(Shared Conference with World Preclinical Congress and IO Pharma Congress)

Cambridge Healthtech Institute’s 8th Annual

Preclinical Strategies, Models & Tools in Oncology

Advancing Translation in Oncology and Immuno-Oncology

June 18-19, 2019

The rise of cancer immunotherapy instigated a wide range of unique preclinical and translational challenges. The demand for predictive and robust preclinical models and approaches to minimize translational failures in immuno-oncology is at an all-time high. The need for leveraging phenotypic features of models, for early identification of predictive biomarkers, for rational design of combination therapies, and for researching the cancer-immune cell interactions add to the complexity of translational research in immuno-oncology. Cambridge Healthtech Institute’s Eighth Annual Preclinical Strategies, Models & Tools in Oncology conference is designed as a forum for ideas and opinions exchange on how to decrease the rate of clinical failures in oncology and immuno-oncology.

Final Agenda

Stay on to attend Wednesday, June 19 - Thursday, June 20

Patient-Derived Tumor Organoids

Recommended Short Courses

SC6: Targeted Protein Degradation Using PROTACs and Molecular Glues
SC10: In vitro and in vivo Modeling for Cancer Immunotherapy s

Tuesday, June 18

7:00 am Registration Open and Morning Coffee


8:00 Chairperson’s Remarks

Elaine Pinheiro, PhD, Senior Principal Scientist, Oncology, Merck

8:10 Mastering Translational Immuno-Oncology

Emma Lees, PhD, Vice President and Oncology Site Head, Bristol-Myers Squibb

This talk will address translational strategies, reverse translation and multidisciplinary approaches to new immuno-oncology agents discovery and development. The new BMS site located in Cambridge, MA will be introduced to the IO community.

8:40 Reverse Translational Studies to Guide Cancer Combination Strategies in the Clinic

Pinheiro_ElaineElaine Pinheiro, PhD, Senior Principal Scientist, Oncology, Merck

Immunotherapeutic strategies, such as checkpoint blockade, have changed the way cancers are being treated, providing significant benefit to patients. Despite success, a large fraction of patients do not respond to single agent therapy. Combination approaches may be the key to improving response rates in these patients. Preclinical immuno-oncology mouse models provide tremendous value to shaping clinical strategies given that countless potential combinations exist with other immunotherapies, radiation, and/or standard of care.

9:10 BCMA-Targeting BiTE® Antibody Constructs for the Treatment of Multiple Myeloma – From Bench to Bedside

Friedrich_MatthiasMatthias Friedrich, PhD, Scientific Director, Comparative Biology and Safety Sciences, Amgen

B-cell maturation antigen (BCMA) is a highly plasma cell-selective protein that is expressed on malignant plasma cells of multiple myeloma patients and therefore is an ideal target for T cell redirecting therapies. We developed Bispecific T cell engager (BiTE®) targeting BCMA and CD3ε and studied their therapeutic impact on Multiple Myeloma.

9:40 Grand Opening Coffee Break in the Exhibit Hall with Poster Viewing


10:25 Chairperson’s Remarks

N. Michael Greenberg, PhD, CSO and Senior Vice President, Atreca Inc.

10:30 Strategies for Generating Novel and Biologically Relevant TcRs for Cancer Cell Therapy

Hurwitz_AndyAndy Hurwitz, PhD, Vice President, Head of Preclinical Research, AgenTus Therapeutics

This presentation will share a mammalian display-based platform for T Cell Receptor (TCR) discovery and identification of novel TCRs targeting NY-ESO-1. Overall translational approaches for TCR-based agents will be discussed.

10:55 COBRA: A Novel Conditionally Active Bispecific Antibody that Regresses Established Solid Tumors in Mice

May_ChadChad May, PhD, Senior Vice President, Research and Development, Maverick Therapeutics

T-cell redirecting bispecific antibodies are so potent that even very low levels of target expression on normal tissues may quickly become a safety liability and prevent the administration of efficacious doses. To overcome this challenge, we have developed a novel recombinant platform that is engineered to pursue more broadly expressed cell surface targets, by limiting T cell engagement to within the tumor microenvironment.

11:25 Presentation to be Announced

11:40 Sponsored Presentation (Opportunity Available)

11:55 Transition to Lunch

12:00 pm Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own

12:30 Session Break

1:05 Chairperson’s Remarks

N. Michael Greenberg, PhD, CSO and Senior Vice President, Atreca Inc.

1:10 Functional Anti-Tumor Antibodies Sourced from Non-Progressing Cancer Patients Undergoing Immunotherapy

Greenberg_NormanN. Michael Greenberg, PhD, CSO and Senior Vice President, Atreca Inc.

We have captured and sequenced the immune B cell repertoires from patients with metastatic non-progressing cancers that received check point inhibitor immunotherapies. Analysis of these datasets allowed us to isolate and identify antibodies that recognized non-autologous human tumor tissues and may cross-react with syngeneic mouse tumor models. Using suitable animal models we have observed antibodies to cause tumor growth inhibition, regression and lasting immunity in vivo. Our ATRC-101 lead program is advancing to the clinic for multiple indications.

1:40 Preclinically Developed Next Generation Selective Estrogen Receptor Degrader (SERD) SAR439859 for ER+ Metastatic Breast Cancer Patients

Sun_FangxianFangxian Sun, MD, PhD, Lead Research Investigator, Pharmacology, Sanofi

Nearly 70% newly diagnosed cases of breast cancer (BC) are estrogen receptor positive (ER+) and approximately 40% of those patients undergone endocrine therapy developed resistance. We developed SAR439859, an orally bioavailable SERD with potent antagonist and degradation activity against ER both in vitro and in vivo. SAR439859 treatment inhibits ER signaling activity in multiple ER+ breast cancer cell lines and patients in clinic. Across a panel of ER+ cells, SAR439859 demonstrated superior ER degradation activity compared with other SERDs that resulted in better growth inhibition. Our results indicated SAR439859 is a novel, oral, nonsteroidal, selective estrogen receptor antagonist and degrader that could provide therapeutic benefit to ER+ breast cancer patients.

2:10 Presentation to be Announced

2:25 Refreshment Break in the Exhibit Hall with Poster Viewing


3:10 PANEL DISCUSSION: Partnering, Preclinical Strategies and Tools, IO Clinical Trials; Capital Invested in IO Relative to Other Oncology Areas

Zawel_LeighModerator: Leigh Zawel, PhD, CSO, Cullinan Oncology


Woo_MichaelMichael Woo, PhD, Head, Search & Evaluation, Immuno-Oncology, Business Development & Licensing, Novartis Institutes for BioMedical Research, Inc.

Williams_SybilSybil Williams, PhD, Director, Biology Oncology Discovery, Merck

Young_PaulPaul Young, PhD, Executive Director, Business Development & Licensing, Merck

Godec_JernejJernej Godec, PhD, Associate, Apple Tree Partners

Adam_StaceyStacey J. Adam, PhD, Director, Cancer Research Partnerships, Foundation for the National Institutes of Health

  • Has the IO bubble popped? Why have no other IO drugs emerged with PD1/PDL1-like efficacy?
  • What combination strategies are being explored to convert poorly PD1 responsive tumors to more responsive ones?
  • Are there new IO monotherapies or combos that appear promising?
  • Is patient stratification practical with IO therapies?
  • What partnering strategies are most effective?
  • What is a recent deal your firm signed that you’re excited about?

4:10 Transition to Keynote


5:20 Welcome Reception in the Exhibit Hall with Poster Viewing

6:35 Find Your Table, Meet Your Moderator

6:40 Breakout Discussion Groups

7:30 Close of Day

Wednesday, June 19

7:00 am Registration Open and Morning Coffee


8:00 Chairperson’s Remarks

Charles Glaus, PhD, Director, Translational Research & Early Clinical, Takeda

8:05 Preclinical and Translational Imaging Methods in the Development of Immuno-Oncology Therapeutics

Glaus_CharlieCharles Glaus, PhD, Director, Translational Research & Early Clinical, Takeda

The primary method to measure biomarkers of IO therapeutic activity in solid tumors is biopsy, yet it is widely understood that biopsies spatially and temporally under-sample the tissues in question. Imaging technologies can provide whole-body, longitudinal, noninvasive monitoring of IO drug distribution, PD, and lymphocyte infiltration. In this talk, we will review examples of advanced imaging biomarkers that will play a key role in the development of new immune-oncology therapeutics.

8:35 CO-PRESENTATION: Determining Markers of Sensitivity to p70S6K/AKT1/3 Inhibition of SCLC PDX Mouse Models: Correlating in vivo Sensitivity with Profiles of Surface Protein Markers and Gene Expression from Individually Dissociated Tumor Cells

Clark_AndersonAnderson Clark, PhD, Director, Translational in vivo Pharmacology, Translational Innovation Platform, Oncology, EMD Serono

Rainer Blaesius, PhD, Technology Manager, BD Technologies and Innovation

Small Cell Lung Cancer (SCLC) is characterized by rapid tumor growth and currently, there are few therapeutic options or predictive biomarkers. In a Phase I clinical trial of the p70S6K/AKT1/3 inhibitor M2698 one SCLC patient had prolonged stable disease while on treatment. A follow-up screen in 45 preclinical in vivo patient-derived xenograft (PDX) models resulted in a tumor control rate of roughly 27%. Failure of “traditional” genomic analyses of the models to identify biomarkers predicting sensitivity in patient tumors, prompted us to pursue a novel approach. Tumors from the 7 most and 7 least sensitive models were re-implanted into mice and the tumors later dissociated for FACS, single cell surface marker profiling and genomic analysis. We will review the data from this study and discuss options to apply the methodology to translational preclinical work and also clinical samples.

9:05 Presentation to be Announced

9:35 Coffee Break in the Exhibit Hall with Poster Viewing


10:20 Utilizing Preclinical in vivo Models to Elucidate Mechanisms of Drug Resistance

Williams_JulietJuliet Williams, PhD, Executive Director, Oncology Drug Discovery, Novartis

Understanding the interactions between human immune cells and tumors is paramount when devising treatment strategies that prevent tumor evasion of immune cells and improve cytotoxic responses. In this talk we will discuss the generation of humanized in vivo models to develop IO therapeutics and how we leverage humanized systems for deciphering mechanism of action and clinical translation.

10:50 Stromal-Imposed Immunosuppression in the Era of Checkpoint Blockade

Viviana Cremasco, PhD, Investigator III, Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research (NIBR)

Despite the increasing interest in targeting stromal elements of the tumor microenvironment, we still face tremendous challenges in developing adequate therapeutics to modify the tumor stromal landscape. The biggest obstacle is represented by our poor understanding of the phenotypic and functional heterogeneity of stromal cells in tumors. Our work aims at addressing some of this ambiguity, focusing on the immunoregulatory roles exerted by specific subsets of mesenchymal cells in the tumor microenvironment.

11:20 The Impact on Tumor Microenvironment by Tissue Type, Genotype, Clonal Diversity and in vitro Culture Artifacts During Tumor Initiation

Chen_ZhaoZhao Chen, PhD, Investigator III, Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research (NIBR)

Cancer immunologists like to farm in the complex tumor microenvironment (TME). Most of us are trying to find the common denominators and make sense out of this mess in order to pin down the key components that we can intervene and tip balance of anti-tumor immunity. We have seen reports claiming many of the biological features possibly having major influences on the TME. However, the truth is most of these factors probably contribute to part of the story, but the importance of each factor maybe highly context dependent or even totally random in some cases. We have done some of the analysis using an engineered organoid tumor system to answer some these basic questions.

11:50 Transition to Lunch


12:30 Transition to Plenary


2:20 Dessert and Coffee Break in the Exhibit Hall with Poster Viewing

3:05 Close of Conference

Stay on to attend Wednesday, June 19 - Thursday, June 20

Patient-Derived Tumor Organoids

Recommended Short Courses

SC6: Targeted Protein Degradation Using PROTACs and Molecular Glues
SC10: In vitro and in vivo Modeling for Cancer Immunotherapy

* The program is subject to change without notice, due to unforeseen reason.

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