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Columbia investigators win Chan Zuckerberg Initiative grants to accelerate development of cellular roadmap of the human body.

In two groundbreaking research projects contributing to the Human Cell Atlas, Columbia University scientists are tasked with mapping complete cells in the immune system and the human spine. The global effort is aiming to identify and define every cell type of the human body and create a collection of maps for navigating the cellular basis of human health and disease.

Peter Sims, PhD
Peter Sims, PhD, assistant professor of systems biology

The Columbia teams, which include co-principal investigators from the Department of Systems Biology Drs. Peter Sims and Raul Rabadan , are among the 38 collaborative science teams launching the Chan Zuckerberg Initiative’s (CZI) Seed Networks for the Human Cell Atlas project announced today. The three-year projects, receiving a total of $68 million in award funding by Seed Networks, are collaborative groups that are bringing together expertise in science, computational biology, software engineering, and medicine to support the ongoing progress of the Human Cell Atlas .

Investigating the Immune System + Aging

Dr. Sims, part of an international team including close collaborator Dr. Donna Farber of the Department of Surgery , is combining single-cell sequencing technologies, data analysis, and immunology expertise to better understand how the immune system ages and gain new insights into how human diseases occur. 

Chaolin Zhang
Chaolin Zhang, PhD, associate professor of systems biology

A new study by researchers in Dr. Chaolin Zhang’s lab at Columbia’s Department of Systems Biology details a novel computational method that models how RNA-binding proteins (RBPs) recognize specific sites in the target RNA transcripts, precisely and accurately. The researchers’ findings include identification of entirely new motifs (RNA sequence patterns), and their research in complex RNA regulation contributes to our understanding of the molecular basis of disease and conditions, and down the road, could aid in the development of targeted therapies. 

The study, led by Dr. Zhang, associate professor of systems biology, with senior co-authors Suying Bao, PhD, and Huijuan Feng, PhD, appears today in Molecular Cell

RNA has traditionally been considered mere “messengers” that transfer genetic information from DNA to proteins that ultimately carry out cellular functions. However, it is now increasingly appreciated that RNA can be tightly regulated to control gene expression and diversity protein products. RNA-binding proteins (RBPs) are at the center of such regulation, with important roles in many cellular processes, including cell function, transport, and location. Gaining mechanistic insights of the binding specificity of RBPs in a genome-wide scale helps advance our knowledge of gene regulation.

“RNA-binding proteins are crucial for gene expression,” says Dr. Feng, coauthor of the study and post-doctoral research scientist in the Zhang lab. “RNA is heavily regulated, and when this regulation goes wrong, instabilities or disease could occur.”  

Dr. Andrea Califano sits down with BioTechniques at AACR. Video: Courtesy of BioTechniques.

At the 2019 annual meeting of the American Association for Cancer Research (AACR), Dr. Andrea Califano sat down with BioTechniques News for an overview on the field of systems biology and its impact in cancer research and in precision medicine. Dr. Califano is a pioneering researcher in the fast-growing field of systems biology whose expertise is in developing innovative, systematic approaches to identify the molecular factors that lead to cancer progression and to the emergence of drug resistance at the single-cell level. A physicist by training, Dr. Califano is the Clyde and Helen Wu Professor of Chemical and Systems Biology, founding chair of the Department of Systems Biology at Columbia University Irving Medical Center, director of the Columbia Genome Center and a program leader at the Herbert Irving Comprehensive Cancer Center.

The video interview is part of the series, Behind the Technqiue by BioTechniques News. 

Brian Ji_2
Systems Biology Graduate Brian Ji, PhD

For Brian Ji, the big draw to systems biology stemmed from his passion for applying quantitative approaches to understanding biology. While an undergraduate at the University of Wisconsin-Madison, Ji studied nuclear engineering and credits that training for the way in which he tackles scientific questions: creatively, and as a problem solver. 

“There is no one right approach to asking a question and setting out to answer it, and that freedom is what makes science fun for me,” he says. 

Ji studied under Dr. Dennis Vitkup in the Vitkup lab and completed his thesis defense for systems biology in the fall of 2018.  Also an MD student in Columbia’s Vagelos College of Physicians and Surgeons , Ji was attracted to Columbia because of the close interplay between the Systems Biology Department and the Columbia University Irving Medical Center. “Ultimately,” he says, “the opportunity to sit at the intersection between math, biology and medicine was too good to pass up.”

Ji’s PhD work focused on understanding spatiotemporal dynamics of human gut microbiota. He developed several frameworks that leveraged the increasing availability of high-throughput sequencing data to better understand and precisely quantify patterns of human gut microbiota variability across time and space. His work showed that characterizing dynamics—changes in bacterial abundances in our gut—are critical to understanding how these ecosystems function and is highly connected to multiple factors such as host diet, travel and diet. 

Ji also spent part of his PhD studying limitations of cancer cell growth in different environmental conditions. He credits Columbia for exposing him to a variety of research topics. 

Phyllis Thangaraj
Phyllis Thangaraj, MD/PhD student (Tatonetti lab)

Aspiring physician-scientists from Columbia's Vagelos College of Physicians and Surgeons presented their research posters at the 14th annual MD-PhD Student Research Symposium on April 25. Their research delved into a range of topics, including Alzheimer’s disease, stroke, and stem cells. The event included a guest lecture by an alumna about her own career path as a physician-scientist, and culminated in the poster session judged by MD-PhD alumni who currently work at the University. Department of Systems Biology’s Phyllis Thangaraj, an MD/PhD student in the Nicholas Tatonetti lab , was named one of five poster winners at the event. 

She presented work on applying machine learning methods to phenotype acute ischemic stroke patients in the electronic health records. In cohort research studies, it is essential to identify a large number of subjects in an accurate and efficient manner, but often this requires time-consuming manual review of patient charts. 

“We applied machine learning methods to data within a patient’s electronic health records to develop a high-throughput way to define research cohorts,” explains Thangaraj. “Our test case is in acute ischemic stroke. We extracted clues within a person’s medical record that required minimal data processing to classify those who have had a stroke. In a separate cohort, the UK Biobank, we were able to use our model to identify patients with self-reported stroke but no mention in their medical data with 65-fold better precision than random selection of patients.” Although stroke was the test case in this particular work, she explained that their workflow could be applied to identify patients for cohorts of other diseases, particularly when the dataset has missing data. 

The Korem Lab

One of the structural variations detected in Anaerostipes hadrus, which is deleted in ~40% of the population (top), and associated with higher disease risk. Genes in this region (bottom) code a composite inositol catabolism - butyrate production pathway, potentially supplying the microbe with additional energy while supplying the host with butyrate, previously shown to have positive metabolic and anti-inflammatory effects. (Credit: Korem lab)

Our gut microbiome has been linked to everything from obesity and diabetes to heart disease and even neurological disorders and cancer. In recent years, researchers have been sorting through the multiple bacterial species that populate the microbiome, asking which of them can be implicated in specific disorders. But a paper recently published in Nature addressed a new question: "What if the same microbe is different in different people?" The study was co-led by Dr. Tal Korem , assistant professor of systems biology and core faculty member in the Program for Mathematical Genomics at Columbia University Irving Medical Center

It has been long known that the genomes of microbes are not fixed from birth, as ours are. They are able to lose some of their genes, exchange genes with other microorganisms, or gain new ones from their environment. Thus, a detailed comparison of the genomes of seemingly identical bacteria will reveal sequences of DNA that occur in one genome and not others, or possibly sequences that appear just once in one and several times over in others. These differences are called structural variants. Structural variants - even tiny ones - can translate into huge differences in the ways that microbes interact with their human hosts. A variant might be the difference between a benign presence and a pathogenic one, or it could give bacteria resistance to antibiotics.

Dr. Raul Rabadan is leading a global research project as part of a new grant from the Pancreatic Cancer Collective to identify high-risk factors of pancreatic cancer. (Courtesy of Stand Up to Cancer)

A global team of researchers led by theoretical physicist Raul Rabadan, PhD, professor of systems biology at Columbia’s Vagelos School of Physicians and Surgeons, and Núria Malats, MD, PhD, head of the Genetic and Molecular Epidemiology Group of the Spanish National Cancer Research Centre (CNIO), are working to develop a comprehensive computational framework that will identify high-risk factors for pancreatic cancer.  

Armed with a new two-year, $1 million grant from the Pancreatic Cancer Collective, the team intends to attack pancreatic cancer research from multiple disciplines—genomics, mathematics and medicine—to provide an integrated, computational approach to studying genomic, environmental and immune factors that could identify populations at high risk of pancreatic cancer. The need for deeper understanding of the contributing factors to this lethal disease is pressing, as pancreatic cancer is projected to become the second leading cause of cancer-related mortality within the next decade. 

Rabadan-led Team for Pancreatic Cancer Collective
Drs. Raul Rabadan and Nuria Malats

Columbia researchers have learned why some glioblastomas—the most common type of brain cancer—respond to immunotherapy. The findings, reported by the CUIMC Newsroom, could help identify patients who are most likely to benefit from treatment with immunotherapy drugs and lead to the development of more broadly effective treatments.

The study, led by Raul Rabadan, PhD, professor of systems biology and biomedical informatics at Columbia University Vagelos College of Physicians and Surgeons and the Herbert Irving Comprehensive Cancer Center, was published online in the journal Nature Medicine

Fewer than 1 in 10 patients with glioblastoma­ respond to immunotherapy, which has shown remarkable success in the past few years in treating a variety of aggressive cancers. But there has been no way to know in advance which glioblastoma patients will respond. Like many other cancers, glioblastomas are able to prevent the immune system from attacking cancer cells. Cancers sometimes put the brakes on the immune system by acting on a protein called PD-1. Immunotherapy drugs called PD-1 inhibitors are designed to release those brakes, unleashing the immune system. Given the success of PD-1 inhibitors in other cancers, doctors were hopeful that the immunotherapy drugs would help patients with glioblastoma. 

To understand why only a few of these tumors respond to the immunotherapy drugs, Dr. Rabadan’s team took a comprehensive look at the tumor microenvironment—which includes the tumor itself and all of the cells that support it—in 66 glioblastoma patients before and after treatment with PD-1 inhibitors (nivolumab or pembrolizumab). Of these, 17 had a response to the drugs of six months or longer.

Nonresponsive tumors had more mutations in a gene called PTEN, which led to higher levels of macrophages, immune cells that usually help the body fight bacteria and other invaders. But in glioblastoma, the macrophages release a number of growth factors that promote the survival and spread of cancer cells.

 

PCF Challenge Award PIs
Principal investigators on the PCF Challenge Award grant, from left to right: Andrea Califano, Michael Shen and Charles Drake.

Columbia University Irving Medical Center experts in prostate cancer will lead a new team research project that tests a novel approach for personalized cancer treatment. 

The two-year project, funded by a $1 million Challenge Award from the Prostate Cancer Foundation (PCF) , combines cutting-edge techniques that include computational methods for targeted drug therapy, single-cell RNA sequencing and novel cancer immunotherapy. The combined approaches are behind a proof-of-concept clinical trial for patients with lethal metastatic prostate cancer.  

PCF Challenge Awards fund projects that bring together experts from a number of related fields to form a team focused on the creation of innovative, effective therapies for advanced prostate cancer. As part of Columbia’s grant, the new clinical trial will take place at the James J. Peters VA Medical Center (also known as the Bronx VA), a partner of Columbia University Irving Medical Center (CUIMC) and New York-Presbyterian .

PCF is recognized as the leading philanthropic organization for prostate cancer research. For the team at Columbia’s Herbert Irving Comprehensive Cancer Center (HICCC ), receiving a Challenge Award from the foundation was more than just an exciting achievement. It underscores CUIMC’s continued commitment to strengthen and expand its expertise in prostate cancer research and care through investments in faculty recruitment, enhanced emphases on bolstering basic science research and clinical trials centered on the disease and direct engagement with PCF. 

Researchers at the Vagelos College of Physician & Surgeons are rewriting the course of scientific investigation, intent on speeding up the process of discovery that will help patients with cancer, Alzheimer’s disease, diabetes, and other intractable diagnoses.

In cancer, Andrea Califano, Dr, the Clyde and Helen Wu Professor of Chemical and Systems Biology and chair of the Department of Systems Biology, decided to turn cancer treatment theory on its head. The first wave of research in pursuit of personalized oncology focused on clues embedded within individual tumors. Decode the nucleic acids gone awry within the DNA of a particular patient’s cancer, or so the thinking goes, to identify treatments tailored to target that specific mutation.

It’s a fine theory, says Dr. Califano in the article, but investigators still have a lot of work to do before the vast majority of cancers yield to that approach. “Only maybe 25 percent of patients have a mutation that could be defined as actionable,” he says.

For more than a decade, Dr. Califano has championed what might be considered an end run around cancer mutations, focusing instead on identifying and blocking the networks of normal proteins—known as master regulators—hijacked by deranged DNA to spur tumor formation and sustain tumor growth. Prevent the signals those proteins send on behalf of a cancerous mutation, and the cancer itself screeches to a halt.

Yufeng Shen Episcore

The epigenomic profile of RBFOX2, a haploinsufficient gene recently identified as a risk gene of congenital heart disease. Each small box represents 100 bp region around transcription start sites (TSSs) and the shade of the color reflect the strength of the histone mark signal in tissues under normal conditions. RBFOX2 has large expansion of active histone marks (H3K4me3 and H3K9ac), especially in heart and epithelial tissues (purple and gray rows), and tissue-specific suppression mark (H3K27me3) in blood samples.(Credit: Shen lab)

The genetics of developmental disorders, such as congenital heart disease and autism, are highly complex. There are roughly 500 to 1,000 risk genes that can lead to each of these diseases, and to date, only about a few dozen have been identified. Scientists have ramped up efforts to develop computational approaches to address challenges in accurately identifying genetic risk factors in ongoing genetic studies, and the availability of such tools would greatly assist researchers in gaining a deeper understanding of the root causes of these diseases. 

Focusing on haploinsufficiency, a key biological mechanism of genetic risk in developmental disorders, Yufeng Shen , PhD, and his lab have developed a novel computational method that enables researchers to find new risk genes in these diseases. Their key idea is that the expression of haploinsufficient genes must be precisely regulated during normal development, and such regulation can be manifested in distinct patterns of genomic regulatory elements. Using data from the NIH Roadmap Epigenomics Project, they showed there is a strong correlation of certain histone marks and known haploinsufficient genes. Then based on supervised machine learning algorithms, they developed a new method, which they call Episcore , to predict haploinsufficiency from epigenomic data representing a broad range of tissue and cell types. Finally, they demonstrate the utility of Episcore in identification of novel risk variants in studies of congenital heart disease and intellectual disability.  

A research team from Columbia University Irving Medical Center has received a 2018 PCF Challenge Award from the Prostate Cancer Foundation (PCF) to advance prostate cancer research. The interdisciplinary team at Columbia includes leading experts in systems biology, cancer research and medicine from Columbia’s Department of Systems Biology and the Herbert Irving Comprehensive Cancer Center (HICCC)

Announced today, PCF is awarding more than $5.5 million in funding to a total of six teams to conduct research with the highest potential for accelerating new and improved treatments for advanced prostate cancer. PCF is one of the largest non-governmental organizations dedicated solely to funding prostate cancer research, and its annual Challenge Awards are highly coveted in the scientific and medical fields. 

In the United States, prostate cancer is the most common non-skin cancer, and 1 out of every 9 men in the U.S. will be diagnosed with the disease in his lifetime. To date, treatment of the most aggressive forms of prostate cancer represents a clinical challenge. After treatment failure with anti-androgen drugs, which are part of the standard of care for advanced metastatic prostate cancer, only few current therapeutic options remain and the impact on patient survival is limited. Indeed, the field needs major innovative, out-of-the-box approaches to new therapies to combat advanced prostate cancer. 

 

DSB Retreat
Members of the Dennis Vitkup Lab, from l to r: Konstatine Tchourine, German Plata and Jon Chang (Credit: Sandra Squarcia); Photo Gallery of the retreat.

Innovative research projects were highlighted at the Department of Systems Biology’s annual retreat, held October 5, at Wave Hill Public Garden and Cultural Center in Riverdale, NY. The retreat, attended by 160 faculty, staff, post-doctoral scientists, students and guests, also provided an opportunity for young investigators to showcase their work during a poster competition. 

Andrea Califano , Dr., chair of the department, opened the day’s sessions with welcome remarks, as the retreat also served as a site visit by the National Cancer Institute for the Columbia University Center for Cancer Systems Therapeutics (CaST) . CaST, co-directors Drs. Califano and Barry Honig , vice-chair of the department, was established in 2016 as one of the key centers in the NCI’s Cancer Systems Biology Consortium (CSBC). The initiative behind CSBC is heavily grounded on innovation—bringing together interdisciplinary teams of clinical and basic cancer researchers with physical scientists, engineers, mathematicians and computer scientists who collaborate to tackle major questions in cancer biology from a novel out-of-the-box point of view. 

 

Andrea Califano
Andrea Califano, Dr.

Andrea Califano , Dr., a pioneer in the field of systems biology and founding chair of the Department of Systems Biology at Columbia University Irving Medical Center (CUIMC), has been elected to the National Academy of Medicine (NAM) . Membership in the NAM is considered one of the highest honors in the fields of health and medicine and recognizes individuals who have demonstrated outstanding professional achievements and commitment to service.  

A physicist by training, Dr. Califano has taken innovative, systematic approaches to identify the molecular factors that lead to cancer progression and to the emergence of drug resistance at the single-cell level. Directing the conversation about cancer research away from focusing solely on gene mutations, Dr. Califano examines the complex and tumor-specific molecular interaction networks that determine cancer cell behavior. Using information theoretic approaches, analysis of these networks can precisely pinpoint master regulator proteins that are mechanistically responsible for supporting tumorigenesis and for implementing tumor cell homeostasis. Dr. Califano and his lab have shown that master regulators represent critical drivers and tumor dependencies, despite the fact that they are rarely mutated or differentially expressed, thus establishing them as a bona fide new class of therapeutic targets.

October 10, 2018

Q+A with Dr. Laura Landweber

Oxytricha

Oxytricha. (Credit: Bob Hammersmith)

Laura Landweber, PhD, loves a challenge. So it’s no surprise that she has built a scientific career unraveling the hows and whys of a unique single-cell organism known for its biological complexity.  

An evolutionary biologist whose work sits at the interface of genetics and molecular biology, Dr. Landweber, for nearly 20 years, has focused much of her research on Oxytricha trifallax , a microbial organism that is prevalent in ponds, feeds on algae and has a highly complex genome architecture, making it an attractive, albeit challenging, model organism to study. Compared to humans, with 46 chromosomes containing some 25,000 genes, Oxytricha is known to comprise many thousands of chromosomes, in the ballpark of 16,000 tiny “nanochromosomes”. Yet not only is it complex in sheer numbers of chromosomes but the information carried in those individual chromosomes can be scrambled, like information compression, and the process of development in Oxytricha must descramble this information so that it can be converted into RNA and proteins.

“DNA can be flipped and inverted in Oxytricha and the cellular machinery actually knows how to restore order,” says Dr. Landweber. “Hence, it’s this wonderful paragon for understanding genome integrity and the maintenance and establishment of genome integrity.” 

Even more perplexing, in cell division, Oxytricha reproduces asexually when it wants to produce more in number, and it reproduces sexually when it needs to rebuild its genome. It also has the ability to “clean up” its genome, so to speak, eliminating nearly all of the non-coding DNA, or so-called junk DNA. Much of why Oxytricha presents such an intricate genomic landscape remains a mystery, and for Dr. Landweber, the leading expert on this single-celled protist, that wide-open field for potential discovery is what got her hooked. 

composite image of the scientists and research figure
Tuuli Lappalainen (top photo) and Stephane Castel co-led the new study. The hypothesis of the study is illustrated here with an example in which an individual is heterozygous for both a regulatory variant and a pathogenic coding variant. The two possible haplotype configurations would result in either decreased penetrance of the coding variant, if it was on the lower-expressed haplotype, or increased penetrance of the coding variant, if it was on the higher-expressed haplotype. (Composite image courtesy of NYGC)

Researchers at the New York Genome Center (NYGC) and Columbia University's Department of Systems Biology have uncovered a molecular mechanism behind one of biology’s long-standing mysteries: why individuals carrying identical gene mutations for a disease end up having varying severity or symptoms of the disease. In this widely acknowledged but not well understood phenomenon, called variable penetrance, the severity of the effect of disease-causing variants differs among individuals who carry them. 

Reporting in the Aug. 20 issue of Nature Genetics, the researchers provide evidence for modified penetrance, in which genetic variants that regulate gene activity modify the disease risk caused by protein-coding gene variants. The study links modified penetrance to specific diseases at the genome-wide level, which has exciting implications for future prediction of the severity of serious diseases such as cancer and autism spectrum disorder.

NYGC Core Faculty Member and Systems Biology Assistant Professor Dr. Tuuli Lappalainen, PhD, led the study alongside post-doctoral research fellow Dr. Stephane Castel.

Suying Bao, PhD
Suying Bao, PhD

Suying Bao, a postdoctoral research scientist in the Chaolin Zhang lab , has been named an inaugural Precision Medicine Research fellow by Columbia’s Irving Institute of Clinical and Translational Research . The two-year fellowship aims to train postdocs to use genomics and complex clinical data to improve personalized and tailored clinical care and clinical outcomes. 

This fellowship “will provide me with more opportunities to translate my findings from basic science research into clinical application,” says Bao, “and pave my way towards an independent researcher in this field.” 

Bao’s expertise lies in RNA regulation at the interface of systems biology, ranging from the specificity of protein-RNA interaction to function of specific splice variants. RNA regulation is critical in proper cellular function; gaining deeper insights into this complex molecular mechanism will promote the development of precision medicine therapies. 

In this project, Bao is aiming to develop new approaches to identify causal noncoding regulatory variants (RVs) modulating post-transcriptional gene expression regulation, such as RNA splicing and stability.  “A majority of genetic variants associated with human diseases reside in noncoding genomic regions with regulatory roles,” notes Bao. “Thus, elucidating how these noncoding regulatory variants contribute to gene expression variation is a crucial step towards unraveling genotype-phenotype relationships and advancing precision medicine for common and complex diseases.”

To identify these RVs, she will leverage massive datasets of high-throughput profiles of gene expression and protein-RNA interactions generated from large cohorts of normal and disease human tissues and cell lines by multiple consortia, such as ENCODE, GTEx and CommonMind, and develop innovative computational methods of data mining. 

Hyundai $2.5M Grant to Columbia
Julia Glade Bender, MD, (center) at the Hyundai Hope on Wheels announcement Mar. 29 during the New York International Auto Show at the Jacob Javitz Center. (Photo courtesy of HHOW)

A team of researchers at Columbia University Irving Medical Center (CUIMC) has recently been awarded a five-year $2.5 million grant from Hyundai Hope on Wheels (HHOW) to fund innovative pediatric cancer research. 

The team at Columbia is being led by principal investigator (PI), Julia Glade Bender , MD, associate professor of pediatrics at CUIMC, with co-PIs Andrea Califano , Dr, chair of Columbia’s Department of Systems Biology and Darrell Yamashiro , MD, PhD, director of pediatric hematology, oncology and stem cell transplantation, along with researchers from Memorial Sloan Kettering, University of San Francisco Children’s and Dana-Farber Cancer Center. 

The Quantum Collaboration award from HHOW is aimed at funding research focused on childhood cancers with poor prognosis. At Columbia, the team will target osteosarcoma, the most commonly diagnosed bone tumor in children and adolescents. No new treatment approaches have successfully been introduced for osteosarcoma in nearly 40 years, and patients with the disease have not benefited from recent breakthroughs like immunotherapy or DNA sequencing and require a shift in the understanding and approach to therapy. 

Califano-Cancer Bottleneck
The N of 1 trial leverages systems biology techniques to analyze genomic information from a patient’s tumor. The goal is to identify key genes, called master regulators (green circles), which, while not mutated, are necessary for cancer cell survival. Master regulators are aberrantly activated by patient-specific mutations (X symbols) in driver genes (yellow circles), which are mutated in large cancer cohorts. Passenger mutations (blue circles) that are not upstream of master regulators have no effect on the tumor. (Image: Courtesy of the Califano Lab)

A novel N of 1 clinical trial led by the Califano Lab at Columbia University Irving Medical Center is focusing on rare or untreatable malignancies that have progressed on multiple lines of therapy, with the goal of identifying and providing more effective, customized therapies for patients. The approach is grounded in a computational platform developed over the last 14 years by the Califano Lab to allow accurate identification of a novel class of proteins that represent critical tumor vulnerabilities and of the drug or drug combination that can most effectively disarm these proteins, thus killing the tumor. Platform predictions are then validated in direct tumor transplants in mice, also known as Patient-Derived Xenografts (PDX). 

“We call these proteins master regulators and have developed innovative methodologies that allow their discovery on an individual patient basis,” said Dr. Andrea Califano , Clyde and Helen Wu Professor of Chemical and Systems Biology and chair of the Department of Systems Biology at Columbia. 

Project GENIE
Richard Carvajal (left) and Raul Rabadan are lead PIs on Project GENIE

Columbia University Irving Medical Center (CUIMC) has recently joined 11 new institutions to collaborate on Project GENIE, an ambitious consortium organized by the  American Association for Cancer Research . An international cancer registry built through data sharing,  Project GENIE , which stands for Genomics Evidence Neoplasia Information Exchange, brings together leading institutions in cancer research and treatment in order to provide the statistical power needed to improve clinical decision-making, particularly in the case of rare cancers and rare genetic variants in common cancers. Additionally, the registry, established in 2016, is powering novel clinical and translational research. In its first two years, Project GENIE has been able to accumulate and make public more than 39,000 cancer genomic records, de-identified to maintain patient privacy. 

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