Non-small cell lung cancer (NSCLC) accounts for more deaths than colon, breast, and prostate cancers combined. Of patients with NSCLC, 20% initially present with stage I or II disease, for which neoadjuvant PD-1 blockade combined with chemotherapy is now the standard of care. The success of PD-1 blockade is predicated on the fact that a critical end-effector of anti-tumor immunity is the T cell. We and others have demonstrated the role of CD4+ (helper) and CD8+ (effector) T cells targeting epitopes derived from tumor somatic mutations (neoantigens) in response to anti-PD-1 in metastatic NSCLC. Additionally, many groups have examined intratumoral characteristics of T cells at the single cell level in human cancers, but these studies suffer from a fundamental limitation: they cannot distinguish true tumor-specific T cells from T cells with irrelevant antigen specificity. In this presentation, I will demonstrate how our lab is developing innovative methods to better detect and study tumor-reactive TIL in the context of resectable lung cancers.

Learning Objectives:

1. Recognize and understand the challenges in identifying true tumor-reactive T cells from bystander cells

2. Demonstrate how we apply innovative methods to study the programming of tumor-reactive T cellsDemonstrate how we apply innovative methods to study the programming of tumor-reactive T cells

3. Discuss the therapeutically relevant biology that we are able to discover by specifically studying anti-tumor T cells rather than all T cells in the TME

Our experience collaborating with oncology and immunology leaders in the pharmaceutical and biotech space has revealed the numerous challenges in every stage of drug development. From target candidate identification to pharmacovigilance, nearly every stage relies on harmonized, well-curated databases to move forward with confidence. But that's not the whole story; advanced, integrated analyses are vital to truly unlock their value.

Customized Analytical Solutions: One size doesn’t fit all. That’s why we create custom project solutions tailored to discover and develop novel cancer therapeutics that matter to you. At QIAGEN Digital Insights Professional Services, we help you extract reliable insights from your multiomics datasets, including genomics, transcriptomics, proteomics, and single-cell and spatial expression profiling data, by combining robust, manually curated databases with the expertise of our scientific consultants.

Learning Objectives:  

1. Assisting clients in identifying alternative indications or disease conditions for existing drugs by providing mechanistic insights that link new and primary indications.  

2. Using context clues from spatial transcriptomics, single-cell transcriptomics and systems biology analyses to trace microenvironmental variations within tumors and understand immune cell recruitment patterns.  

3. Power immunogenicity analyses for neo-antigen discovery with public and proprietary somatic and RNA-seq datasets.

The webinar highlights advances in high-throughput gene and protein synthesis platforms that accelerate antibody discovery and optimization. Using accurate HTP Strings DNA fragments improves cloning efficiency and reduces rework while maintaining sequence diversity. A semi-automated antibody production platform streamlines steps from DNA normalization through purification with full traceability. The new Expi293 PRO expression system further enhances rapid protein production. Finally, the talk addresses scale-up and analysis considerations for multi-specific antibody formats.

Learning Objectives:

1. Demonstrate how high-throughput DNA and protein synthesis platforms accelerate antibody discovery and optimization by improving speed, accuracy, and sequence diversity.

2. Showcase the integrated semi-automated antibody production workflow that enhances efficiency and ensures traceability across all steps.

3. Introduce the Expi293 PRO expression system and discuss strategies for scale-up and analysis of complex, multi-specific antibody formats.

The next leap in oncology therapeutics demands speed, precision, and rapid molecular innovation — and AI-driven antibody design (AIDD) is beginning to deliver. In this talk, we will unveil how our platform leverages artificial intelligence to generate high-purity, diverse antibody-like libraries at unprecedented speed, feeding iterative design loops that accelerate hit-to-lead timelines. We’ll highlight recent platform enhancements, including AI-driven codon optimization and signal peptide selection, which — combined with our upcoming TurboCHO 3.0 expression system — are boosting yields and functional diversity. Two compelling case studies ground our approach: First, we tackle the notorious challenges of VHH (nanobody) library production — instability, aggregation, low expression — and reveal how AI-guided design and expression tuning overcome these hurdles. Second, we explore asymmetric bispecific antibodies, engineered to simultaneously engage tumor antigens and immune cells, and demonstrate their growing relevance in solid and hematologic cancers. Our upgraded platform aims to support the exploration of novel scaffolds and designing next-gen multispecifics, for smarter, faster, more effective cancer drug discovery.

Learning Objectives:

1. Next-Gen platforms are required to deliver on AI-accelerated antibody drug discovery.

2. How closed-loop optimization with real-time feedback can be achieved.

3. Mitigating late-stage risks early.

From 12-1 PM PT on the day of the event, Labroots is excited to offer a variety of interactive networking opportunities designed to help you engage, explore, and expand your network.

Connect with fellow attendees in the social space through Speed Networking, chat with poster authors during our live Poster Discussion, and earn bonus points by visiting booths in our Exhibit Hall. See you there!

Bi-specific antibodies have gained traction in cancer drug development due to their ability to target two distinct antigens, thereby enhancing therapeutic efficacy simultaneously. They overcome limitations of traditional monoclonal antibodies by redirecting immune effector cells to tumor sites, blocking multiple oncogenic pathways, or bridging tumor cells with cytotoxic T-lymphocytes. Key mechanisms include T-cell engagement through CD3 binding, dual checkpoint inhibition, and simultaneous targeting of resistance pathways. Bi-specific antibodies, however, are challenging to develop and produce. GenScript offers an advanced integrated development platform that addresses development and manufacturing challenges through expedited processes, and novel expression systems and purification strategies, enabling scalable production of stable, potent bi-specific constructs with improved safety profiles and enhanced anti-tumor activity. 

Learning Objectives:

1. Learn about challenges in developing bi-specific antibodies.

2. Learn about methodologies for development.

3. Learn how GenScript's solutions can accelerate your development.

Advances in next-generation sequencing (NGS) and synthetic DNA technologies are reshaping oncology research by enabling earlier cancer detection, more accurate biomarker discovery, and sensitive monitoring of disease progression. This webinar will explore how Twist Bioscience’s customizable genomic solutions—including DNA/RNA panels, cfDNA/cfRNA liquid biopsy workflows, and innovative methylation detection systems—support research across the oncology journey. Through real-world case studies in pediatric cancer profiling, colorectal cancer screening, and minimal residual disease detection, attendees will learn how to apply scalable, cost-effective, and high-performance NGS tools to accelerate discoveries and advance precision oncology.

Learning Objectives:

1. Understand how custom NGS panels, liquid biopsy assays, and methylation profiling can improve cancer detection, monitoring, and biomarker discovery.

2. Explore case studies demonstrating the application of advanced genomic technologies in pediatric cancer research, colorectal cancer screening, and minimal residual disease detection.

Analytical developoment and quality control plays pivotal roles in drug development. Validated and ready-to-use analytical tools can streamline the process and accelerate regulatory approvals.    

GenScript offers a comprehensive suite of analytical and quality control (QC) solutions to accelerate the development and manufacturing of advanced therapeutics for oncology research and treatment development, spanning from cell therapies to antibody drugs. Our portfolio includes our first-to-market universal and high-specificity CAR-detection antibodies, ultra-sensitive and fast-protocol ELISA kits, and stable cell lines of ADC targets and immune checkpoint targets. Together, these products empower biopharmaceutical developers with end-to-end analytical capabilities that enhance accuracy, throughput, and confidence from early discovery through commercial manufacturing.

Learning Objectives:

1. How can universal CAR detection antibody escalate CAR-based cell therapy development?

2. How can fast-protocol ELISA kits streamline your analytical and QC workflow?

3. How can ready-to-use stable cell lines for immune checkpoints and ADC targets speed up your oncology drug discovery and development?

Humanized immune system (HIS) mouse models have become indispensable for advancing translational research in immuno-oncology, autoimmune disorders, and infectious disease. This webinar will begin with an overview of HIS models, focusing on the NOG platform with CD34+ hematopoietic stem cell (HSC) engraftment. Attendees will gain an understanding of the benefits and limitations of HSC-based humanization, key considerations for experimental design, and how model selection impacts study duration and translational relevance.  

A major challenge in this field is variability stemming from donor differences, which can complicate data interpretation and hinder reproducibility. To address this, we will introduce Taconic’s huSelect™ suite of services, which supports researchers with HLA-based donor selection, access to pre-characterized CD34+ HSC donors, and expanded immune profiling capabilities by flow cytometry. 

This webinar will highlight how circular RNA overcomes key challenges in in vivo CAR-T therapy, with case examples from YXgene’s circRNA platform.

In vivo CAR-T therapy is emerging as a transformative approach to overcome the limitations of traditional ex vivo manufacturing. Circular RNA (circRNA) offers unique advantages—prolonged expression, reduced immunogenicity, and enhanced reprogramming efficiency—making it an ideal tool to enable in vivo CAR-T applications. In this webinar, we will discuss how circRNA addresses key challenges in safety, efficacy, and scalability, and share insights from YXgene’s proprietary circRNA technology platform that supports translational research and clinical development.

Learning Objectives:

1. Understand the key challenges of in vivo CAR-T therapy and how circular RNA technology can address limitations in safety, efficacy, and manufacturing scalability.

2. Explore the unique properties of circular RNA—including prolonged expression, reduced immunogenicity, and high reprogramming efficiency—that make it an enabling tool for next-generation CAR-T development.

3. Gain insights into practical applications of circRNA platforms in supporting translational research, clinical development, and future collaborations in the in vivo CAR-T field.

Cells in the body never experience the 21 percent oxygen levels of a standard incubator, yet much of biomedical research is still carried out under these artificial conditions. This webinar highlights why adopting physiologically relevant oxygen levels is essential for accurate, reproducible science. Dr. Krista Rantanen will explain how shifting from traditional normoxia to physioxia can transform cell culture studies, improve drug development models, and reveal hidden biological effects that high oxygen levels mask. Join this session to see how small changes in experimental oxygen conditions can make a big difference in advancing discovery and translational research.

Effective functioning of the immune system relies upon systems of checks and balances; too little activity results in overwhelming infection, too much activity results in excessive damage to the host. The importance of balance is particularly notable in cancers of the immune system, such as Cutaneous T-cell Lymphoma (CTCL), a cancer of skin-homing T-lymphocytes. Advanced CTCL causes inflammatory tissue damage in CTCL-involved skin and defects in cell-mediated immunity that lead to frequent Staphylococcus aureus (S. aureus) skin and soft tissue infections (SSTI) associated with high morbidity and mortality. The mechanisms that lead to defects in cell-mediated immunity and inflammatory tissue damage in CTCL remain poorly defined. We previously identified high levels of LAIR2, a decoy protein for the inhibitory immune receptor LAIR1, in advanced CTCL. Available evidence supports the notion that LAIR proteins likely function in inflammatory responses in infection, including RSV infection, severe COVID-19, and pediatric malarial infection. Given their immunosuppressive function and high expression in some hematologic malignancies, LAIR proteins have also been evaluated as targets for cancer therapy. Mice do not have a LAIR2 homolog, so we used Lair1 knock-out (KO) mice to model LAIR2 overexpression. In a model of subcutaneous S. aureus skin infection, Lair1 KO mice had significantly larger abscesses and areas of dermonecrosis compared to WT. Lair1 KO exhibited a pattern of increased inflammatory responses in infection and sterile immune stimulation, including increased production of proinflammatory cytokines and myeloid chemokines, neutrophil ROS, and collagen/ECM remodeling pathways. CTCL skin lesions harbored similar patterns of increased expression in cytokine and collagen/ECM remodeling pathways, suggesting that high levels of LAIR2 in CTCL recapitulates Lair1 KO, causing inflammatory tissue damage and compromising host defense against S. aureus infection.

Learning Objectives:

1. Describe the role of LAIR proteins in regulating immune responses during bacterial infection and cancer.

2. Explain how Lair1 knock-out mouse models are used to study the effects of LAIR2 overexpression on inflammation and host defense.

3. Analyze the parallels between immune dysregulation in Lair1 KO mice and inflammatory tissue damage observed in advanced cutaneous T-cell lymphoma (CTCL).

Infiltration of the tumor microenvironment (TME) with cytotoxic T cells (CTLs) which recognize tumor-associated antigens (TAAs and TSAs) is required for the clinical efficacy of immunotherapy and for long-term effectiveness of chemo- and radiotherapies. Our group developed type-1-polarized dendritic cells (DC1) matured in the conditions of acute viral infections (dsRNA, type-1 and type-2 interferons) which selectively activate type-1 immunity and promote selective intratumoral entry of CTLs but not Tregs. Polarized DC1s show enhanced ability of DCs to cross-resent TAAs and induce DNAM1- and NKG2D-expressing CTLs which use these NK receptors to amplify weak TCR signals, enhancing the sensitivity and selectivity of recognition of cancer (but not healthy) cells which express both TAAs and NKR ligands.
Similar features can be induced in endogenous DCs by the “chemokine-modulatory” regimen (CKM) combining TLR3-ligand and IFN CKM selectively targets (NFB-high) cancer lesions, but not healthy tissues, allowing its systemic application to promote uniform CTL infiltration of multiple “cold” tumors. Our pilot trial NCT03403634 tested the safety and immunologic efficacy of systemic (i.v.) IFN2b and selective TLR3-ligand (rintatolimod/Ampligen) in patients with metastatic triple-negative breast cancer (TNBC). We observed very good tolerability, average of 10.3-fold increases in intratumoral CTL markers and preliminary indications of potential clinical activity. Analogous immunologic efficacy was observed on study NCT04081389 (neoadjuvant CKM plus chemotherapy in TNBC) and NCT02432378 (i.p. CKM plus chemotherapy in advanced ovarian cancer), with 7 of 9 patients displaying pathologic complete responses (pCR) or microscopic disease at the time of tumor resection, known to predict positive long-term outcomes. 
Our upcoming trials will test combinations of CKM and DC therapies with immune checkpoint inhibitors (ICI) and adoptive T cell therapies (ACT).
Supported by NIH/NCI grants (P01CA132714, P01CA234212, P30A016056, P50CA159981, K08CA279766), NIH/NCATS grants (UL1TR001412, KL2TR001413, R03TR004607), DOD grant W81XWH-19-1-0674, and grants from the Pittsburgh Foundation, Jacobs Family Foundation, Rustum Foundation, Roswell Park Alliance Foundation and Roswell Park Institutional Funds.

Learning Objectives:

1. Describe how type-1–polarized dendritic cells (αDC1) enhance CTL activation and tumor recognition compared to conventional DCs.

2. Explain how chemokine-modulatory regimens (CKM) promote endogenous DC activation and cytotoxic T cell infiltration in “cold” tumors.

3. Discuss recent clinical trial outcomes using DC-based and CKM approaches in combination therapies for triple-negative breast and ovarian cancers.

Functional imaging of cancer typically involves the use of fluorodeoxyglucose-positron emission tomography (FDG-PET) in combination with computerized tomography (CT) for anatomical mapping. Standard clinical imaging for central nervous system (CNS) malignancies is magnetic resonance imaging (MRI), due to its superior soft tissue resolution compared to CT. We developed a novel functional MRI technique that uses oral deuterated water labeling followed by deuterium MRI (dMRI) for the initial diagnosis of brain tumors and treatment response assessment, including detection of pseudo-progression. Deuterated water (d-water) is NOT radioactive and safe to imbibe. Deuterium-enriched tissues/cells can be differentially detected by MRI. Standard MRI uses magnetic waves to image protons abundant within normal human tissues and provides anatomical mapping. Deuterium MRI detects deuterium-labeled tissues, i.e., providing functional or molecular imaging. Deuterium labeling can be achieved by drinking deuterated water, which looks and tastes like regular water. Deuterated water preferentially labels highly proliferating cells including tumors, which then have an increased dMRI signal compared no healthy tissues as a result of their rapid growth. Additionally, using our d-water-dMRI approach we have been able to detect pseudo-progression, a recognized pattern of tumor response to therapy. Pseudo-progression is a challenge and an impactful barrier for drug development because it’s a false signal of tumor progression that can lead to patients discontinuing effective therapies prematurely. Pseudo-progression is seen by anatomical imaging (including MRI) as an initial increase in tumor size/volume, which is eventually followed by tumor shrinking. Pseudo-progression is more commonly seen in the setting of immunotherapy compared to chemotherapy and radiation and can lead to effective treatments being halted and patients undergoing additional unnecessary biopsies to identify the next therapy for their “progressing” tumor. We have been able to differentiate pseudo-progression from true tumor progression by d-water labeling (oral) followed by d-MRI. In August 2025 we opened an investigator initiated clinical trial at the Roswell Park Comprehensive Cancer Center (PI Buxbaum) using dMRI in patients with primary CNS lymphoma. 

Learning Objectives:

1. Describe how deuterium magnetic resonance imaging (dMRI) works and how it differs from standard MRI and FDG-PET.

2. Explain how deuterated water labeling highlights proliferating tumor cells for functional imaging.

3. Assess the potential of dMRI to distinguish pseudo-progression from true tumor progression in cancer patients, particularly in the context of immunotherapy.

Cancer remains one of the most pressing health challenges of our time, yet drug development in oncology faces persistent hurdles. Despite billions invested, nearly 90% of drugs that succeed in animal studies ultimately fail in human trials, largely due to the poor translatability of preclinical data. The FDA Modernization Act 2.0, passed in late 2022, marks a pivotal shift by allowing non-animal testing methods to replace animal models in preclinical research.
This change is particularly significant for oncology, where human-relevant models are urgently needed to accelerate the development of safer, more effective drugs and therapies. The Act prioritizes New Approach Methodologies (NAMs)—such as microphysiological systems (organs-on-a-chip), induced pluripotent stem cells, and in silico modeling—that more accurately reflect tumor biology and patient diversity. These innovations promise not only to reduce attrition in cancer drug pipelines but also to create opportunities for more personalized and predictive translational research.
This talk explores what the FDA Modernization Act 2.0 means for cancer research and translational medicine, how NAMs are reshaping preclinical pipelines, and how clinical labs can position themselves competitively by embracing modern informatics tools. Attendees will leave with practical strategies for operationalizing regulatory change while improving efficiency, compliance, and translational outcomes.

Learning Objectives:

1. Identify the key provisions of the FDA Modernization Act 2.0 and their specific impact on research and drug development.

2. Discuss how NAMs such as organs-on-a-chip and in silico models are advancing research.

3. Recognize the operational and regulatory challenges oncology labs and clinical trials face as they implement these new methodologies and learn how a LIMS can support compliance with the FDA Modernization Act 2.0.

Pancreatic ductal adenocarcinoma (PDAC) is a disease characterized by hypovascularization and poor perfusion. Malignant and stromal PDAC cells actively suppress vascularization and impair blood vessel function resulting in cancers that are amongst the most poorly perfused. The profound limitations in perfusion cause metabolic stresses in the tumor microenvironment (TME) that influences the behavior and biology of both PDAC and stromal cells. I will discuss our team's work measuring the metabolic content of the TME to identify the metabolic stresses that malignant and stromal cells face. I will also discuss our efforts to develop model systems that incorporate TME metabolic stress and the findings we have made regarding the role of metabolic stress in drug response using these model systems.

Learning Objectives:

1. Identify that the tumor microenvironment of solid tumors contains abnormal levels of nutrients.

2. Discuss how abnormal access to nutrients in tumors affects the biology of cancer cells.

3. Discuss how nutrient starvation in tumors affects the response of cancer cells to chemotherapeutics.

Mitochondria are central hubs for cellular stress adaptation, with their function integrated with both apoptosis and autophagy pathways that determine cell fate. Alterations in mitochondrial morphology and inter-organellar communication shape these outcomes. In this presentation, I will first provide an educational overview of how mitochondrial dynamics (fusion, fission) intersect with intrinsic apoptosis and mitophagy/autophagy regulation. Particular emphasis will be placed on how live-cell high- and super-resolution microscopy has advanced our understanding of these processes, revealing the spatial and temporal coordination of organelle remodeling under stress. In the second part of the talk, I will highlight recent findings from my laboratory on FATE1 (Fetal and Adult Testis Expressed 1), a cancer/testis antigen aberrantly expressed in cancer cells. Unlike its homolog mitochondrial fission factor (Mff), FATE1 does not promote mitochondrial fragmentation but instead preserves mitochondrial networks and prevents stress-induced breakdown. Given that FATE1 is recognized as a factor promoting cancer cell survival, these activities may be integrated with mechanisms that allow tumor cells to resist apoptosis and maintain their survival under chemotherapies. Together this dual focus will illustrate both fundamental principles of mitochondrial stress responses and a concrete example of how a cancer-selective regulator exploits these pathways for oncogenic advantage.

Learning Objectives:

1. Explain how mitochondrial dynamics influence intrinsic apoptosis and autophagy

2. Describe how advanced live-cell and super-resolution microscopy can be used to study mitochondrial stress responses

3. Analyze how mitochondrial remodeling contributes to cancer cell survival and therapy resistance

Engineered immune cell therapies offer the promise of more tailored interventions than traditional systemic checkpoint blockades, but so far remain ineffective across the majority of clinical settings, especially solid tumors. To overcome the slew of resistance mechanisms cancers present, various screening modalities have nominated numerous gene knockouts, gene overexpression, and synthetic CAR and TCR sequences to further refine T cell therapies. But among this abundance of gene targets, effective methods to directly compare large numbers of potential clinical constructs to engineer immune cells are lacking. Further, the association of these synthetic genetic sequences with the functional phenotype they impart on an engineered cell is costly, time consuming, and low throughput. Here, we developed Modular Pooled Knockin Screening (ModPoKI), a highly scalable platform to rapidly associate large pools of T cell genetic modifications with high dimensional single cell phenotypes across diverse cancer immunotherapy contexts. We built libraries of transcription factors (TFs) and natural and synthetic surface receptors, including numerous proposed constructs under clinical investigation. Over 20 ModPoKI screens across dozens of healthy human donors in both TCR and CAR T cells in diverse conditions built a high dimensional genotype x phenotype map which benchmarked existing clinical constructs and nominated unique novel cell therapy targets for further clinical development which overcame cancer resistance mechanisms and showed improved in vitro and in vivo performance. Analysis across these diverse functional contexts identified a transcription factor AP4 (TFAP4) construct that enhanced long-term T cell fitness and anti-cancer function in vitro and in vivo. ModPoKI’s modularity further allowed us to generate a ∼10,000-member library of TF combinations, revealing unexpected functional relationships within CAR T cells with synthetic transcriptional programs. Non-viral knockin of a combined BATF-TFAP4 polycistronic construct further enhanced function in vivo. ModPoKI facilitates scalable discovery of complex gene constructs to program and improve engineered immune cell functions tailored to specific cancer resistance mechanisms.

Learning Objectives:

1. Describe how Modular Pooled Knockin Screening (ModPoKI) enables scalable genetic discovery in human T cells.

2. Compare the functional outcomes of different genetic modifications, including transcription factors and synthetic receptors, in engineered immune cells.

3. Assess how genotype–phenotype mapping through ModPoKI can identify novel constructs that enhance T cell fitness and anti-cancer function.

Survival for women with HR+ breast cancer has increased over the past several decades.  However, estrogen- and progesterone-receptor positive (HR+) Her2neg breast cancer continues to exhibit tremendous metastatic capability, as evidenced by the fact that 73.1% of women with metastatic breast cancer were diagnosed with HR+ disease. Successfully preventing metastatic dissemination remains a significant barrier to reducing mortality associated. Here, we explore the link between the gut microbiota, mammary tissue microenvironment, and lungs - defining how an unhealthy and inflamed gut microbiome impacts long-term susceptibility to metastatic breast cancer. 

Learning Objectives:

1. Learn what gut microbial dysbiosis is and understand the systemic consequences of an unhealthy gut microbiome. 

2. Understand different mechanisms whereby the host microbiome can impact metastatic breast cancer. 

3. Explain how interactions between the gut microbiota and mammary/lung microenvironments contribute to metastatic progression.