The unique strengths of the Center for Cancer Research (CCR) are the exceptional quality of its faculty and the ways in which the CCR's basic scientists collaborate with Mass General’s leading oncologists, surgeons, radiologists, pathologists, and other health care professionals to advance the frontiers of cancer medicine.
Welcome to the website for the Center for Cancer Research. This center serves as the engine for discovery. We have 41 independent laboratories with faculty drawn from all departments of Harvard Medical School. Our faculty study everything from Cancer cell genetics and epigenetics, metabolism and microenvironments, cell signaling and DNA damage, with studies of cultured cells, all the way to patient derived samples and specimens. I encourage you to visit our website, view all the investigators summaries, look through our news and events, and our current publication highlights.
Explore the work of The Bardeesy Lab, led by Principal Investigator Nabeel M. Bardeesy, PhD, focusing on pancreatic ductal adenocarcinoma.
Featured Recent Publications from the Center for Cancer Research [Archive of Past Publications]
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Nabeel Bardeesy and Julien Fitamant
YAP Inhibition Restores Hepatocyte Differentiation in Advanced HCC, Leading to Tumor Regression.
In this March 2015 paper in Cell Reports, Julien Fitamant from Nabeel Bardeesy’s laboratory and colleagues identify the Yap pathway as a novel therapeutic target in liver cancer, the second most common cause of cancer-related deaths worldwide. Main findings include that YAP functions as a rheostat to control hepatocyte differentiation, and that targeting YAP restores cell differentiation and leads to pronounced tumor regression in a mouse model.
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Erin Sennott, Leanne Ahronian and Ryan Corcoran
Clinical acquired resistance to RAF inhibitor combinations in BRAF-mutant colorectal cancer through MAPK pathway alterations.
Drug regimens that include RAF inhibitors show promise in BRAF-mutant colorectal cancer (CRC). In this February 2015 Cancer Discovery paper, shared first authors Erin Sennott and Leanne Ahronian from the labs of Ryan Corcoran and Jeffrey Engelman identified MAPK pathway alterations driving resistance to these regimens, highlighting the critical dependence of BRAF-mutant CRCs on MAPK signaling and suggesting strategies to overcome resistance.
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Lee Zou and Jian Ouyang
Noncovalent Interactions with SUMO and Ubiquitin Orchestrate Distinct Functions of the SLX4 Complex in Genome Maintenance.
In this January 2015 paper published in Molecular Cell, first author Jian Ouyang from Lee Zou’s group analyzed the multifunctional DNA repair protein SLX4. The authors show that the binding of SLX4 to SUMO or ubiquitin promotes its functions in distinct contexts, revealing an intriguing mechanism to orchestrate the context-specific functions of this protein.
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Johnathan Whetstine and Capucine Van Rechem
Lysine Demethylase KDM4A Associates with Translation Machinery and Regulates Protein Synthesis.
In this January 2015 paper published in Cancer Discovery, Capucine Van Rechem and co-workers from Johnathan Whetstine’s laboratory describe an unexpected novel function for the KDM4A lysine demethylase as a regulator of protein translation. In a second paper in the same journal this group also describes a KDM4A coding polymorphism associated with altered sensitivity to mTOR inhibitors.
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Patient-derived models of acquired resistance can identify effective drug combinations for cancer.
In this December 2014 paper in the journal Science a group of authors led by senior investigators Cyril Benes and Jeffrey Engelman describe how combined genetic analysis and pharmacological screening of biopsied drug resistant lung tumors allowed the rapid discovery of drug combinations that overcome resistance. Further refinement of this novel analytical platform could direct therapeutic choices for individual patients.
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Nick Dyson and Wayne Miles
Post-transcriptional gene expression control by NANOS is up-regulated and functionally important in pRb-deficient cells.
In this October 2014 paper published in The EMBO Journal, first author Wayne Miles from Nick Dyson’s group describes a new mechanism that allows cells to cope with loss of the pRb tumor suppressor. pRb is inactivated in most cancers and its loss affects many processes, yet pRb mutant cells have few defects. The authors report that an evolutionary conserved post-transcriptional mechanism involving pRb target NANOS1 allows cells to deal with loss of pRb.
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Mario Suva, Bradley Bernstein and Anoop Patel
Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma.
In this June 2014 paper in the journal Science, first author Anoop Patel working with senior authors Mario Suva and Bradley Bernstein reports the first use of single-cell RNA sequencing to probe tumor heterogeneity. Sequencing of 430 single cells from five human glioblastomas revealed an unanticipated high level of heterogeneity both between and within tumors, which has profound implications for glioblastoma prognosis and therapy.
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Lee Zou and Ching-Shyi Wu
SUMOylation of ATRIP potentiates DNA damage signaling by boosting multiple protein interactions in the ATR pathway.
Maintaining genome integrity is essential since DNA damage often leads to cancer. In human cells, the ATM and ATR protein kinases are activated by specific forms of DNA damage, and coordinate the DNA damage response. In this August 2014 Genes and Development paper, first author Ching-Shyi Wu from Lee Zou's lab describes that SUMOylation of ATRIP potentiates DNA damage signaling by enhancing multiple protein interactions in the ATR pathway.