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The QMUL Centre of the Cell, the first informal science learning centre to be located within a working research facility, are running a training workshop for researchers within CRUK RadNet City of London.

The session will give researchers of all levels and experience the skills to run a successful public engagement activity.

Equally, if interested, researchers can apply their training by taking part in a short series of patient/researcher workshops to be carried out in the near future.

When? Virtual session from 2-5pm on the 14th June (Zoom).

What? Topics covered include (i) who the public are and (ii) what public engagement is. It will also look into (iii) what makes a good presentation, and (iv) provide tips on how to maximise your engagement with your audience.

How do I take part? Email info@centreofthecell.org

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CRUK RadNet City of London Seminar Series #7

Radiotherapy-induced in situ immunization: Mechanisms and barriers.

18th May 2021 at 3:00-4:00 pm GMT

Hosted by Dr Anthony Kong Reader and Honorary Consultant Clinical Oncologist at King’s College London, we will be exploring the mechanisms and barriers of Radiotherapy-induced situ immunisation with guest speaker, Dr Sandra Demaria from the Weill Cornell Medical College.

A bit about our speaker:

Sandra Demaria, M.D. is currently Professor of Radiation Oncology and Pathology and Laboratory Medicine at Weill Cornell Medicine in New York City. Dr. Demaria is internationally known for her studies demonstrating the synergy of radiotherapy with immunotherapy in pre-clinical cancer models. She was the first to show that radiotherapy can convert tumors unresponsive to immune checkpoint inhibitors into responsive ones, a finding being translated in several clinical trials at multiple institutions.

Her lab has a central interest in addressing the molecular mechanisms that regulate ionizing radiation’s ability to generate an in situ tumor vaccine in both preclinical models as well as cancer patients. Her group has recently demonstrated the development of neoantigen-specific T cells in lung cancer patients treated with focal radiotherapy and ipilimumab. As a breast cancer pathologist Dr. Demaria also studies the immunological microenvironment of breast cancer in patients, and therapeutic strategies to modulate the immune infiltrate in preclinical models and in patients.

She has authored more than 120 articles and has received awards from the US National Cancer Institute, American Cancer Society, the Department of Defense CDMRP, and several private Foundations, and serves in the editorial board of Cancer Immunology Research, and the Journal for the ImmunoTherapy of Cancer. She is currently the Chair of the AACR Cancer Immunology Working Group, and has previously served in the board of the Society for the Immunotherapy of Cancer (SITC) and the Radiation Research Society (RRS).

To watch a full recording of the seminar with Dr Sandra Demaria, click here.

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CRUK RadNet City of London Seminar Series #6

Mechanisms that Maintain Genome Stability.

7th May 2021 at 2:30-3:30pm GMT

Hosted by Dr Ivana Bjedov, Group Leader at the Molecular Biology of Cancer Research Group, we will be exploring the mechanisms that maintain genome stability with guest speaker, Andre Nussenzweig Ph.D., National Cancer Institute.

A bit about our speaker:

Dr. Nussenzweig is a leading contributor to the study of mechanisms that maintain genomic stability and prevent cancer. His laboratory has elucidated many fundamental features of DNA damage and repair proteins and revealed the critical role they play in both normal and pathogenic states. Ongoing studies have emphasized the importance of DNA repair pathways as drivers of specific hematological malignancies and as contributors to chemoresistance/sensitivity in breast and ovarian cancers. The goal of his program is to use hypothesis-driven approaches to develop therapeutic strategies in the treatment of cancers.

Areas of Expertise

1) genomic Instability, 2) DNA damage/repair, 3) breast/ovarian cancers, 4) recombination/replication, 5) chromosomal translocations, 6) adult/pediatric leukemias

To watch a full recording of our seminar with Andre Nussenzweig, click here. 

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The GOOD, the ELDER & the UGLY: RNA Vaccine & Radiotherapy to fight Cancer

19th April 2021 at 09:15 – 10:15 GMT

Hosted by Dr Anthony Kong Reader and Honorary Consultant Clinical Oncologist at King’s College London, we will be exploring the relationship between the RNA vaccine and radiotherapy with guest speaker, Dr Fulvia Vascotto, leader of Vaccine and Cellular Immunotherapy at TRON.

A bit about our speaker:

Dr. Fulvia Vascotto graduated in Molecular Biology at University of Trieste and obtained a PhD in Molecular Immunology at ICGEB Trieste working on the development of blocking intracellular antibodies against viral (Rotavirus) proteins.

After a first post-doctoral training in the laboratory of Dr. Ana-Maria Lennon-Duménil, in the unit of Dr. Sebastian Amigorena at the Institute Curie in Paris on the cell biology of B cells and dendritic cells. She identified myosin II as the actin cytoskeleton motor protein involved in the regulation of antigen uptake, trafficking, processing, and presentation. Then she moved to Harvard Medical School, Boston, in the laboratory of Prof. Dr. Ulrich von Andrian, extending immunology experience in vivo in mice in particular in the field of NK and regulatory T cell biology in contact hypersensitivity model using multicolor flow cytometry multiphoton and confocal microscopy.

Since 2011, she has worked at TRON, leading the unit of Vaccine and Cellular Immunotherapy. Her work focuses on several pre-clinical cancer models using combinatorial immunotherapies based on RNA vaccines, chemotherapy, local radiotherapy and antibody therapy aiming to understand the cellular and molecular mechanisms involved in the synergistic therapeutic effects and on the composition and phenotype of the tumor immune environment (TiME).

To watch the seminar in full, click here. 

We look forward to seeing you there.

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– For our upcoming seminar, you have chosen to focus on the communication between DNA damage and immune response. Why you’ve chosen this topic and why you think it’s an important subject to be talking about?

This is a fascinating topic that speaks to many issues related to disease etiology and therapy. It involves the communication of DNA damage from individual cells to the entire organism. We were originally interested in this topic because of longstanding observations that radio- and chemo- therapies were less effective in immune deficient mice. What it indicated was that DNA damaging modalities necessitate an immune response against the tumor in order to maximize their clinical efficacy. At the time, the basic question of how DNA damage in the nucleus communicated with the immune system was enigmatic to say the least. Different DNA damaging agents elicit a robust response to the damage within seconds. On the other hand, it was known to take days for DNA damaging agents to cause an inflammatory response that could attract immune cells. We demonstrated that passage through mitosis in the presence of a damaged genome was the gatekeeper to this response. This occurs in part by missegregation of damaged chromosomes into the cytoplasm where they are subsequently recognized by proteins that typically sense viral DNA. Passage through mitosis to activate these pathways is also necessary for a systemic immune response to irradiated tumors.

Interestingly, there is a second component to this response that involves RNA recognition by additional RNA-sensing pattern recognition receptors. We are currently trying to understand how mitotic progression creates immunogenic RNA species in the cytoplasm.   The work has many implications for radio- therapy. We can enhance this response by driving cells into mitosis, whereas a low mitotic index or loss of specific pattern recognition receptors reduces it. It’s an exciting prospect to be able to harness the immune system to increase responses to cancer therapy in a rationally designed manner. I am certain there are many important discoveries remaining.

– Can you tell us more about the methodologies you’ve developed to help visualise the major steps of homologous recombination?

Homologous recombination is a fundamental mechanism for error-free repair of DNA damage. It is essential for genome integrity from bacteria to humans. This classically occurs in a manner that depends on the breast and ovarian cancer suppressor proteins, BRCA1 and BRCA2. When these genes are mutated, genome instability arises and mutation carriers have a high risk of cancer development. Interestingly, some cancers acquire an unusual form of homologous recombination and use this to maintain their chromosome ends (known as telomeres) during each cell division. This process is called ALT and occurs in approximately 10% of cancers, often portending a poor prognosis. ALT does not rely on BRCA1 and BRCA2, but is instead executed by a poorly understood recombination mechanism.

We developed a system to study ALT by directing a nuclease specifically to telomeres. This creates DNA double-stranded breaks at the telomeres and initiated the ALT process in a relatively synchronous manner, which allowed us to visualize the process in real-time. What we showed in a series of publications is that damaged telomeres move large distances in the nucleus before pairing up with telomeres on other chromosomes to form recombination centers. This resulted in homologous recombination DNA synthesis for up to 70 kilobases, or to the end of the chromosomes. We developed the methods to visualize the telomere mobility and synthesis as it occurred and named this process Break Induced Telomere Synthesis (BITS). In unpublished studies, we’ve extended this capacity to monitor homologous recombination by purifying the entire DNA damage response on the broken telomeres. We are currently investigating how this response allows telomeres to execute the unusual form of recombination during ALT.

– How do you hope your research will benefit patient outcomes?

As a basic scientist, my mission is to understand how processes work at a molecular level and how this affects both cell autonomous and organismal behaviors. Asking fundamental questions at this level is always the first step in what I do. We try to relate this to human disease whenever possible, often in collaboration with more translationally oriented investigators. This has led to identification of gene mutations responsible for cancer predisposition and also for developmental syndromes. We’ve also discovered new drug targets that create selective vulnerabilities in BRCA and other homologous recombination deficient cancers, and revealed approaches to combine DNA damaging agents with immune therapies that have inspired clinical trials. We make efforts to work with clinicians and the biotech sector to develop our basic findings into therapies that can benefit cancer patients.

– What research developments do you most hope to see in your field within the next decade?

The DNA damage response field is developing at an extremely rapid pace. It is an incredibly exciting topic and I would argue one of the most intellectually challenging aspects of biology. There has also been a renewed enthusiasm for targeting the DNA damage response for cancer therapy. I hope to see a better understanding of how these basic molecular mechanisms of genome maintenance impact human biology. We are gaining such detailed insight at the molecular and cellular level into processes that orchestrate genome integrity.

However, we understand very little about all of the influences emanating from tissue architecture, cell-cell contacts and other endogenous sources. This is in large part due to the difficulty of studying molecular processes in more complex model systems. It is also a consequence of intense specialization of scientists in a particular aspect of the damage response. I think that integration of information and approaches will lead to a better understanding of how DNA damage signals at an organismal level.

– What are you most looking forward to about your upcoming seminar with CRUK RadNet City of London?

My understanding is that the audience will consist of scientists and clinicians with broad expertise in DNA repair, radiobiology, and cancer therapy. This is a great opportunity for me to receive input on our studies from a prominent group of individuals with many different perspectives. I am looking forward to the question and answer session and am optimistic that it will be an opportunity for a stimulating exchange of ideas.

For more information about our upcoming seminar with Professor Roger Greenberg and to book your place, click here. 

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UCL have been awarded £790,000 from the Medical Research Council (MRC) to develop an exciting new training programme to help improve the use and curation of medical imaging data in research.

The new programme, Health and Bioscience IDEAS – Imaging, Data structures, genetics and Analytical Strategies, will focus on building researchers’ skills in data management and analysis.

Imaging data and associated information are playing an increasing role in research – helping with prevention, monitoring, diagnosis and treatment of multiple conditions, as well as advancing our scientific understanding of how the body functions. As a result, a larger and more diverse pool of researchers needs to be equipped with the skills to accurately analyse and securely manage often complex and sensitive imaging data.

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