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15-Track, 3-Day, Leading Precision Medicine Agenda

Largest & Original Forum for Precision Medicine

15-Track, 3-Day, Leading Precision Medicine Agenda

Facilitating Collaboration in the Field of Personalized Patient Care

The Largest & Original (Est. 2009) Forum for Precision Medicine

Facilitating Collaboration in the Field of Personalized Patient Care

The Largest & Original (Est. 2009) Forum for Precision Medicine

15-Track, 3-Day, Leading Precision Medicine Agenda

Facilitating Collaboration in the Field of Personalized Patient Care

15-Track, 3-Day, Leading Precision Medicine Agenda

The Largest & Original (Est. 2009) Forum for Precision Medicine

Facilitating Collaboration in the Field of Personalized Patient Care

The Largest & Original (Est. 2009) Forum for Precision Medicine

15-Track, 3-Day, Leading Precision Medicine Agenda

The Largest & Original (Est. 2009) Forum for Precision Medicine

15-Track, 3-Day, Leading Precision Medicine Agenda

Facilitating Collaboration in the Field of Personalized Patient Care

15-Track, 3-Day, 400-Speaker Precision Medicine Agenda

SPEAKERS / HONOREES

-Select:

Mary-Claire King
University of Washington School of Medicine

PMWC 2027 PIONEER HONOREE
BRCA1 Discovery Pioneer

David Baker
University of Washington

PMWC 2027 LUMINARY HONOREE

2024 Nobel Laureate

Emmanuelle Charpentier
Max Planck Unit for the Science of Pathogens

PMWC 2027 J. CRAIG VENTER VISIONARY HONOREE

Nobel Laureate (CRISPR)

Daniel Drucker
Sinai Health System

PMWC 2027 PIONEER HONOREE
2025 Breakthrough Prize (GLP-1)

Thomas C. Südhof
Stanford

PMWC 2027 PIONEER HONOREE

Nobel Laureate

Fei-Fei Li
Stanford

PMWC 2027 PIONEER HONOREE

Godmother of AI

Randy Schekman
UC Berkeley

PMWC 2027 PIONEER HONOREE

Nobel Laureate

Andrew Ng
DeepLearning.AI

PMWC 2027 LUMINARY HONOREE

Google Brain Founder

Bringing Together

DAYS

ATTENDEES (35 COUNTRIES)

EXHIBITORS

PARALLEL TRACKS

Format

The conference format consists of five parallel talks spanning 3 full days. Main Tracks 1-4 include sessions by leaders in the commercial, pharmaceutical, academic, government, regulatory, venture capital, and non-profit arenas that deliver a broad and up-to-date array of content across the various facets of precision medicine. Session discussions focus on time-relevant aspects with a selected set of key stakeholders, while commercial sessions cover the latest developments in technologies that are instrumental for the success of further adoption of precision medicine.

Additional 2 Tracks, feature Showcases: companies and research institutions can promote their platforms, launch products, and share research developments to a targeted audience – Apply.

For over a decade, PMWC has recognized individuals who have played a significant role in transforming health care by advancing precision medicine in the clinic with the Luminary and Pioneer Awards. The honorees’ numerous technological and scientific contributions have expedited this transformation as demonstrated by the clinical adoption of precision medicine, and the ongoing introductions of novel clinical applications. For a deeper look into the fascinating achievements of our past awardees see the awards page.

Receive the latest news about the field of precision medicine, and the conference from Tal Behar, PMWC’s President:

Interview Questions for Samir Hanash

Interview with Samir Hanash, MD Anderson Cancer Center

Responses to interview questions from Tal Behar, Precision Medicine World Conference

Samir Hanash, The University of Texas MD Anderson Cancer Center | PMWC 2027 Silicon Valley, Track 3, Day 1, Session 2: The End of One Size Fits All

Interview Personalized Cancer Screening Proteomics & AI

View the Developing PMWC 2027 Program

Beyond Age-Based Screening: Personalizing cancer detection around individual risk

Hanash argues that reducing cancer deaths starts with determining who is at risk and for which cancer. He points to blood-based risk assessment across nine common cancers as a way to personalize screening and potentially enable prevention.

Q1 You pursued blood-based cancer detection long before it became a major field. What did you see that others did not, and what still must happen before early detection meaningfully reduces cancer deaths?

A: It became clear that the foundation for reducing death due to cancer is to determine who is at risk and for which cancer. This allows for screening to be personalized based on risk. At present screening is largely based on age and for just a few common cancers. Determining an individual’s cancer risk based on a blood test like we have done for nine common cancers provides a real time assessment of risk to tailor screening accordingly. Determining risk also provides an opportunity for prevention like eventually with a cancer vaccine for which an individual is found to be at risk or other means.

When Is a Multi-Cancer Test Ready? Cancer-specific evidence and cost effectiveness

For broad clinical adoption, Hanash calls for test performance to be calibrated for each cancer type. Mortality reduction remains the ultimate goal, with cost effectiveness and potential health care savings also part of the evaluation.

Q2 Blood-based early detection must distinguish true early disease from biological noise while avoiding unnecessary downstream procedures. What evidence should the field require before a multi-cancer test is ready for broad clinical use?

A: The performance of the test has to be calibrated on a cancer type by cancer type basis. Because some cancers are more common than others, one size does not fit all. Although the ultimate benefit is mortality reduction, in addition to performance, cost effectiveness meaning health care costs saved through the implementation of the test have to be taken into account.

From Proteomics to Prevention: Integrating multi-omics and AI

Hanash sees proteomics as essential for characterizing proteins and their locations. As vast proteomic datasets are combined with other omics and individual characteristics, AI becomes critical to translating that complexity into useful discoveries.

Q3 You helped establish HUPO and have watched cancer proteomics mature over decades. Looking ahead, how do you see proteomics, other omics, and AI working together to shift cancer care from late diagnosis toward interception and prevention?

A: Proteomics, other omics and AI can contribute substantially to shifting cancer care. First proteomics is essential to identify forms of proteins and their subcellular locations whether for diagnostics or therapeutics At present with the advances in proteomics technologies from one biological sample terabytes and terabytes of data can be generated for discovery that can be incorporated with other omics data and with subject characteristics making the use of AI essential to derive the most benefit from such data.

Explore the PMWC 2027 Program

07 Oct ,2026

Interview Questions for Jay Bradner

Interview with Jay Bradner, M.D., Amgen

Responses to interview questions from Tal Behar, Precision Medicine World Conference

James “Jay” Bradner, M.D., Executive Vice President, Research and Development, Artificial Intelligence and Data, Amgen

Interview Drug Discovery & Chemical Biology AI & Data in R&D

View the Developing PMWC 2027 Program

Reaching the Undruggable Proteome: Molecular glues, degraders and what remains out of reach

Bradner describes how chemical biology, molecular glues and induced proximity are opening historically intractable targets, particularly in gene control. But intrinsically disordered proteins and the intracellular delivery of large biomolecules remain major challenges.

Q1 Much of the proteome was once considered undruggable. Molecular glues, degraders, and induced proximity have changed that premise. What can we reach today that was out of reach ten years ago, and what still feels out of reach?

A: The chemical biology mindset has contributed meaningful in-roads to the discovery of new molecules working in new ways, in many cases on historically intractable targets. Molecular glues, which remain a focus of my research, leverage large protein interfaces adjacent to binding sites to complete molecular recognition events, allowing the engagement of protein targets that would otherwise not be “druggable”. This has been particularly exciting in the field of gene control, which for years was the focus of my scholarship as an investigator. Gene control proteins, in particular transcription factors, frequently possess intrinsically disordered regions that rare adopt coherent secondary structures. High entropic penalties and absent binding sites continue to challenge the drug hunter. Beyond small molecules, approaches to deliver large biomolecules into cells remains a grand challenge, which we and others are working on to this day.

Where AI Is Changing Drug Development: From protein design to agentic workstreams

Bradner points to concrete AI applications across discovery, regulatory work and clinical development. His strongest near-term excitement is around agentic workstreams, while emphasizing that AI works best in the hands of disciplinary experts rather than as a substitute for them.

Q2 Your current role brings research, development, AI and data under one remit. Where is AI genuinely changing the probability of developing a successful medicine, and where is the field still mistaking hype for progress?

A: Artificial Intelligence is proving to be a powerful catalyst for biomedical discovery research and therapeutic development, with a growing number of high-impact applications. Protein structure prediction accelerates both de novo discovery of active large molecules, as well as their optimization for drug-like properties. Document authoring decreases the time to regulatory filing. Pattern recognition identifies new target pathways in complex genomic and phenotypic datasets. Forecasting and clustering optimize clinical trial enrollment. Together, these and other tools cut through complexity, improve decision-making and ultimately improve the probability of success. Most exciting to me at this moment is the systematic application of agentic workstreams to critical phases of pharmaceutical science, and business. AI is an instrument best played by a disciplinary expert, who has accepted the invitation to approach their work in a new way. While there remains some distracting hype around AI across sectors, there is no question that AI is emerging as a powerful adjacency for biomedicine – which we call convergent innovation.

What JQ1 Taught Us: Open chemical probes can accelerate an entire field

The JQ1 experience became a case study in how an openly shared chemical probe can accelerate biology far beyond its original hypothesis. Bradner traces its impact from BRD4 biology to protein degradation, oncogenic transcription factors and therapeutics now in clinical development.

Q3 JQ1 became one of the most widely shared chemical probes in modern biology, yet BET inhibitors have proven difficult to convert into approved medicines. What did that teach you about the distance between a beautiful hypothesis and a drug — and about how openly discovery should be shared?

A: In this post-genomic era, biomedicine is best practiced by hypothesis-testing. Where available, incisive prototype drugs paired with predictive pre-clinical models can expedite therapeutic translation. The experience of creating, characterizing, studying and sharing the BET bromodomain inhibitor, JQ1, provided a powerful learning. Open access to chemical probes opens up a field of study and accelerates medical progress. In the few years following the publication of JQ1, hundreds of laboratories worked with the molecule to learn about the biology of BRD4 in cancer, heart disease, fibrosis, inflammation, fertility, and most importantly the fundamental role of BRD4 in gene control (transcription elongation). In this way, JQ1 powerfully accelerated scientific discovery, bringing BRD4 biology into view in many disparate fields of study. Years later, scientists have used JQ1 as a work-horse of protein degradation, since our publication of the chemical solution to protein degradation and the molecule dBET1. Others have used JQ1 to recruit BRD4 to oncogenic transcription factors, such as the Androgen Receptor (at Halda, now J&J). JQ1-derived therapeutics are presently in advanced stages of clinical investigation as cancer therapies and for cardiovascular disease. I am hopeful that patients will benefit from the learnings of this remarkable molecule.

Explore the PMWC 2027 Program

05 Oct ,2026

Interview Questions for Nickolas Papadopoulos

Interview with Nickolas Papadopoulos, Ph.D., Johns Hopkins University

Responses to interview questions from Tal Behar, Precision Medicine World Conference

Nickolas Papadopoulos, Ph.D., Professor of Oncology and Pathology, Johns Hopkins Sidney Kimmel Comprehensive Cancer Center

Director of Translational Genetics, Ludwig Center at Johns Hopkins University

Interview Early Cancer Detection Multi-Cancer Screening

View the Developing PMWC 2027 Program

From Early Detection to Cancer Interception: Finding the lesions that will become dangerous

Detecting cancer earlier is only part of the challenge. The next frontier is identifying which precancerous lesions are biologically destined to progress. Papadopoulos points to combinations of DNA, RNA, proteins and other biomarkers, as well as sampling bodily fluids closer to the lesion, as promising ways to find these elusive signals.

Q1 Your newest work points to a harder problem than detecting cancer early: distinguishing a precancerous lesion that will become dangerous from one that may never progress. Which biological signals look most promising, and what is your team pursuing next to make cancer interception possible?

A: Precancerous lesions still have genetic and epigenetic changes much like cancers. So, similar signals look promising. The issue with developing liquid-biopsy-based tests to detect precancerous lesions is the scarcity of the cancer signal, i.e. biomarkers, in blood, which affects the sensitivity of an assay.

One approach is to identify some combination of biomarkers that could increase the sensitivity. There is work being done on this and, in addition to DNA, other biomarkers are being studied, like proteins and RNA.

Another approach is to use a different medium than blood, like bodily fluids that are closer to the source of the lesions desired to be detected. For example, the use of urine for detecting bladder lesions.

What NHS-Galleri Really Tells Us: Stage shift alone is not enough

The first randomized MCED trial to report results raised a more fundamental question about how these tests should be judged. Papadopoulos argues that simply counting Stage III and IV cancers misses important differences among tumor types. Future trials will need to show whether screening finds cancers when cure is realistically possible, while also measuring survival, benefits and harms.

Q2 The NHS-Galleri trial, the first randomized MCED trial to report results, found 14% fewer Stage IV diagnoses after three annual screenings, but missed its primary endpoint of reducing combined Stage III–IV cancers. What do you believe the trial actually proved, and what must the next generation of MCED tests and trials do differently?

A: Although the primary endpoint had to do with reduction of Stage III–IV cancers, an in-depth analysis of the data is needed. Some of these data were presented at ASCO 2026.

What is important is to look at the type of tumors identified and at what stage. For some tumor types Stage III is manageable, while for other tumor types even Stage I is not.

Future randomized controlled prospective interventional studies should focus not only on the reduction of stage. For example, the endpoints should include a more detailed view that includes the cancer types detected, the stages identified, in how many cases there is an opportunity to treat people with intent to cure, and cancer-specific survival, to mention a few.

We need to know the benefits as well as the harms of MCED tests before widespread adoption.

The Bar for Routine Screening: High specificity, meaningful cancers and an opportunity to cure

For population screening, false positives can quickly overwhelm the benefits of a test because cancer remains uncommon among asymptomatic people. Papadopoulos says the strongest case for MCED will come from finding cancers that currently lack standard screening tests, before symptoms appear and while treatment still has curative potential.

Q3 What evidence would convince you that multi-cancer blood testing is ready for routine screening, and what finding would make you pull back?

A: I will start with what would make me pull back. That would be low specificity. This test is meant to be used as a screening test. Cancer in asymptomatic individuals is rare, approximately 1% depending on the age of the population. So, the test needs to be specific, avoiding a large number of false-positive results which could lead to unnecessary procedures.

What will keep me going is detection of cancers for which we do not have standard-of-care tests, detected before symptoms at stages where there is an opportunity to manage these individuals with intent to cure.

I see early detection of cancer as being proactive, instead of reactive, about detecting the disease to address underdiagnosis. Earlier detection of cancer will result in the reduction of sickness and death from cancer. It provides an opportunity to deliver management, including surgeries and therapies, with intent to cure and not just to prolong life. Drugs that are now used to treat metastatic stages of cancer should have better results in individuals whose cancer was detected earlier.

I do not mean to minimize other aspects associated with the successful clinical implementation of a test, like cost, accessibility, etc. I have focused my answer on why it is worth trying to deliver such a test.