background preloader

Research

Facebook Twitter

Stanford

Stand Up To Cancer — This Is Where The End Of Cancer Begins. Next generation biomarker detects tumour cells and delivers anti-cancer drugs. Nanyang Technological University (NTU) has invented a unique biomarker with two exceptional functions. First, it lights up when it detects tumour cells to allow scientists to take a better look. And it can also release anti-cancer drugs at the same time to the specific cells. This new biomarker, which has immense potential for drug development, is made from a nanophosphor particle, ten thousand times smaller than a grain of sand. NTU associate professors Zhang Qichun and Joachim Loo have found a way to make the nanoparticle light up when it is activated by near-infrared light emitted by an imaging device and only if tumour cells release small signalling molecules. Prof Zhang said the use of near-infrared light, which is invisible to the human eye, is unique as most imaging techniques use ultraviolet light or visible light.

"Near-infrared light can penetrate 3 to 4 cm beyond the skin to deep tissue, much deeper than visible light. The new biomarker also has other advantages. Novel therapeutic cancer vaccine reaches human clinical trials. A cross-disciplinary team of scientists, engineers, and clinicians announced today that they have begun a Phase I clinical trial of an implantable vaccine to treat melanoma, the most lethal form of skin cancer. The effort is the fruit of a new model of translational research being pursued at the Wyss Institute for Biologically Inspired Engineering at Harvard University that integrates the latest cancer research with bioinspired technology development. It was led by Wyss Core Faculty member David J. Mooney, Ph.D., who is also the Robert P. Pinkas Family Professor of Bioengineering at the Harvard School of Engineering and Applied Sciences (SEAS), and Wyss Institute Associate Faculty member Glenn Dranoff, M.D., who is co-leader of Dana-Farber Cancer Institute's Cancer Vaccine Center.

Most therapeutic cancer vaccines available today require doctors to first remove the patient's immune cells from the body, then reprogram them and reintroduce them back into the body. The Conspiracy To End Cancer. The hero scientist who defeats cancer will likely never exist. No exalted individual, no victory celebration, no Marie Curie or Jonas Salk, who in 1955, after he created the first polio vaccine, was asked, So what’s next?

Cancer? — as if a doctor finished with one disease could simply shift his attention to another, like a chef turning from the soup to the entrée. Cancer doesn’t work that way. It’s not just one disease; it’s hundreds, potentially thousands. “This disease is much more complex than we have been treating it,” says MIT’s Phillip Sharp. So it will take not one hero but many. Cancer research — indeed, most medical research — is typically about the narrowly focused investigator beavering away, one small grant at a time. So what does it take to transform the way an entire medical ecosystem functions? “When you have to answer to Nobel laureates and others, it’s a very tough review team,” says Dr.

And for patients, it’s happening where the chemo hits the cancer. Scientists create extremely potent and improved derivatives of successful anticancer drug. Scientists at The Scripps Research Institute (TSRI) have found a way to make dramatic improvements to the cancer cell-killing power of vinblastine, one of the most successful chemotherapy drugs of the past few decades. The team's modified versions of vinblastine showed 10 to 200 times greater potency than the clinical drug. Even more significantly, these new compounds overcome the drug resistance that emerges upon treatment relapse, which renders continued or subsequent vinblastine treatment ineffective in some patients. The TSRI researchers expect that similar modifications will boost the effectiveness of vincristine, a closely related drug that is commonly used against childhood leukemias and Hodgkin's disease.

"These new compounds should improve on what are already superb anticancer drugs," said Dale L. Boger, who is the Richard and Alice Cramer Professor and Chair of the Department of Chemistry at TSRI. Anticancer Agents Developing Extraordinary Potency. Depletion of 'traitor' immune cells slows cancer growth in mice. When a person has cancer, some of the cells in his or her body have changed and are growing uncontrollably. Most cancer drugs try to treat the disease by killing those fast-growing cells, but another approach called immunotherapy tries to stimulate a person's own immune system to attack the cancer itself. Now, scientists at the University of Washington have developed a strategy to slow tumor growth and prolong survival in mice with cancer by targeting and destroying a type of cell that dampens the body's immune response to cancer.

The researchers published their findings this week (Sept. 16) in the Proceedings of the National Academy of Sciences. "We're really enthusiastic about these results because they suggest an alternative drug target that could be synergistic with current treatments," said co-author Suzie Pun, a UW associate professor of bioengineering. Our immune system normally patrols for and eliminates abnormal cells. Scientists develop ground-breaking new method of 'starving' cancer cells. Engineered T cells kill tumors but spare normal tissue in an animal model. The need to distinguish between normal cells and tumor cells is a feature that has been long sought for most types of cancer drugs.

Tumor antigens, unique proteins on the surface of a tumor, are potential targets for a normal immune response against cancer. Identifying which antigens a patient's tumor cells express is the cornerstone of designing cancer therapy for that individual. But some of these tumor antigens are also expressed on normal cells, inching personalized therapy back to the original problem. T cells made to express a protein called CAR, for chimeric antigen receptor, are engineered by grafting a portion of a tumor-specific antibody onto an immune cell, allowing them to recognize antigens on the cell surface. Early first-generation CARs had one signaling domain for T-cell activation. Importantly, CARs allow patients' T cells to recognize tumor antigens and kill certain tumor cells.

To address this issue, Daniel J.

John Hopkins

Reprogrammed immune cells might give doctors an edge in rallying the body's defenses against tumor growth. Genetic abnormalities accrued by tumor cells lead to inappropriate production of proteins at the wrong time or place, or even the synthesis of unusual hybrid proteins not found in normal cells. Such abnormalities can serve as 'red flags' that alert the immune system that something has gone awry, triggering proliferation of cytotoxic T lymphocytes (CTLs) that can recognize and destroy defective cells based on these protein signatures.

Unfortunately, cancers ultimately deploy defensive strategies that render the body's natural immune response incapable of stopping cancerous growth, and scientists have encountered only limited success with vaccines and other strategies that help 'super-charge' the anti-tumor immune reaction. Now, new stem cell research by Hiroshi Kawamoto and colleagues at the RIKEN Research Center for Allergy and Immunology promises to greatly bolster the effectiveness of such approaches1. Made to order Testing the troops.

Cold Spring Harbor Laboratory

Learn About Cancer. Cancer Institute of New Jersey. Weizmann Institute of Science. Fred Hutchinson Cancer Research. Virginia Commonwealth University. University of California (San Diego) University of Missouri. NIH National Human Genome Research. Science.