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.

Featured Recent Publications from the Center for Cancer Research [Archive of Past Publications

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Rushika Perera and Nabeel Bardeesy

Rushika Perera and Nabeel Bardeesy

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.

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Joshua Black, Johnathan Whetstine, Elnaz Atabaksh

Joshua Black, Johnathan Whetstine, Elnaz Atabaksh

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.

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Eduardo Reátegui and Shannon Stott

Eduardo Reátegui and Shannon Stott

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.

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Nabeel Bardeesy and Julien Fitamant

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

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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Jian Ouyang

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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Capucine Van Rechem

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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Jeffrey Engelman

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.