The Ludwig Institute for Cancer Research Ltd (LICR)is a non-profit research organization committed to improving the control of cancer through Integrated laboratory and clinical research and novel therapeutic strategies based on the emerging understanding of cancer. The Institute translates these strategies into applications for human benefit by coupling discoveries from its basic laboratory research and renowned scientists with strong intellectual property positions,clinical development expertise and the conduct of Institute-sponsored, GCP compliant clinical trials.
Researchers elucidate how precise chemical modifications across the genome turn genes on and off during early human development—and how those mechanisms are disrupted in cancer
May 9, 2013, New York, NY and San Diego, CA - A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis in the current issue of the journal Cell of how genes are turned on and off to direct early human development. Led by Bing Ren of the Ludwig Institute for Cancer Research, Joseph Ecker of The Salk Institute for Biological Studies and James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences.
New research reveals how the tumor suppressor p53 is shut down in metastatic melanoma - and how it can be revived
April 25, 2013, New York, NY and Oxford, UK - Cancer cells are a problem for the body because they multiply recklessly, refuse to die and blithely metastasize to set up shop in places where they don’t belong. One protein that keeps healthy cells from behaving this way is a tumor suppressor named p53. This protein stops potentially precancerous cells from dividing and induces suicide in those that are damaged beyond repair. Not surprisingly, p53’s critical function is disrupted in most cancers.
April 21, 2013, New York, NY and San Diego Calif. – Ludwig researchers Arshad Desai and Christopher Campbell, a post-doctoral fellow in his laboratory, were conducting an experiment to parse the molecular details of cell division about three years ago, when they engineered a mutant yeast cell as a control that, in theory, had no chance of surviving. Apparently unaware of this, the mutant thrived.
April 11, 2013, Stockholm, Sweden - At their regular meeting on April 26, 2013, the Trustees of the Nobel Foundation will elect Carl-Henrik Heldin of Uppsala as a new member of the Nobel Foundation’s Board of Directors. Heldin was born in 1952 and is a member of the Royal Swedish Academy of Sciences, professor of molecular cell biology at Uppsala University, branch director of the Ludwig Institute for Cancer Research in Uppsala and Vice President of the European Research Council (ERC).
April 10, 2013, New York, NY – A dozen Ludwig scientists from around the world presented the latest advancements in basic and clinical cancer research at this week’s American Association for Cancer Research (AACR) Annual Meeting 2013. Progress in immunotherapy and epigenetics led the program with important diagnostic and treatment implications for emerging cancer therapy.
WASHINGTON, D.C. - Researchers using a tool called BEAMing technology, which can detect cancer-driving gene mutations in patients’ blood samples, were able to identify oncogenic mutations associated with distinct responses to therapies used to treat patients with gastrointestinal stromal tumors (GIST), according to a researcher who presented the data at the AACR Annual Meeting 2013, held in Washington D.C., April 6-10.
April 8, 2013, New York, NY and San Diego Calif. - Proteins that control cell growth are often mutated in cancer, and their aberrant signaling drives the wild proliferation of cells that gives rise to tumors. One such protein, the epidermal growth factor receptor (EGFR), fuels a wide variety of cancers - including a highly malignant brain cancer known as glioblastoma. Yet drugs devised to block its signaling tend to work only for a short while, until the cancer cells adapt to evade the therapy. So far, much of the research examining such drug resistance has focused on how mutations of other proteins in cancer cells allow them to resist drugs.
March 26, 2013, New York, NY - Three Ludwig scientists were named as Fellows in the inaugural class of the AACR Academy, the most prestigious honor bestowed by the American Association for Cancer Research.
February 26, 2013, New York, N.Y. and San Diego, Calif. – Glioblastoma, the most common and lethal form of brain tumor in adults, is challenging to treat because the tumors rapidly become resistant to therapy. As cancer researchers are learning more about the causes of tumor cell growth and drug resistance, they are discovering molecular pathways that might lead to new targeted therapies to potentially treat this deadly cancer.
Vogelstein is among 11 recipients of inaugural Breakthrough Prize in Life Sciences, world's richest academic prize for medicine, biology school of medicine
February 21, 2013, Baltimore, US - Ludwig scientist Bert Vogelstein at Johns Hopkins, a pioneer in the field of cancer genomics, is among 11 scientists named the first winners of the world's richest academic prize for medicine and biology. News of the award was first reported today by The New York Times.
February 18, 2013 , New York, NY and Melbourne, Australia - A Melbourne-based research team has discovered a genetic defect that can halt cell growth and force cells into a death-evading survival state. The finding has revealed an important mechanism controlling the growth of rapidly-dividing cells that may ultimately lead to the development of new treatments for diseases including cancer.
Monday, Feb. 4, 2013- STANFORD, Calif. - An antibody that binds to a molecule on the surface of a rare but deadly tumor of the gastrointestinal tract inhibits the growth of the cancer cells in mice, according to researchers at the Stanford University School of Medicine.
An analysis of how the epigenetic marker 5-hydroxymethylcytosine is interpreted by neural cells opens the door to studying its role in developmental disorders and disease
February 4, 2013, New York, NY and Oxford, UK - Nearly every cell in the human body carries a copy of the full human genome. So how is it that the cells that detect light in the human eye are so different from those of, say, the beating heart or the spleen?