Cancer Genomics

Forum Chairs

Dana-Farber Cancer Institute
Wellcome Sanger Institute

Forum Description


  1. Molecular Analysis of Cancer Genomes I
  2. Molecular Analysis of Cancer Genomes II
  3. Evaluation of Genetic Variation in Cancer
  4. From Genomics to Therapy

Cancer is a genetic disease. Increased cancer susceptibility can result from inherited mutations in tumor suppressor genes and oncogenes as well other genes. In addition, in both inherited and the much more common sporadic cancers, mutations arise that drive the development and progression of the cancer. Decades of research have led to an understanding of the types of pathways that become genetically and epigenetically compromised in cancer; however, a comprehensive understanding of the genetics of all tumor types is not yet available. In recent years it has been possible to bring to the clinic therapies that are targeted to genetic defects found in cancer. The classic example is the treatment of Chronic Myelogenous Leukemia (CML). This disease is characterized by a specific chromosomal translocation resulting in the breakage and fusion of two genes to create the novel, mutant BCR-ABL fusion gene. The expression of this fusion gene drives tumorigenesis in this disease.

The development of a class of agents that inhibit the BRC-ABL oncoprotein, which is only expressed in CML cells, has dramatically improved the prognosis of patients diagnosed with CML. Many other such anti-cancer drugs have been developed or are under development for treating other types of cancer. However, the ability to more broadly implement these types of therapies will require a much more comprehensive understanding of the genetic and epigenetic changes in different cancers. Since the successful sequencing of the human genome, there have been rapid advances in the development of genomic technologies.

These new technologies, which are advancing and evolving at a rapid rate, have made it possible to gain a much more detailed understanding of the types of genetic changes present in cancers. For example, it is now possible to detect genetic changes that occur at low frequencies in different cancer types and begin to explore whether such mutations are bystander mutations or whether they influence the development and progression of cancer, and therefore might guide the development of targeted therapeutics. In addition, it is also possibly to map the types of genome rearrangements that occur in cancers in much greater detail.

In parallel with these developments has been the development of sophisticated bioinformatics needed for analyzing the much larger data sets being generated. Over the next few years, it is likely that our ability to explore the genetics of individual cancers will expand by a previously unanticipated extent. In this rapidly evolving field, the meeting, to be led by Dr. Richard Kolodner of the Ludwig Institute for Cancer Research and Dr. Michael Stratton of the Sanger Center, will provide an important opportunity to explore our current state of knowledge of Cancer Genomics and the directions in which the field is moving.

Forum Summary

The focus of the 2010 Forbeck Foundation was on the rapidly moving field of cancer genomics. It is generally accepted that cancer is caused by the accumulation of mutations or epigenetic modification that affect specific genes. The identity of the affected genes provides clues to the cellular processes underlying tumorigenesis and has proven useful for diagnostic and therapeutic purposes. To date, however, only a small fraction of the genes has been analyzed and the number and type of alterations responsible for the development of common tumor types are not well known. Much of our current knowledge of the genetic and epigenetic alterations in cancers has come from decades of work cloning and analyzing individual genes in human cancers. The insights from these studies have provided diagnostic tools for analyzing inherited cancer susceptibility and linking genetic changes in cancer to sensitivity and resistance to chemotherapy as well as providing predictions of prognosis and survival.

A key insight in the applicability of cancer genetics to cancer treatment came from the development of drugs that successfully target the oncoprotein encoded by the BCR-ABL translocation, a genetic alteration that underlies Chronic Myelogenous Leukemia. This development has led to the common view that many other successful cancer treatments that target genetic alterations, so-called personalized therapy, can be developed. However, implementation of personalized therapies will require a much more comprehensive knowledge of the genetic and epigenetic changes in different cancers.

The completion of the human genome sequence greatly facilitated the types of studies required to identify the diversity of genetic and epigenetic changes in different cancers. In the last several years, facilitated by the knowledge of the human genome sequence, there has been the rapid development of ever more powerful methods for analyzing genetic and epigenetic changes on a genome-wide scale. The rapidly decreasing cost of genome-wide analysis and the continued development of bioinformatics methods have brought us to the point where the results of genome-wide analysis of genetic and epigenetic changes are becoming available for many different tumor types.

The 2010 Conference brought together a group of experts in Cancer Genomics to discuss progress and the challenges in transforming the results of current Cancer Genomics initiatives into practical treatments that can impact the prognosis for cancer patients. A session chaired by Dr. Joe Gray focused on the genomic analysis of a number of cancer genomes, with a primary focus on the use of whole genome and whole exome sequencing methods. The discussions in this session also triggered a debate about how to distinguish which identified mutations were “driving” cancer from those that are merely “passengers” and whether or not this driver/passenger dichotomy was even useful or legitimate for understanding cancer biology.

Dr. James Downing discussed collaborative efforts to perform large-scale genomic analysis of leukemias using sequencing approaches to detect mutations and genome rearrangements and array based methods to detect copy number changes. These efforts were directed at both understanding the genetic changes in primary leukemias as well as in understanding relapse cases. These efforts have revealed information about the prevalence of mutations in different cancer-relevant genes, such as PAX5, in different leukemias as well as demonstrating how copy number changes can lead to clinically relevant alterations in gene expression. Mutations that can predict relapse have been identified, and interestingly, it was demonstrated that relapses could result from leukemia cells present in the original cancer population but are distinct from the major clone present in the original leukemia. Finally, recent results on mutations affecting DNA methyl transferase genes in leukemias were discussed providing an interesting linkage between the development of some leukemias and epigenetic processes.

Dr. David Huntsman discussed his efforts to use whole-genome analysis to address clinical questions in ovarian cancer. Of particular importance in this disease is the development of molecular markers for sub-classifying ovarian cancer to better understand both prognosis and treatment options. Ovarian cancers with BRCA1 or BRCA2 mutations are sensitive to PARP inhibitors, and these mutations are currently used to select patients for PARP inhibitor therapy. Conversely, he showed that there are PARP inhibitor sensitive ovarian cancers without defects in BRCA1 or BRCA2, illustrating the need for a molecular signature for identifying this ovarian cancer sub-type. Related to this problem, Huntsman also described ongoing genomic analysis of ovarian cancers that had acquired resistance to PARP inhibitors to understand the mechanism of resistance.

Dr. Victor Velculescu discussed his laboratory’s collaborative efforts to systematically study the cancer genome through analysis of the majority of protein coding genes in breast, colorectal, pancreatic, ovarian and brain cancers. Their analysis to date has focused on direct resequencing of all of the currently annotated genes in the human genome. They have identified mutations both in genes previously known to be mutated in human cancer and in a wealth of new mutated genes, implicating new pathways as playing roles in human cancer. Their results indicate that the genetic landscape of human cancers include both commonly mutated genes as well as genes that are mutated at lower frequencies. Importantly, their data has allowed them to calculate the number of driver mutations in different cancer types and show that each type of cancer has a different, but characteristic, number of driver mutations. These studies define the genetic landscape of human cancers, open fertile avenues for basic research in tumor biology, and provide new targets for personalized diagnostic and therapeutic intervention.

Dr. Tom Hudson discussed examples of ongoing initiatives that were established to accelerate the translation of new cancer mutation discoveries into clinical applications. He focused on inherited common risk alleles that were identified by Genome-Wide Association Studies (GWAS). Individually, these common alleles confer only small increases in risk of developing colorectal cancer (CRC), but by combining these alleles with age and family history, they observed that population subgroups can be identified with a predicted absolute CRC risk sufficiently high as to merit surveillance/intervention. He also focused on the analysis of somatic mutations acquired during the development of tumors. Here, the International Cancer Genome Consortium (ICGC) was formed with the aim of generating comprehensive catalogues of genomic abnormalities (somatic mutations, abnormal expression of genes, epigenetic modifications) in tumors in 50 different cancer types and/or subtypes and to make the data available to the research community. In this context, Hudson presented a design for a clinical trial underway in Canada that is sequencing a large set of cancer genes in tumors from patients with advanced cancer, in order to select therapies that are based on mutation status.

A session chaired by Dr. Victor Velculescu focused on the structure of cancer genomes integrating a number of approaches including analysis of copy number variation, mapping of genome rearrangements and both whole genome and targeted gene sequencing. Dr. Sharon Diskin (Forbeck Scholar) discussed her laboratory’s efforts to understand the genetic and environmental factors that cause sporadic neuroblastoma (NB), which remain largely unknown. They have been comparing germline genome-wide single nucleotide polymorphism (SNP) genotypes from 5,000 NB patients to 10,000 controls in order to discover SNP and copy number variation (CNV) associations. To date, they have genotyped over 3,800 neuroblastoma cases and have reported six loci containing common SNPs and a common CNV each highly associated with sporadic NB. To begin to understand the biological relevance of these associations, they are performing correlative and mechanistic studies in lymphoblastoid cell lines (LCLs) as well as matched primary NB tumor tissues and NB cell line models. Together, their data provide evidence for at least two distinct genetic subtypes of NB at the level of tumor initiation, and illustrate the utility of combining germline and somatic data in assessing GWAS signals in cancer. Additional NB associated variants, both common and rare, have been identified and validation efforts are ongoing.

Dr. Michael Stratton primarily focused on his laboratory’s use of Next Generation DNA sequencing technologies to perform high-density mapping and sequencing of the genome rearrangements found in human tumors. Their data indicated that each tumor had its own genome rearrangement signature. A particularly interesting use of this information was illustrated by a study of several patients in which it was possible to follow the genome rearrangement signatures for the primary tumor and subsequent relapse and metastatic tumors. This allowed them to characterize tumor clonality and evolution through the course of disease development and progression.

Dr. Rick Wilson described the development and use of Next Generation sequencing technology at the Sequencing Center at Washington University in St. Louis to study cancer genomes. The work he described illustrated that early stage sequencing can sometimes miss important mutations and that there is considerable value to continuing to analyze larger numbers of tumors with newer, improved technology as this can reveal important cancer-related genetic variation. The work also illustrated the enormous amount of genetic variation in tumors that is being revealed by sequencing studies and the enormous challenge this presents in classifying these potential genetic changes, validating the genetic changes and ultimately determining their significance to cancer biology.

Dr. Christopher Putnam (Forbeck Scholar) discussed his efforts to understand the nature of genome instability. The genomes of many types of cancers are extensively rearranged and show evidence of ongoing instability. This instability is likely to be due to accumulated defects in processes that maintain normal genomes in non-cancerous cells and such defects could play a role in initiation or progression of cancer. He described studies of genome instability in a model organism, the yeast Saccharomyces cerevisiae. These studies have identified genes in which mutations result in increased rates of accumulating genome rearrangements and have revealed that the types of genome rearrangements that occur, which resemble those discovered in human tumors, are strongly influenced by which underlying genetic defects causes the increased genome instability observed. These studies also suggest that genetic defects underlying increased genome instability might be identified through analysis of the spectrum of genome rearrangements present in an individual tumor and, because many of these genetic defects give rise to sensitivity to DNA damaging agents, that rearrangement spectra could eventually be used to help guide treatment choice.

Dr. Jessica Zucman-Rossi discussed her team’s efforts to identify new carcinogenesis pathways and provide molecular classifications for benign and malignant liver tumors using functional genomics approaches. Their strategy enabled them to identify a broad diversity of genetic lesions that will have important implications for patients with liver disease. For example, dissection of molecular pathways in hepatocellular adenoma identified new risk factors (obesity) and genetic susceptibility (germline HNF1A and CYP1B1 mutations) that promote the development of benign liver tumors. Moreover, new pathways of tumorigenesis (HNF1A, STAT3, ß-catenin and others) showed a close relationship with the clinical and pathological features of both tumors and patients. As a result of this analysis, it was possible to identify small homogeneous sub-groups of tumors which will allow modification of prevention, diagnosis and treatment strategies for patients leading to more efficient personalized treatment.

A session chaired by Dr. Tom Hudson, focused on evaluating the significance of genetic variation in cancer genomes through the identification genetic and epigenetic changes that are of significance to the development of cancer. Dr. David Adam’s work is focused on using functional assays in mice as a model system to identify tumor suppressor genes. He described the largest and most comprehensive forward genetic screen in the mouse for genes that play a role in tumorigenesis. The screen was performed in Apc mutant mice for bowel cancer genes. His critical finding was that there were many more genes than previously thought that can contribute to tumor formation. These results challenge the dogma that that there are just a few major genes in which defects result in cancer formation and suggested that as many as 20 genes can contribute to tumorigenesis in each clonal cancer. Interestingly, this number of genes falls within the range of the number of driver mutations in individual cancer identified by Velculescu’s studies.

Dr. Andrea Califano discussed the use of Systems Biology to identify critical pathways in different cancers. Reverse engineering of cell context specific molecular interactions has unveiled the complex structure and control of regulatory networks in normal cell physiology and in disease. Interrogation of these networks using cancer specific signatures has identified an intermediate layer of transcriptional regulation, responsible for the integration of a broad spectrum of signals that are altered in specific tumor subtypes. For instance, his laboratory demonstrated that a small module regulated by the two transcription factors C/EBP(b/d) and Stat3 is responsible for the synergistic integration of genetic alterations contributing to expression of mesenchymal genes in High Grade Glioma. Activation of the mesenchymal program is associated with the poorest prognosis in these tumors. Similarly, Nf-kB was shown to integrate aberrant signals associated with an entire spectrum of genetic alterations in upstream signal transduction genes, such as CARD11, A20, TRAF2, TRAF5, TAK1, and RANK, among others, specific to the more aggressive ABC subtype of Diffuse Large B Cell Lymphoma compared to the GCB subtype. These results suggest that while sequencing can identify key oncogenes and tumor suppressors associated with tumor initiation and tumor progression, analysis of regulatory networks can provide a complementary and valuable perspective by identifying genes acting as key integrators of these aberrant signals. These approaches have the potential to provide more general targets for single- and combination drug therapy as well as more informative and universal biomarkers that are causally relate to the presentation of the tumor subtype.

Dr. Richard Kolodner discussed his laboratory’s efforts to use the yeast Saccharomyces cerevisiae as a model system to identify the genes and pathways that cells use to prevent genome instability. It is well known that many cancers have ongoing genome instability that potentially reflects a defect in a gene or pathway required for maintenance of genome stability, and work with PARP inhibitors has suggested that such defects may be a cancer therapeutics target. However, the range of genetic defects that result in increased genome instability is largely unknown. A series of quantitative genetic assays for detecting increased genome instability has been developed and through a combination of genetic screens and bioinformatics analysis, a series of 510 yeast genes predicted to act to prevent genome instability has been developed and partially validated. Initial attempts to mine cancer genome mutation data sets to determine if the human homologues of these genes are mutated in human cancers has suggested that a significant number of these genes are potentially mutated in some human cancers; however, functional studies will be required to validate the presumptive mutations.

Dr. Peter Laird discussed his work demonstrating that genomic loci that are involved in cellular differentiation and are targeted by Polycomb Group Repressors in embryonic stem cells are predisposed to become methylated in cancer cells, suggesting that an epigenetic block to cellular differentiation may sometimes be an initiating event in carcinogenesis. DNA methylation changes contribute directly to cancer by transcriptional silencing of tumor-suppressor genes through promoter CpG island hypermethylation. His group demonstrated very strong associations between distinct epigenetic subtypes, such as CpG Island Methylator Phenotypes (CIMP) and specific somatic genetic events, such as BRAF mutation in colorectal cancer and IDH1 mutation in glioblastoma multiforme. These associations are consistent with an early role for DNA methylation, and suggest these epigenetic modifications provide a cellular context for the subsequent somatic mutation that is favorable for disease progression. This session, chaired by Dr. Jessica Zucman-Rossi, focused on the prospects and challenges for using the results of genomic analysis to direct cancer therapy.

Dr. Benjamin Berman (Forbeck Scholar) discussed his efforts to develop DNA methylation profiles for evaluating different cancers. Epigenetic mechanisms play important roles in the development of cancer, and DNA methylation has been used as both a biomarker and a target for therapeutics. He applied a new sequencing technology (massively parallel MethylCseq) to a paired colon tumor and normal colon mucosa sample to determine the complete map of DNA methylation at single base-pair resolution, the first such "methylome" map of a tumor. This high resolution map revealed a number of novel features, including the presence of methylation differences at two distinct spatial scales. Long (>100 kb) blocks of reduced methylation in the tumor corresponded to silencing domains associated with the nuclear periphery, and within these were thousands of short (~1 kb) CpG island elements with increased methylation in the tumor. Profiling additional types of cancer in this way is expected to yield insights into the regulatory changes that occur in the development of cancer, and guide the use of different treatment regimens.

Dr. Levi Garraway discussed the many challenges involved in bringing genomic information into clinical practice. The key questions he discussed are whether ongoing genomic studies will provided all of the clinically relevant data needed to drive future application, what are the challenges in actually using genomic information to guide clinical decisions, how do we use genomic information in the clinical setting so that we know it is actually useful and what types of clinical and translational research will be needed once genomic information is readily available. Appropriately addressing these questions will be required to ensure that patients fully benefit from cancer genomics.

Dr. Derek Chiang (Forbeck Scholar) discussed his studies aimed at understanding the many mechanisms of drug resistance in tumors and the identification of therapeutic targets that will be suitable for developing combination therapies that can target drug resistant tumors. Toward this end, they have performed an RNA interference screen to identify kinases that may confer sensitivity to sorafenib combinations. Computational analyses of signaling pathways identified in this screen found a surprising but potentially useful link between Toll-like receptor signaling and sorafenib in liver cancer cell lines.

Dr. Joe Gray focused on the use of “omic” information on breast cancer to address the poor survival duration (<25% 5 year survival) experienced by patients with metastatic breast cancer. One approach he suggested for dealing with this problem was early detection of metastasis prone breast cancer. He described their efforts to develop sensitive and specific detection reagents for MRI/PET imaging and multiplex immunohistochemical detection designed for specific detection of cancers that will metastasize with high probability. These studies are being guided by “omic” information on gene expression, alternative mRNA splicing, fusion genes, DNA methylation profiles, copy number abnormalities and promoter methylation. The second approach he suggested for dealing with this problem was improved treatment of metastatic disease. He described their efforts to screen next generation drugs singly and in combination in a panel of well-characterized cell lines where complete genomic profiles are becoming available to identify molecular determinants of response. They are focusing on identification of response predictors that are not influenced by variations in the microenvironment, in order to make therapies robust across the diverse microenvironments in which metastatic tumor cells reside.

In summary, the 2010 conference was an exciting meeting held at a pivotal time in the development of the field of Cancer Genomics. The discussion revealed that the wealth of genomic information about cancer that is currently being generated suggests that we are on the verge of having enough data to make personalized cancer treatment a reality for many different types of cancer. Yet, as exciting as the promises of these new advances are, the discussion also revealed that key challenges remain in the interpretation and integration of this data in ways that will allow these results to be applied routinely in the clinic.

Quotes from Participants
“The meeting last weekend was a clear example of how your group has had a direct impact on the enterprise of cancer research. The meeting was unlike any other I have attended. It was fantastic to be able to get together with the leaders of the field of cancer genomics and discuss in an open forum where the field has been, and where it needs to go. The combination of scientific sessions, breaks, lunch out on the point and the leisurely walks back to the hotel, and the evening receptions provided the ideal balance of setting to allow the participants to not only discuss science, but to also interact outside the bounds of our often competitive existence. Again, thank you for everything you do.” -- James R. Downing, M.D., St. Jude Children's Research Hospital, Memphis, TN

“The meeting really was special and unlike any other I've attended before. Having just 12 participants and restricting the number of slides really helps promote discussion.” -- David Adams, Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Cambridge, UK

Venue & Travel Information

Geneva National Resort

1221 Geneva National Avenue, South

Lake Geneva, WI 53147


Travel Forms

Travel forms are due 30 days prior to the start of the meeting to allow enough time to plan transportation.

Milwaukee's General Mitchell International Airport (MKE) is the preferred airport as it is only 45 minutes from the meeting location.

  • Arrivals - Thursday around 1 PM, 3 PM and 5 PM
  • Departures - Sunday around 10 AM and 12 PM

Chicago's O'Hare Airport (ORD) is 1 1/2 hours from the meeting location without traffic. The Foundation tries to prioritize International Flights and situations where flying into ORD is significantly cheaper than connecting to MKE. The times below are for guidance only, and depending on the volume of travelers, we may add an additional shuttle to and from the airport.

  • Arrivals - Thursday around 3 PM
  • Departures - Sunday around 10 AM
October 4, 2010
submit travel form

Travel Policy

Please familiarize yourself with our policies and procedures for travel. We truly appreciate you taking the time to participate in this meeting. As you make your plans, please remember that we are a nonprofit organization dependent on donations and volunteers. We do NOT pay for upgrades, change fees, incurred costs resulting from a flight change, transportation to or from your local (home side) airport, meals or other incidentals.

  • Travel Confirmation will be sent out within 1 week of the meeting. This will include a hotel confirmation number, if there is one, and airport transfer details. We have to wait until we receive almost everyone’s travel to book airport transfer. Due to frequent airline changes, we wait until the week of the meeting to send this out.
  • Airport transfer is provided by Foundation staff, volunteers or arranged shuttle at specific times. If you opt to utilize Foundation airport transportation on your travel form, please be patient in receiving this information. We will send it to the week of the meeting.
  • Speaker agenda is not sent out prior to the meeting. It will be provided upon arrival in the meeting packet. We do not tell people when they are speaking because we expect everyone to attend all sessions. Sessions are all day Friday and Saturday.
  • REMINDER: We do not reimburse for home side airport transfer or incidentals while traveling. We will not honor miscellaneous receipts sent for these expenses.
  • Spouses are welcome to come with you at their own cost but are not allowed to attend the meeting. Please no children.

What the Foundation Pays

Accommodations and meals are provided by the foundation during the meeting. Airfare will be covered only if booked through our travel agent. The Foundation will also cover airport transportation on the meeting side at the designated shuttle times. You can select not to utilize Foundation arranged transportation at your own expense when completing the travel form. Once your travel form is received your accommodations and airport transfer will be confirmed. Please let us know of any food allergies or other information we should be aware of on the travel forms.

  • If you would like your airfare covered by the Foundation, you must book with our travel agent. Note we do not cover upgrades, changes, late bookings, etc.
  • Flights must be booked at least 30 days prior to the meeting to confirm your accommodations and airport transfer.
  • As a nonprofit we utilize volunteers and other methods to maximize our efforts (or our donor support) when making accommodations and arranging ground transportation. Ground transportation will be provided upon your arrival either by a foundation volunteer or arranged shuttle. You will be provided airport transportation information the week of the meeting. We do not reimburse for home side airport transfer or incidentals while traveling.


Abstracts are due 30 days prior to the start of the meeting to allow enough time to prepare the meeting book.

The abstracts should be only one or two paragraphs outlining the theme of your presentation and should reflect the objective and spirit of the meeting (see above). Abstracts will be circulated about one week before the meeting. The meeting organizer will start requesting them a month before the meeting.

abstracts DUE:
October 4, 2010
submit abstract

Meeting Structure

The meeting structure has been developed over years of experience.

  • Participants have approximately 45 minutes, depending on the number of participants, for their presentation and discussion. The presentation is meant as a conversation start and should last about twenty minutes briefly covering background information and areas that are new or need further input. This should be structured in such a way as to lead to a lively discussion. Participants are encouraged to interrupt to ask questions or start discussions.
  • A MAXIMUM of 5 slide equivalents per presentation is allowed (Power point slides should not contain more than one graph or gel per slide and no more than 5 bullet points to stress the points being made by the presenter.) We appreciate cooperation with the spirit of this guideline. Handouts are welcome but should be distributed before sessions.
  • Everyone is expected to actively participate in every session and discussions.
  • The time spent at the meeting is relatively short, so please be familiar with papers received prior to the meeting.
  • It is very important that you commit to all sessions of the 2 days of meetings.

Forbeck Scholars Participation

Scholars are selected for each Forbeck Forum. These are outstanding junior clinical or post-doctoral fellows selected based on the quality and relevance of science.

  • Scholars present for 30-45 minutes, depending on the number of participants
  • The same presentation rules apply for scholars
  • After the Forum you are selected to attend, you will attend three years of Scholar Retreats held in Lake Geneva, WI. If you attend a Fall Forum, you will attend the Spring Retreat. If you attend a Spring Forum you will attend a Fall Retreat.
  • Scholars are selected by the Foundation Scientific Advisory Board and peer reviewers selected from past Forbeck Scholars.

General Program

The outline below illustrates a typical program schedule. You will receive a complete schedule, including speaking times, the Thursday the meeting starts.

Arrival Day
1:00 PM Arrivals
6:00 PM Cocktails (opt'l)
7:00 PM Dinner
Meeting Day 1
7:00 AM Breakfast
8:00 AM Scientific Sessions
12:00 PM Lunch
1:30 PM Scientific Sessions
6:00 PM Cocktails & Dinner
Meeting Day 2
7:00 AM Breakfast
8:00 AM Scientific Sessions
12:00 PM Lunch
1:30 PM Scientific Sessions
6:00 PM Cocktails & Dinner
Departure Day
7:00 AM Breakfast
8:00 AM Departures

Frequently Asked Questions

Below are some of our most Frequently Asked Questions. If you have something new to ask, please feel free to contact us.

  • Travel Confirmation will be sent out within 1 week of the meeting. This will include a hotel confirmation number, if there is one, and airport transfer details. We have to wait until we receive almost everyone’s travel to book airport transfer. Due to frequent airline changes, we wait until the week of the meeting to send this out.
  • Airport transfer is provided by Foundation staff, volunteers or arranged shuttle at specific times. If you opt to utilize Foundation airport transportation on your travel form, please be patient in receiving this information. We will send it to the week of the meeting.
  • Speaker agenda is not sent out prior to the meeting. It will be provided upon arrival in the meeting packet. We do not tell people when they are speaking because we expect everyone to attend all sessions. Sessions are all day Friday and Saturday.
  • Frequently airport transfer is provided by volunteers. Please be patient on receiving this information. Airport transfer will be sent out prior to arrival.
  • REMINDER: We do not reimburse for home side airport transfer or incidentals while traveling. We will not honor miscellaneous receipts sent for these expenses.

Forum Participants

Wellcome Sanger Institute
Columbia University
James R.
St Jude Children's Research Hospital
Dana-Farber Cancer Institute
Joe W.
Lawrence Berkeley National Laboratory
Ontario Institute for Cancer Research
University of British Columbia
Peter W.
University of California Los Angeles
Johns Hopkins Medicine
Richard K.
Washington University in Saint Louis
University Paris Descartes

Forum Scholars

Benjamin P. Berman, PhD
USC Epigenome Center
Derek Y. Chiang, PhD
Sharon J. Diskin, PhD
Children’s Hospital of Philadelphia
Chris Putnam, PhD
Ludwig Institute for Cancer Research