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Center for Cancer Research
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.
[Archive of Past Publications]
Genome-wide identification of microRNAs regulating cholesterol and triglyceride homeostasis. In this October 2015 paper in Nature Medicine Alexandre Wagschal from Anders Näär’s lab, and co-authors from MGH and elsewhere, report that 4 microRNAs located near SNPs associated with altered blood lipid levels regulate key proteins involved in cholesterol-lipoprotein trafficking. Functional studies support that altered microRNA expression contributes to abnormal blood lipid levels and may predispose individuals to cardiometabolic disorders.
Distinct but Concerted Roles of ATR, DNA-PK, and Chk1 in Countering Replication Stress during S Phase. In this September 2015 paper in Molecular Cell, Rémi Buisson and Jessica Boisvert from the labs of Cyril Benes and Lee Zou report that cells in early S-phase undergo mitotic catastrophe when subjected to ATR inhibition (ATRi). This reflects a key role for ATR in coordinating RRM2 accumulation and origin firing. Importantly, the level of ATRi-induced ssDNA can serve as a biomarker predicting the ATRi sensitivity of cancer cells.
Transcriptional control of autophagy–lysosome function drives pancreatic cancer metabolism. In this July issue of Nature, Rushika Perera from Nabeel Bardeesy’s laboratory and colleagues identify a transcriptional program regulating nutrient scavenging pathways (autophagy and the lysosome) in pancreatic cancer. They show that increased function of these pathways allows efficient recycling of proteins and other cargo, which sustains intracellular amino acid levels and supports tumor growth.
Hypoxia drives transient site-specific copy gain and drug-resistant gene expression. In this May 2015 paper in Genes & Development co-first authors Joshua Black and Elnaz Atabaksh from Johnathan Whetstine’s lab report that hypoxia drives sites-specific gene copy number gains in normal as well as in tumor cells. This evolutionary conserved response depends on the KDM4A histone demethylase and is blocked by inhibiting this enzyme. CSK1B, implicated in chemotherapy resistance, is among the genes amplified in response to hypoxia.
Tunable nanostructured coating for the capture and selective release of viable circulating tumor cells. In the March 2015 issue of the journal Advanced Materials, Eduardo Reátegui from Shannon Stott’s laboratory describes a stable degradation resistant ultra-thin membrane that can rapidly dissolve under temperature shifts. Use of this membrane in a microfluidic device, the CTC-chip, allows the isolation of rare circulating tumor cells from patient blood, providing a snapshot of a patient’s tumor and bringing us closer to personalized medicine.
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.
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.
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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