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Genome Integrity Discussion Group February 2017

Genome Integrity Discussion Group February 2017

Monday, February 6, 2017

The New York Academy of Sciences

The connection between cancer and genome integrity is widely appreciated. Importantly, the greater New York Metropolitan area is unparalleled in the concentration of world leading research on chromosome biology and function, as well as for research at the interface between chromosome integrity and the dynamics of malignancy. The Genome Integrity Discussion Group capitalize on this concentration of excellence, providing a forum for interaction between basic- and clinically-oriented research groups working in these fields. These meetings not only facilitate synergy between labs, but also provide a context in which previously unappreciated complementarities can be revealed.

In that spirit, the talks will cover a broad range of areas, including, but not limited to the DNA damage response and cancer predisposition, DNA replication, transcription, chromatin modification, recombination, cell cycle control, telomeres, chromosome segregation, epigenetic states, as well as the emergence of new technologies relevant to research in genome integrity. Although a primary focus is upon basic mechanisms and processes, these areas are pertinent to cancer and myriad human disease states, and it is expected that this will be reflected in the substance of our discussions. At each of the meetings, two early career scientists (students or postdocs) are selected to present data.

Genome Integrity Discussion Group meetings are organized under the leadership of Susan Smith (NYU Langone Medical Center), Lorraine Symington (Columbia University Medical Center), and Scott Keeney (Memorial Sloan Kettering Cancer Center).

Call for Student/Postdoc Presentation Abstracts: Deadline January 6, 2017

Two abstracts will be selected for short talks by students/postdocs. Please submit in CSHL format with file name via email to Prof Smith at by January 6th, 2017.

Registration Pricing

Member (Student / Postdoc / Resident / Fellow)$0
Nonmember (Academia)$65
Nonmember (Corporate)$75
Nonmember (Non-profit)$65
Nonmember (Student / Postdoc / Resident / Fellow)$30


* Presentation times are subject to change.

Monday, February 6, 2017

1:00 PM

Registration Opens

1:30 PM

Welcome and Introductory Remarks
Caitlin McOmish, PhD, The New York Academy of Sciences
Susan Smith, PhD, NYU School of Medicine

1:40 PM

Breaking and Chewing DNA in Meiosis
Scott Keeney, PhD, Memorial Sloan Kettering Cancer Center

2:10 PM

Repeated Losses of PRDM9-Directed Recombination Despite the Conservation of PRDM9 Across Vertebrates
Molly Przeworski, PhD, Columbia University

2:40 PM

Mechanisms to Maintain Centromere Stability in Human Cells
Simona Giunta, PhD, The Rockefeller University (Funabiki Lab)

2:55 PM

Coffee Break

3:25 PM

Effect of DNA Interstrand Crosslink (ICL) Structure on Lesion Bypass by DNA Polymerases
Upasana Roy, Stony Brook University (Schärer Lab)

3:40 PM

Stress Response at the Replication Fork
Agata Smogorzewska, MD, PhD, The Rockefeller University

4:10 PM

Regulation of PARP1 Retention at the DNA Damage Foci
Shan Zha, MD, PhD, Columbia University Irving Medical Center

4:40 PM

Networking Reception

5:30 PM



Scott Keeney, PhD

Memorial Sloan Kettering Cancer Center

Susan Smith, PhD

NYU Langone Medical Center

Lorraine Symington, PhD

Columbia University Irving Medical Center

Sonya Dougal, PhD

The New York Academy of Sciences

Caitlin McOmish

The New York Academy of Sciences


Simona Giunta, PhD

The Rockefeller University (Funabiki Lab)

Simona Giunta is a Research Associate in the laboratory of Prof. Funabiki at the Rockefeller University, where she is developing assays to examine the integrity of human centromeres tandem DNA repeats in proliferating cells. Originally from Rome, Simona earned her PhD in Cancer Research in the laboratory of Prof. Steve Jackson at the University of Cambridge, where she analysed the fate of DNA double strand breaks during mitosis and reported the suppression of late signaling events in the mitotic DNA damage response. Following a short-term project at the CSIRO in Australia as a UICC Fellow investigating the protective impact of resveratrol on oxidative damage, she started her postdoctoral work at the Rockefeller University on human centromeres stability. Simona was an American Italian Cancer Foundation Fellow from 2012–2014 and a Rockefeller Women & Science Fellow in 2012–2013.

Scott Keeney, PhD

Memorial Sloan Kettering Cancer Center

Molly Przeworski, PhD

Columbia University

Molly Przeworski received a BA in Mathematics from Princeton University and a PhD in Evolutionary Biology from the University of Chicago. Her postdoc was in the Statistics Dept. of the University of Oxford, and was followed by a two year stint as a research scientist at the Max Planck Institute for Evolutionary Anthropology. Before moving to Columbia University, she was a faculty member at the University of Chicago (where she was also a Howard Hughes Medical Institute Early Career Scientist) as well as, briefly, at Brown University. Her work focuses on understanding how natural selection shapes patterns of genetic variation in humans and on elucidating the evolution of recombination and mutation processes across vertebrates.

Upasana Roy

Stony Brook University (Schärer Lab)

Upasana Roy is a PhD candidate in Dr. Orlando Schärer's lab at the Department of Chemistry in Stony Brook University. She uses chemically modified DNA to understand how the structure of DNA interstrand crosslinks (ICLs) affect lesion bypass during ICL repair. Upasana holds a BS in Chemistry from St. Stephen's College, India, and an MS in molecular biology from the Tata Institute of Fundamental Research, India. Her Masters thesis focused on understanding the mechanisms by which micro-RNAs are regulated. In particular, she studied the effect of histone deacetylase Sirt1 on micro-RNA expression, and the regulation of miR-9 in mouse pancreatic β-cells.

Agata Smogorzewska, MD, PhD

The Rockefeller University

Dr. Smogorzewska received her BS in molecular biology and biochemistry from the University of Southern California in 1995, her PhD from The Rockefeller University in 2002 working with Dr. Titia de Lange and her MD from Weill Cornell Medical College in 2003. Following a residency in clinical pathology at Massachusetts General Hospital, she joined Harvard Medical School as a postdoctoral fellow in Dr. Stephen Elledge's lab in 2005. She joined The Rockefeller University as an assistant professor in 2009 and became an associate professor in 2015. Dr. Smogorzewska's lab focuses on understanding the mechanism of DNA damage response and repair during DNA replication. Most of the work in the lab concerns DNA interstrand crosslink (ICL) repair with the overall goal to gain insights into the cellular and organismal consequences of deficiencies in this type of repair.

Shan Zha, MD, PhD

Columbia University Medical Center

Dr. Shan Zha’s research is focused on how cells efficiently and accurately repair DNA breaks and respond to persistent DNA damage to support normal immune function and prevent human cancers. Lymphocytes are a type of human immune cells that are specialized in fighting infectious diseases. The efficient generation and function of lymphocytes require multiple rounds of physiological DNA breaks and repair. As a result, inefficient DNA repair cause primary immunodeficiency in children. Inaccurate repair join different chromosomes together to form chromosomal translocations that are associated with lymphoma and leukemia — the most common types of malignancy in children. DNA damage responses factors also eliminate cells with persistent DNA damage or inaccurate repair to prevent cancer. Dr. Zha’s laboratory uses innovative genetically engineered mouse models to study the mechanisms of DNA repair that have important implications in cancer biology and cancer therapy. Her lab has discovered phosphorylation-dependent structural functions of ATM, DNA-PKcs and other related kinases in DNA repair and elucidate the molecular mechanism underlying the primary immunodeficiency and recurrent chromosomal translocation in human patients with defects in DNA double stand breaks repair pathways.

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