Announcing 2017 KRAS Fellowship and KRAS Travel Scholarship Funding Opportunities

Awards available for researchers studying KRAS in pancreatic cancer. View in browser.

Marco Biancucci, PhD
Postdoctoral research fellow, Northwestern University – Chicago Campus
Recipient, 2016 Pancreatic Cancer Action Network – NCI Frederick National Laboratory for Cancer Research
KRAS Fellowship funded in memory of Samuel Stroum
Announcing 2017 KRAS Fellowship and KRAS Travel Scholarship Funding OpportunitiesDear RAS research community,

The National Cancer Institute’s (NCI) Frederick National Laboratory for Cancer Research (FNLCR) and the Pancreatic Cancer Action Network have joined together again to further cutting-edge research on pancreatic cancer and KRAS that integrates with NCI’s RAS Initiative. For 2017, two types of awards are available.

Expanded! KRAS Fellowship
Amount: $100,000 | Duration: Two years
Supports a postdoctoral or clinical research fellow to conduct KRAS research that is directly relevant to pancreatic cancer with aims aligned with the RAS Initiative
Application deadline: October 27, 2016, Noon EDT

KRAS Travel Scholarship
Amount: Depending on need
Provides travel support to a researcher at any career stage, during or after the postdoctoral level, to visit FNLCR to pursue KRAS research that is directly relevant to pancreatic cancer with aims aligned with the RAS Initiative
Application deadline: Rolling


For questions about proposed projects and resources at FNLCR, please contact Dwight V. Nissley, PhD, Director, Cancer Research Technology Program, FNLCR:

For general questions about the award or our other funding opportunities, please contact:

The RAS Initiative
The National Cancer Institute’s RAS Initiative was launched in 2013 to deepen knowledge of several aspects of RAS genes – their protein products, role in cell signaling, and functions in health and disease – with the explicit goals of improving treatment, diagnosis, and prevention of the many human cancers driven by mutant RAS genes. The Initiative operates as a research hub based at the NCI Frederick National Laboratory for Cancer Research (FNLCR) in Frederick, Maryland, with spokes reaching into all corners of the extramural research community. The RAS Initiative is led by Dr. Frank McCormick, a distinguished RAS investigator from the University of California, San Francisco, and is managed for NCI by Leidos Biomedical Research, Inc.

The Pancreatic Cancer Action Network
The Pancreatic Cancer Action Network is the national organization creating hope in a comprehensive way through research, patient support, community outreach and advocacy for a cure. The organization is leading the way to increase survival for people diagnosed with this devastating disease through a bold initiative – The Vision of Progress: Double Pancreatic Cancer Survival by 2020. To continue to accelerate progress, a goal to raise $200 million by 2020 has also been established to allow the organization to significantly increase its investment in research efforts. Together, we can Wage Hope and rewrite the future of pancreatic cancer.

Frederick National Laboratory for Cancer Research
8560 Progress Drive
Frederick, MD 21701
301-496-4345Pancreatic Cancer Action Network
1500 Rosecrans Ave., Suite 200
Manhattan Beach, CA 90266

Meeting Report: Society for Melanoma Research 2015 International Congress

Meeting Report: Society for Melanoma Research 2015 International Congress


November 18-21, 2015

Ana Neto, Postdoctoral Fellow, Ceol Laboratory, UMass Medical School, USA

I had the opportunity to attend the Society for Melanoma Research 2015 International Congress in San Francisco, CA (18th-21st of November). Several aspects of melanoma research were covered: genetics, genomics, immunotherapy, models of melanoma, targeted therapy, and resistance to targeted therapy, between others. The goal of the Society and the meeting is to promote the unification of the field by improving the communication between different areas of melanoma research. Approximately 1200 delegates with different backgrounds basic, translational and clinical research attended this meeting. Several companies that supported the meeting were represented in exhibitors (Novartis Oncology, Amgen, Genentech, Brystol-Myers Squibb, Merck and Castle Biosciences Incorporated).

This meeting had oral communications from great speakers. A. Hunter Shain gave an insightful talk about the genetic evolution of melanoma from precursor lesions. Sean Morrison shared his new results about how oxidative stress restricts metastasis spreading to distant locations. Marcus Bosenberg showed how melanoma genotype defines melanoma phenotype using mice as model system. In Ashani Weeraratna’s talk we could learn that aging could affect the signaling of melanoma cells. These were only a few examples of the talks that the attendees from this meeting could enjoy. Liz Patton and Jacqueline Lees were amazing ambassadors of the melanoma research using zebrafish as model system. They delivered great talks where they refer the potential of the zebrafish for melanoma modeling and chemical screening. Indeed, Lees’ laboratory just developed a model of uveal melanoma that recapitulates the human disease, where new drug therapies could be screened. The participants from zebrafish laboratories were only a few: Milena Zimmer (Richard White’s laboratory), Mitch Levesque and students, Penny Lovat and myself (from Craig Ceol’s laboratory) (I hope I didn’t miss anyone). It would be good to increase the participation of zebrafish researchers to this type of meetings to enhance the impact and visibility of zebrafish as a disease model, so we improve funding in our research.

The congress has several moments for social interaction, breakfast, lunch and dinner for the SMR awards ceremony. The work of James P. Alison, Suzanne Topalian, Daniel Peeper and Georgina Long was recognized and it was also a moment of mixing between all investigators.

It was an enthusiastic meeting and the next year’s venue will be in Boston, a meeting organized by Keith Flaherty.

Live imaging reveals how wound healing influences cancer

Live imaging reveals how wound healing influences cancer

Live imaging reveals how wound influences cancer (2015) 

Click here to read article on 

Researchers in the United Kingdom and Denmark have studied the “see-through” larvae of zebrafish to reveal how wound healing leads to skin cancer. Live imaging shows neutrophils, the protective inflammatory cells of the body’s immune system, diverted from an induced wound to any nearby precancerous skin cells. The newly arrived neutrophils cause rapid division of these skin cells, which may cause them to progress to melanoma. The results are published in The EMBO Journal.

“Our results provide direct visual evidence of a physical link between wound-associated inflammation and the development of skin cancer,” says EMBO Member Paul Martin, Professor at Bristol University and the University of Cardiff. “White blood cells, in particular neutrophils, that typically serve as part of the body’s built-in immune system are usurped by nearby precancerous skin cells in a way that leads to the proliferation of tumour cells in our zebrafish model experimental system of human melanoma.”

Scientists have known for some time that inflammation is one of the ten hallmarks of cancer. Cancer has also been described as a “wound that does not heal.” However details about how physical damage to body tissues might influence the progress of cancer have remained scarce.

The researchers used genetically modified larvae of zebrafish to watch the relationship between wound-associated inflammation and melanoma as the cancer took hold in the living fish. The cellular events and changes were observed by live imaging with a special confocal laser-scanning microscope.

In further experiments, the researchers were also able to show that a specific type of signaling molecule released by neutrophils, prostaglandin E2, is part of the signal that drives the splurge of cell growth linked to the cancer in their experimental system. High levels of neutrophils were also detected in human clinical samples of melanomas that had been obtained from individuals whose cancers had open ulcers. Importantly, neutrophils were linked to increased proliferation of melanoma cells and poor survival, which suggests that these findings in fish may have considerable relevance to cancer patients.

The authors note that the findings of the study may have implications for cancer surgery. Minimally invasive surgery is beneficial to cancer patients in many situations and often the preferred treatment. However, particularly in cases where all cancerous tissue cannot be removed, the inflammatory response might influence the remaining cancer cells in the body. “Our studies to date suggest that several strategies might improve outcomes for patients including the possible use of therapeutics to dampen damage-induced inflammatory responses,” adds Martin.

Further work is in progress to better understand the relationship between the inflammatory response and skin cancer in the zebrafish model system. Studies are also needed to investigate what therapeutic or other strategies might bring better interventions for patients who have adverse tissue inflammation due to planned (for example biopsy or surgery) or unplanned (e.g. ulceration) tissue damage.

Full research paper can be found in The Embo Journal. Click here to read the full paper

The wound inflammatory response exacerbates growth of pre-neoplastic cells and progression to cancer”

Nicole Antonio, Marie Louise Bønnelykke-Behrndtz, Laura Ward, John Collin, Ib Jarle Christensen, Torben Steiniche, Henrik Schmidt, Yi Feng, Paul Martin

Models of Transparency

Models of Transparency

Heath, J.K. Langenau, D. Sadler, K.C. and White, R. (2013) Models of Transparency. The Scientist.

Read Full Article Here

Researchers are taking advantage of small, transparent zebrafish embryos and larvae—and a special strain of see-through adults—to understand the development and spread of cancer.

The zebrafish model offers a major opportunity to discover impor­tant pathways underlying cancer and to identify novel therapies in high-throughput drug screens, in a way that mice never could.

From frogs to dogs and people, cancer wreaks havoc across the animal kingdom—and fish are no exception. Coral trout, for example, develop melanoma from overexposure to sun, just as humans do. Rainbow trout develop liver cancer in response to environmental toxins. And zebrafish—small, striped fish indigenous to the rivers of India and a widely used model organism—are susceptible to both malignant and benign tumors of the brain, nervous system, blood, liver, pancreas, skin, muscle, and intestine.

Importantly, tumors that arise in the same organs in humans and fish look and behave alike, and the cancers often share common genetic underpinnings. As a result, most researchers believe that the basic mechanisms underlying tumor formation are conserved across species, allowing them to study the formation, expansion, and spread of tumors in animal models with the hope of eventually finding new insights into cancer in people.

Zebrafish are an increasingly popular choice among cancer biologists. Between 1995 and 2012, there was a 10-fold increase in the number of yearly PubMed citations of cancer studies in the species, with more than 200 research papers published last year.  Although dwarfed by cancer studies using human tissue and mouse models, the optical transparency of zebrafish embryos and larvae—and now, adult fish of a recently created strain—allows researchers to track tumors in a way that is not possible in other vertebrate models. Furthermore, their small size—embryos are small enough to be reared in 96-well plates—make them a more practical laboratory system than other cancer models. Indeed, researchers are now using these fish to identify druggable oncogenic drivers of specific tumor types, to tease apart the complex network of cancer genes that cooperate in tumor formation and progression, to probe the interplay between the genes that govern embryonic development and those that cause cancer, and to uncover how tumors metastasize and kill their host. The zebrafish model offers a major opportunity to discover important pathways underlying cancer and to identify novel therapies in high-throughput drug screens in a way that mice never could.

Z ebrafish (Danio rerio) have fast made their way from pet stores and home aquaria into research laboratories worldwide. Their weekly matings produce 100 to 200 embryos that rapidly and synchronously march through embryonic development, so that within 5 days of fertilization, they are mature, feeding larvae. Zebrafish are small and inexpensive to maintain in high numbers, facilitating large-scale experimentation and cheap in vivo drug screens. Famously, the fish are transparent during early larval stages, allowing investigators to directly observe internal development and making the fish a favorite of developmental biologists since the 1960s. But in recent years, the utility of zebrafish has been proven beyond developmental fields, and they are now being found in more and more laboratories studying behavior, diabetes, heart disease, regeneration, stem cell biology—and cancer.

Critically, zebrafish can be used to identify the important pathways and processes that cause cancer in people. Common organ systems and cell types are shared between human and zebrafish, and whether induced by transgenesis or carcinogens, cancers arising from the blood (leukemia and lymphoma), pigmented cells of the skin (melanoma), and the cells that line the bile ducts (cholangiocarcinoma) have microscopic features that are essentially indistinguishable between humans and zebrafish.

The zebrafish model offers a major opportunity to discover impor­tant pathways underlying cancer and to identify novel therapies in high-throughput drug screens, in a way that mice never could.

Comparing gene-expression profiles of tumors across various species provides a powerful mechanism for identifying genes that likely represent core functions of cancer. For example, microarray gene-expression analyses have compared the gene signatures of fish hepatocellular carcinoma to that of human liver, gastric, prostate, and lung tumors. Remarkably, this analysis revealed that fish and human liver tumors are more similar to each other than either tumor type is to human tumors derived from different tissues. Moreover, comparative studies can often be used to pinpoint pathways that are active in human disease. This is illustrated by work on a zebrafish model of rhabdomyosarcoma (RMS), a cancer of skeletal muscle, which revealed a gene signature that is also commonly found in human RMS, highlighting the importance of the RAS signaling pathway in the genesis of human RMS

Read Full Article Here