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 Dyson Lab, led by Principal Investigator Nicholas Dyson, PhD, focusing on E2F-, pRB- and tumorigenesis.
Featured Recent Publications from the Center for Cancer Research
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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.
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Supriya Saha, Nabeel Bardeesy and Christine Parachoniak
Mutant IDH inhibits HNF-4α to block hepatocyte differentiation and promote biliary cancer.
In this July 2014 Nature paper, Supriya Saha and Christine Parachoniak from Nabeel Bardeesy’s lab describe how mutations in metabolic enzymes isocitrate dehydrogenase 1 or 2 (IDH1/2) cause a deadly form of liver cancer. Mutations in IDH1/2 block the expression of HNF4alpha without which liver stem cells fail to mature. The paper also describes a novel genetically engineered mouse model that should be useful in further studies of this lethal cancer.
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Isolation and molecular characterization of circulating melanoma cells.
In this May 2014 paper, first author Xi Luo from the labs of Shyamala Maheswaran and Daniel Haber, describes the characterization of melanoma cells isolated from the blood of tumor bearing mice and patients. Providing another illustration of the unique power of the microfluidic platform developed at MGH, targeted therapy reduced the number of circulating tumor cells (CTCs), which expressed genes implicated in cell motility and tumor invasiveness.
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Mario Suva, Esther Rheinbay and Bradley Bernstein
Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.
In this April 2014 Cell paper, co-first authors Mario Suva and Esther Rheinbay from Brad Bernstein’s lab, describe the transcriptional circuitry underlying the development of glioblastoma (GBM), an aggressive brain tumor. They found that 4 transcription factors (TFs) and their associated networks control the tumor-propagating potential of GBM stem cells, and identified subunits of an epigenetic regulator complex as candidate therapeutic targets.
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Nicholas Dyson and Amity Manning
Suppression of genome instability in pRb-deficient cells by enhancement of chromosome cohesion
In this March 2014 Molecular Cell paper, Amity Manning and co-workers from Nick Dyson’s lab show that loss of the retinoblastoma protein (pRB) alters centromeric heterochromatin and chromosome cohesion. These changes contribute to chromosome segregation errors, explaining how loss of pRB reduces genome stability. Because pRB loss is common in cancer, interventions that increase cohesion may reduce cancer-associated genome instability.