available online GEO database (NCBI), we compared expression levels of ER negative (ER-) tu-
mours to ER positive (ER+) tumours. 7 protein coding genes were identified as candidate functional genes,
-31
where their expression was significantly up-regulated in ER- tumours (log2 FC= 1.02-1.24, P = 2.98E -
-19
6.47E ) which correlated with reduced survival using distant metastasis free survival in Kaplan-Meier
plotter (Log rank test, P = 0.0013-0.033). Next, we will determine the effect of copy number changes, the
functions of the genes in triple negative breast cancers and in cellular pathways, and then validate these
results in the laboratory to test their potential as novel therapeutic targets in aggressive cancers and as bio-
markers to predict prognosis or metastases.

60. CRUK-MedImmune Alliance Laboratory: a unique partnership in the discovery and

development of novel biologics

Sebastian Fielder, Denice Chan

Cancer Research UK-MedImmune Alliance Laboratory, The Portway Building, Granta Pk, Cambridge CB21
6GS, UK

In September 2014 Cancer Research UK (CRUK) and MedImmune entered into an innovative collabora-
tion with the aim of setting up a laboratory in Cambridge to develop novel cancer drugs for patients. As
part of its research review, CRUK identified that it needed to better leverage its biological expertise and
play a more prominent role in biotherapeutic discovery. At the same time, MedImmune were driving for-
ward towards the potential of more cures and realized the role key collaborations with organizations like
CRUK could play in the generation of novel oncology therapeutics. Crucial to the success of the Alliance
is for the lab to receive target proposals from researchers across the UK with and without CRUK funding.
Our mission: (1) to maximise cancer patient benefit; (2) to run a collaborative research laboratory; (3) to
actively engage the oncology research community; (4) to partner closely with investigators.

61. Using tumour deconvolution to identify determinants of anti-tumour immunity and
checkpoint blockade response

2
2
1
2
3
Ankur Chakravarthy , Andrew Furness , Kroopa Joshi , Ehsan Ghorani , Kirsty Ford , Matthew
4
3
3
1
2
J. Ward , Emma V. King , Matt Lechner , Teresa Marafioti , Sergio A. Quezada , Gareth J.
5
Thomas , Andrew Feber , Tim R. Fenton 6
3
1 Department of Oncology, UCL Cancer Institute, University College London, London WC1E 6BT, UK; present
address: Princess Margaret Cancer Centre, Toronto, Ontario M5G 2C4, Canada
2 Department of Haematology, UCL Cancer Institute, University College London, London WC1E 6BT, UK
3 Cancer Sciences Unit, University of Southampton, Tremona Road, Southampton SO16 6YD, UK
4 Department of Pathology, UCL Cancer Institute, University College London, London WC1E 6BT, UK
5 Division of Surgery and Interventional Science, University College London, London WC1E 6BT, UK
6 School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK
The nature and extent of immune cell infiltration into solid tumours are key determinants of therapeutic
response. Using a DNA methylation-based approach to tumour cell fraction deconvolution, we report the