Original Agenda
We are actively working with our speakers to confirm their availability for the virtual event. Initial response from our speakers has been very positive, and we are optimistic we will have the new programs ready to share here soon.

Modulating the Tumour Microenvironment track banner

Our understanding of mechanisms in the tumour microenvironment is increasing year-on-year. Research this year reveals a focus on checkpoint blockade mechanisms and agonisitc and antagonistic approaches to overcome their limitations. There is huge interest in macrophagres and monocytes. Having previously been considered suppressive, investigators are discovering macrophage and monocyte subsets that activate the immune system, and are finding ways to stimulate this. There are exciting new developments with cytokines, some engineered to become active only at the site of disease, and others engineered to bind better to fusion proteins.

Monday, 9 November

08:00 Short Course Registration
09:00 Recommended Short Course*
SC2: The Tumour Microenvironment and Response to Cancer Immunotherapy

*Separate registration required. See short course page for details.

12:00 Conference Registration


13:30 Welcome by Conference Organizer

Mimi Langley, Senior Conference Director, Cambridge Healthtech Institute


Chairperson's Opening Remarks

Dario Neri, PhD, Full Professor, Chemistry & Applied Biosciences, ETH Zurich
13:45 Targeting Intratumoral Treg and CD8+ T Cells by Isotype-Optimized Blocking/Depleting and Agonist Anti-TNFR2 Antibodies
Björn L. Frendeus, PhD, CSO, BioInvent International AB

Fine-tailoring antibody Fv- and Fc- interactions is needed to optimize anti-TNFRs antibodies’ activity. Here, the potent antitumor activity of isotype-optimized ligand-blocking, or agonist, antibodies to the T cell co-stimulatory receptor TNFR2 is described. Both types of mAbs eradicated large solid tumors through mechanisms involving intratumoral Treg-depletion and/or CD8+ T cell expansion, alone or in combination with anti-PD-1. BI-1808 has completed GLP toxicology and is scheduled to enter the clinic in 2020.

14:15 Overcoming Resistance to MAb Therapy
Mark S. Cragg, PhD, Professor, Cancer Immunology Pathway, Medicine, Southampton General Hospital

There is growing appreciation of the depth of interaction between tumour cells and their microenvironment serving to modulate tumour growth, proliferation and immune suppression. Although these interactions have long been known to limit responses to conventional treatments such as chemotherapy, their impact on antibody immunotherapy is less clear. This presentation will discuss several key interactions between the host and the tumour that impact antibody immunotherapy and how they might be targeted to improve treatment efficacy.


A Tumor-Targeted CD40 Agonistic DARPin® Molecule Leading to Anti-Tumor Activity with Limited Systemic Toxicity

Nicolo Rigamonti, PhD, Therapeutic Area Leader, Cancer Immunology, Molecular Partners AG

Systemic administration of some agonistic anti-CD40 antibodies has shown some signs of activity in cancer patients, but dose-limiting toxicity has prevented the exploration of the full dose range, and possibly has impaired clinical efficacy. To overcome this issue, we developed a multispecific DARPin® therapeutic candidate, MP0317, intended to activate CD40 receptor locally, rather than systemically, in the tumor microenvironment through cross-linking with fibroblast activation protein (FAP). In vitro and in vivo data will be presented showing that MP0317 is able to activate the CD40 receptor locally in FAP-positive tumors, producing significant antitumor activity in the absence of systemic toxicity.

15:15 Sponsored Presentation (Opportunity Available)
15:45 Networking Refreshment Break



Keynote Chairperson's Remarks

Denise L. Faustman, MD, PhD, Associate Professor & Director, Immunobiology Labs, Massachusetts General Hospital
16:20 Learning from What Works: Dissection of Successful Cancer Clearance by the Immune System
Andrew Sewell, PhD, Distinguished Research Professor and Wellcome Trust Senior Investigator, Division of Infection and Immunity, Cardiff University School of Medicine

What is the key to success? How do some rare patients spontaneously clear extreme cancer? What is being recognised by T cells during successful tumour-infiltrating lymphocyte or T cell checkpoint therapy? We have developed two new methodologies that allow rapid determination of the ligand recognised by any ‘orphan’ T cell clone. These techniques have enabled us to address these questions and discover novel cancer-associated epitopes expressed by most cancers.


mAbs vs. Bugs: Antibody Therapies for Infectious Disease

Steve Martin, PhD, Vice President, Biopharm Discovery, GlaxoSmithKline

This year’s coronavirus pandemic has provided a stark reminder of the threat to global health posed by infectious disease and the need for new treatments. Renewed attention has been brought to the potential of antibodies as anti-infective therapeutics, which historically has been a challenging area for drug discovery. Synergies between modern vaccine development approaches and antibody discovery technologies offer new opportunities in the fight against our microbial foes.

17:50 Welcome Reception in the Exhibit Hall with Poster Viewing
19:00 End of Day

Tuesday, 10 November

07:45 Registration and Morning Coffee



Chairperson's Opening Remarks

Björn L. Frendeus, PhD, CSO, BioInvent International AB
08:35 From Dud to Diamond: Unlocking Potent Pharmacology in a PD1-VEGFR2 Cross-Reactive IgG
Jamie Coleman, PhD, Co-Founder & Chair, UltraHuman Ltd.

Bispecifics can potentially improve solid tumour therapy, but synergistic pathways have been hard to identify. The PD(L)1 and VEGF pathways are both immunosuppressive in the TME, with combinations of extant drugs showing improved efficacy in the clinic over monotherapy. We have developed an IgG, of standard antibody structure, that exhibits high-potency dual antagonism of both PD1 and VEGFR2, but with a reduced toxicity potential that opens up new polytherapy opportunities.

09:05 Dominant Antagonism of the TNF Superfamily
Denise L. Faustman, MD, PhD, Associate Professor & Director, Immunobiology Labs, Massachusetts General Hospital

One limitation of checkpoint inhibitors is Treg escape.  We believe it is possible to only target the highly immunosuppressive Tregs of the tumor microenvironment. The TNFR2 receptor is massively expressed in the tumor microenvironment on Tregs and the design of dominant TNFR2 antagonists has been possible. The unique structural biology of this dominant receptor agonism has been determined to represent the stabilization of the anti-parallel proteins.  This structural motif is now being mirrored by many large pharma efforts for various receptors.

09:35 Problem Solving Breakout Discussions*

*Topics to be announced.

10:30 Coffee Break in the Exhibit Hall with Poster Viewing


11:15 KEYNOTE PRESENTATION: Immunocytokines with "Activity on Demand"
Dario Neri, PhD, Full Professor, Chemistry & Applied Biosciences, ETH Zurich

Engineered cytokines are gaining importance for the treatment of cancer and of chronic inflammatory conditions. In this seminar, I will present strategies and experimental results for the creation of antibody-cytokine fusions, which display a preferential activity at the site of disease, helping spare normal tissues.

11:45 KEYNOTE PRESENTATION: Novel Cytokine-Grafting Technique Generates Potent Interleukin-2 Immunotherapy with Efficacy in Multiple Cancer Models
Onur Boyman, Professor & Chair, Immunology, University Hospital Zurich

We developed a novel strategy to permanently graft human interleukin-2 (IL-2) to its antigen-binding groove on anti-human IL-2 antibody NARA1, thereby generating NARA1leukin. NARA1leukin was unable to bind to IL-2 receptor alpha, and thus showed uncompromised selectivity for effector immune cells in vitro and in vivo. This translated into efficacious anti-tumor responses in several cancer models with superior effects on metastatic lesions. NARA1leukin is a novel and potent IL-2 immunotherapy.

12:45 Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own
13:45 Dessert Break in the Exhibit Hall with Poster Viewing



Chairperson's Opening Remarks

Sophia N. Karagiannis, PhD, Professor, Translational Cancer Immunology & Immunotherapy, Kings College London
14:20 Regulation of Macrophages in the Tumour Microenvironment and Monocytes in the Peripheral Blood by Means of IgE Immunotherapy
Sophia N. Karagiannis, PhD, Professor, Translational Cancer Immunology & Immunotherapy, Kings College London

In several models and functional evaluations, anti-tumour IgE immunotherapy can restrict cancer growth by immune effector mechanisms employed by this antibody class against parasites. IgEs recognizing tumour-associated antigens potentiated re-activation of monocytes and recruitment of stimulated macrophages into the tumour microenvironment. We will discuss the clinical development of a first-in-class IgE and the mechanisms by which IgE can reconfigure the tumour microenvironment and activate previously untapped immune mechanisms against tumours.

15:20 The Tumor Microenvironment Instructs Divergent Monocyte Fates that Determine Response to Anti-PDL1 Treatment
Shahram Salek-Ardakani, PhD, Senior Director, Cancer Immunology Discovery, Pfizer Inc.

The tumor microenvironment is rich with immune suppressive macrophages that are associated with cancer progression and resistance to immune checkpoint therapy. Using pre-treatment tumor biopsies complemented with single-cell RNA-Seq, we characterized the intratumoral heterogeneity of myeloid cells to unveil potential mechanisms of resistance to anti-PD-L1 treatment. To our surprise, we identified a distinct proinflammatory macrophage population that was associated with response, rather than resistance, to anti-PDL-1 therapy.

15:50 Sponsored Presentation (Opportunity Available)
16:20 Refreshment Break in the Exhibit Hall with Poster Viewing


17:00 Manipulating Dendritic Cell (DC) Biology to Impact T Cell Functional Differentiation
Tariq Ghayur, PhD, Distinguished Research Fellow, Foundational Immunology, Abbvie

DCs are efficient antigen processing and presenting cells that influence T cell functional differentiation (Th1,Th17, Treg, etc.) during an immune response within lymphoid organs and autoimmune – and tumor – microenvironments. Therefore, modulating DC biology is an attractive therapeutic approach for both autoimmune and cancer indications. DCs express a variety of cell surface receptors, and mAbs to some of these receptors modulate DC biology, and thereby, T cell differentiation. Generation and characterization of mAbs targeting specific DC receptors, their effect on DC biology, and T cell functional outcomes will be discussed.

17:30 Oncolytic Virus and Antibody-Drug Conjugate-Based Therapeutic Combinations: Different Modalities – Common Themes
Philipp Mueller, PhD, Senior Principal Scientist, Cancer Immunology & Immune Modulation, Boehringer Ingelheim Pharma GmbH & Co KG

Despite the clinical breakthroughs achieved with checkpoint blockade, the overall proportion of patients experiencing durable responses remains relatively small. Therefore, the real promise for most cancer patients lies in complementary combination therapies, combining checkpoint blockade with the immune-promoting/supporting properties of other therapeutic modalities, which help breach physical barriers, overcome immunosuppression, and improve immune cell infiltration in tumors. This talk will compare and highlight two of the latter categories: antibody-drug conjugates and oncolytic viruses.

18:00 Multispecific Nanofitin Assemblies for Modulating the Tumor Microenvironment
Mathieu Cinier, PhD, Scientific Director & CSO, Affilogic

Many efforts have been devoted in recent years towards reconditioning the tumor microenvironment to mount an immune response against the tumor. While holding promises, our understanding of the manipulation of the immune system remains limited and has to be addressed with other technical challenges, such as tumor penetration, off-target systemic toxicity, and simultaneous co-engagement of several tumor progression pathways. We will be sharing our strategy to answer these different challenges using the Nanofitin scaffold, with examples of multispecific constructions directed against several tumor progression pathways (angiogenesis, T cell population, and macrophage differentiation).

18:30 Close of Modulating the Tumour Microenvironment