The Gene Regulation & Cell Proliferation Program is an interdisciplinary effort focused on understanding the mechanisms that govern both normal and cancerous cell growth. The researchers in this program combine traditional experimental biology with cutting-edge technology to gain significant insights into DNA replication, epigenetics, and RNA biology.
Research in the Gene Regulation and Cell Proliferation program explores how these cellular processes drive the pathogenesis of human cancer. Scientists in this Program have identified numerous epigenetic vulnerabilities in aggressive cancers. The Program has also discovered aberrantly expressed non-coding RNAs and splicing alterations that provide the rationale for a potential new class of cancer therapeutics. In addition, significant advances have been made in our understanding of the mechanisms and regulation of DNA replication.
The Program is increasingly extending its studies to single cell biology and cancer metabolism, in an effort to understand the complexity and diversity of tumor cell types. There are numerous interactions among Program members and clinical researchers both locally and around the world. As a result, researchers in the Gene Regulation and Cell Proliferation Program continue to make seminal discoveries about the mechanisms that govern cell proliferation.
Christina Renna Foundation gives $35k for pediatric cancer research
February 7, 2019
The Christina Renna Foundation donated $35,000 to CSHL for continued work on Sarcoma Research Project and research into RMS.
Friends of T.J. donate $50k for sarcoma research
October 9, 2018
Associate Professor Chris Vakoc and his team receive a donation to further their rhabdomyosarcoma research.
Christina Renna Foundation raises $30,000 for continuing pediatric cancer research at CSHL
January 22, 2018
The Christina Renna Foundation donates over $30,000 for rhabdomyosarcoma research, and honors Associate Professor Chris Vakoc with its research award
Molecular decoy helps researchers halt and reverse acute leukemia in mice
January 8, 2018
By throwing a molecular wrench into the gears of a machine that sets genes into motion, researchers were able to get leukemias to 'melt away.'
David Spector is named ASCB Fellow
December 11, 2017
David L. Spector was named a fellow of The American Society for Cell Biology
Research profile: Leemor Joshua-Tor
November 27, 2017
A CSHL faculty member since 1995, a professor since 2005, Joshua-Tor is among the most distinguished members of the Laboratory community.
Friends of T.J. present $50,000 gift for ongoing rhabdomyosarcoma research
November 7, 2017
The Friends of T.J. Foundation presented CSHL Associate Professor Chris Vakoc with a check for $50,000 for his ongoing rhabdomysarcoma research
Cryo-EM imaging suggests how the double helix separates during replication
October 23, 2017
Special cryo-EM imaging helps figure out how the double helix of DNA separates when it replicates
Halfway around the world, a reunion of friends opens door to a cancer discovery
August 31, 2017
After interviewing for a position in a pancreatic cancer lab at Cold Spring Harbor Laboratory, 7,000 miles from his hometown in South Korea, Chang-il.
Structural view suggests RNAi machinery multiplies its efficiency in repressing gene expression
August 3, 2017
Leemor Joshua-Tor publishes atomic-resolution pictures and an analysis of RNAi machinery
Long-sought mechanism of metastasis is discovered in pancreatic cancer
July 27, 2017
An epigenetic factor reprograms gene enhancers, enabling cancer cells to “remember” an earlier developmental state and causing metastasis.
Freeze-frames of enzymes in action have implications for a new cancer treatment concept
July 3, 2017
TUTase enzymes interact with let-7, a regulator of development; targeting them could help control certain cancers.
Newly identified small RNA fragments defend the genome when it’s ‘naked’
June 29, 2017
Fragments snipped from tRNAs protect embryonic stem cells while they’re being epigenetically reprogrammed.
A protein that stem cells require could be a target in killing breast cancer cells
June 1, 2017
Cancer cells, like stem cells, have the ability to multiply indefinitely but epigenetic factor BPTF may be a shared weakness.
Redefining biologists, redefining genes
May 16, 2017
Drs. Molly Hammell and Thomas Gingeras talk about redefining what a biologist is and what genes are.
CSHL’s Dr. Leemor Joshua-Tor is elected to The National Academy of Sciences
May 2, 2017
Professor Leemor Joshua-Tor has been elected to The National Academy of Sciences (NAS).
Dark matter of the genome, part 2
April 15, 2017
This episode of Base Pairs deals with the myth of "junk DNA" and why scientists are interested in non-coding portions of the genome.
CSHL’s Dr. Leemor Joshua-Tor Elected to American Academy of Arts and Sciences
April 14, 2017
Professor Leemor Joshua-Tor is among 228 newly elected members of The American Academy of Arts and Sciences
Protein complex that takes first steps in human DNA replication dance is captured at high atomic resolution
March 16, 2017
Human ORC complex captured in action in x-ray crystallography and cryo-EM
Focus on quiescent cells brings to light the essential role of RNA interference in transcription control
November 9, 2016
RNAi and other epigenetic processes induce changes in where and when specific genes are expressed without altering their genetic code.
Non-coding portions of genome are found to play role in cancer
September 27, 2016
CSHL scientists test an antisense method of targeting long noncoding RNAs overexpressed in breast cancers.
Why calling childhood cancers “rare” is missing the point
September 19, 2016
Associate Professor Christopher Vakoc on why calling pediatric cancers "rare" actually hurts their chances of being studied.
To divide or not: a cellular feedback loop that enables new cells to make a fateful decision
July 21, 2016
Team explains a key mechanism to prevent aberrant cell proliferation
Academic-industry collaboration generates elegant way of pinpointing how a new drug exerts beneficial effects
July 5, 2016
Researchers identify a new drug target in leukemia and creation of a candidate drug that hits the target.
One experiment: How the breast “remembers” a first pregnancy
July 2, 2016
Professor Greg Hannon and his team, including Assistant Professor Camila dos Santos, learn more about breast cells and tissue.
Unusual drug target and drug generate exciting preclinical results in mouse models of metastatic breast cancer
December 22, 2015
Researchers publish preclinical data suggesting the promise of a novel drug directed against a novel target n malignant mammary tumors.
New method prevents cells from prematurely halting protein production in certain genetic illnesses
December 14, 2015
Research team succeeds in paradoxically inhibiting a process cells have evolved to prevent imperfect proteins from being synthesized
Unassuming “Swiss Army knife”-like protein proves lynchpin in a new cancer drug’s therapeutic action
November 30, 2015
Researchers report a surprising mechanism through which an important new candidate drug against leukemia exerts its therapeutic effect.
Breast cancer survivors show Camila dos Santos what’s important about her research
November 17, 2015
Camila dos Santos talks about what she has learned by talking with breast cancer survivors.
Rhabdomyosarcoma (RMS) research bolstered by $50,000 gift from Friends of TJ
October 20, 2015
The Friends of TJ Foundation presented a check for $50,000 to CSHL Associate Professor Chris Vakoc
Research connects specific variations in RNA splicing with breast cancer causation
October 1, 2015
Researchers have identified cellular changes that may play a role in converting normal breast cells into tumors.
Scientists discover how a promising anti-leukemia drug harms cancer cells
May 14, 2015
Inhibiting a protein called BRD4 critical to the survival of acute myeloid leukemia (AML) cells has shown to be an effective therapeutic strategy.
Using CRISPR, biologists find a way to comprehensively identify anti-cancer drug targets
May 11, 2015
Researchers use CRISPR to find binding pockets inside cancer cells, that when blocked, prevent the cells from proliferating and cause them to die.
Scientists show the mammary gland ‘remembers’ prior pregnancy, spurring milk production
May 7, 2015
Anecdotal reports of nursing mothers have long suggested that giving milk is a lot easier in second and subsequent pregnancies.
Cancer researcher Dr. Chris Vakoc to receive AACR’s Outstanding Achievement Award
April 17, 2015
Assistant Professor Christopher R. Vakoc, receives the 35th annual AACR Outstanding Achievement in Cancer Research Award
Twin copies of a gene pair up in embryonic stem cells at a critical moment in their differentiation
March 5, 2015
Team finds that both copies of the Oct4 gene come together just as embryonic stem cells begin to develop into tissue-specific cell types
In a role reversal, RNAs proofread themselves
January 29, 2015
Molecular photographs of an enzyme bound to RNA reveal a new, inherent quality control mechanism
Christina Renna Foundation raises $30,000 for pediatric cancer research at CSHL
January 26, 2015
The Christina Renna Foundation presented $30,000 to Cold Spring Harbor Laboratory (CSHL) at their 8th annual Angel's Wish Gala
One experiment: Sometimes our cells express only one gene copy. Why?
June 1, 2014
Professor David L. Spector and team discover some monoallelically expressed genes encoded extra RNA, even though they are missing their other gene.
Among the changes that occur during pregnancy, those affecting the breasts have been found to subsequently modify breast cancer risk. My laboratory investigates how the signals present during pregnancy permanently alter the way gene expression is controlled and how these changes affect normal and malignant mammary development.
Only a small portion of the RNAs encoded in any genome are used to make proteins. My lab investigates what these noncoding RNAs (ncRNAs) do within and outside of cells, where regulators of their expression are located in the genome, and how perturbations of ncRNAs and their regulators contribute to disease.
To ensure that cells function normally, tens of thousands of genes must be turned on or off together. To do this, regulatory molecules - transcription factors and non-coding RNAs – simultaneously control hundreds of genes. My group studies how the resulting gene networks function and how they can be compromised in human disease.
Our cells depend on thousands of proteins and nucleic acids that function as tiny machines: molecules that build, fold, cut, destroy, and transport all of the molecules essential for life. My group is discovering how these molecular machines work, looking at interactions between individual atoms to understand how they activate gene expression, DNA replication, and small RNA biology.
From regulating gene expression to fighting off pathogens, biology uses DNA sequence information in many different ways. My research combines theory, computation, and experiment in an effort to better understand the quantitative relationships between DNA sequence and biological function. Much of my work is devoted to developing new methods in statistics and machine learning.
Our DNA carries the instructions to manufacture all the molecules needed by a cell. After each gene is copied from DNA into RNA, the RNA message is "spliced" - an editing process involving precise cutting and pasting. I am interested in how splicing normally works, how it is altered in genetic diseases and cancer, and how we can correct these defects for therapy.
Chromosomes are covered with chemical modifications that help control gene expression. I study this secondary genetic code - the epigenome - and how it is guided by small mobile RNAs in plants and fission yeast. Our discoveries impact plant breeding and human health, and we use this and other genomic information to improve aquatic plants as a source of bioenergy.
Transposable elements make up half of our DNA. They control gene expression and have been a major evolutionary force in all organisms. The Schorn lab investigates how small RNAs identify and silence transposable elements when they become active during development and disease.
The immense amount of DNA, RNA and proteins that contribute to our genetic programs are precisely organized inside the cell's nucleus. My group studies how nuclear organization impacts gene regulation, and how misregulation of non-coding RNAs contributes to human diseases such as cancer.
Despite the development of preventive vaccines, human papillomaviruses (HPVs) still infect more than five million women each year, significantly increasing their risk of cervical cancer. I am working to identify how HPV multiplies so that we may develop drugs that can defeat the virus once it has infected an individual.
Every time a cell divides, it must accurately copy its DNA. With 3 billion “letters” in the human genome, this is no small task. My studies reveal the many steps and molecular actors involved, as well as how errors in DNA replication are involved in diseases that range from cancer to rare genetic disorders.
Cancer cells achieve their pathogenicity by changing which genes are on and off. To maintain these changes in gene expression, cancer cells rely on proteins that interact with DNA or modify chromatin. My group investigates how such factors sustain the aberrant capabilities of cancer cells, thereby identifying new therapeutic targets.
The research in my laboratory addresses a central question in hematopoiesis—which is how self-renewal and differentiation are properly balanced in the hematopoietic stem and progenitor cell population. We utilize both CRISPR/Cas functional genomic and chemical genomic approaches to identify novel regulators of self-renewal and aim to develop novel therapeutic strategies for hematopoietic diseases and malignancies.