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New immune system-boosting cancer drugs have in clinical trials saved the lives of many people with seemingly untreatable melanoma or lung cancer, but the drugs seem useless against colon cancer. One exception-a man with colon cancer whose metastatic tumors vanished for several years after he was treated in 2007-piqued researchers' interest. They suspected his recovery might have to do with the large number of mutations in his tumors. Now, a small clinical trial suggests that even cancer patients with types of tumors that were thought to be impervious to the new drugs could benefit if those malignancies have the right error-riddled DNA signature, a result that could help 3% to 4% of cancer patients.

When a person dies from cancer, the culprit is usually not the original tumor but rather the cancerous cells that spread throughout the body and replicate in distant organs, a process called metastasis. Researchers have long known that metastasizing cancer cells slip their bonds and avoid immune detection by altering the sugars on their surfaces. They've even come up with a would-be drug to prevent such sugar alterations. But that compound interferes with needed sugars on normal cells, too, with lethal results in animals. Now, Dutch researchers report that they've packaged the drug in nanoparticles targeted exclusively to cancer cells, and they've shown that this combination prevents cancer cells from metastasizing in mice.  

The US Food and Drug Administration has approved a first-of-a-kind drug that uses the herpes virus to infiltrate deadly skin cancer tumours, reducing their size in some cases.

"Designing drugs" sounds trendy, but it accurately describes how some remarkably effective drugs are developed. In this case study we'll follow the steps of drug design, from initial research on the targeted disease, to the drug's use in humans. Gleevec (STI-571) is our example.

This dilemma/decision case study is intended to demonstrate how knowledge of signal transduction pathways can be applied to the pharmaceutical industry and within a medical setting. The case scenario revolves around a physician scientist's analysis of a chronic myelogenous leukemia (CML) patient's resistance to the cancer drug Gleevec® (imatinib). Students explore the molecular targets of drugs that inhibit cell signaling, while considering the best course of treatment for the medical patient. Written for an undergraduate sophomore level cell biology course, the case is also suitable for general biology, genetics, molecular biology, pharmacology, and cancer biology.

Panobinostat is a new type of drug that works by blocking an enzyme responsible for modifying DNA at the epigenetic level. Epigenetics refers to chemical marks on DNA itself or on the protein "spools" called histones that package DNA. These marks influence the activity of genes without changing the underlying sequence, essentially acting as volume knobs for genes. Earlier genomic studies showed that about 80 percent of DIPG tumors carry a mutation that alters a histone protein, resulting in changes to the way DNA is packaged and tagged with those chemical marks. This faulty epigenetic regulation results in activation of growth-promoting genes that should have been turned off, and shutdown of others that should have acted as brakes to cell multiplication. Cancer is the result. Panobinostat appears to work by restoring proper functioning of the cells' chemical tagging system.

Inflammation may help you fight off invading microbes, but it can also kill you, leading to insufficient blood flow and even organ failure. A new study shows that some cancer drugs may be able to quell the excessive inflammation that occurs in conditions such as sepsis, which is responsible for more than 250,000 deaths in the United States each year.

The UK's leading cancer charity yesterday welcomed work by British scientists who created a breed of genetically modified hens that can produce cancer-fighting medicines in their eggs. The research could slash the cost of producing drugs and potentially save the NHS millions of pounds.

This clicker case was designed to teach students about basic enzyme structure, mechanisms of enzyme inhibition, and mechanisms of drug resistance. The story follows Oliver Casey, a patient afflicted with Chronic Myelogenous Leukemia (CML). CML is caused by a chromosomal mutation that affects the tyrosine kinase ABL, an enzyme important in regulating cell growth and proliferation. The chromosomal mutation gives rise to the BCR-ABL fusion gene that produces a constitutively active ABL kinase, which causes the leukemia. In May 2001, the Food and Drug Administration approved the use of a rationally designed tyrosine kinase inhibitor, imatinib (Gleevec®), for the treatment of CML. During that same month, Gleevec made the cover of TIME magazine, described as "new ammunition in the war on cancer." The case is structured for a flipped classroom environment in which students view preparatory videos (including one by the author) on their own before beginning the case. Written for a first-year introductory biology course, the case could also be adapted for AP/Honors high school biology or a cancer biology course.

When Jordan is diagnosed with brain cancer (glioblastoma multiform), his college plans are unexpectedly put on hold. This scenario is presented in order to teach students about gene regulation, as the efficacy of the drug Jordan receives for post-surgical treatment is dependent upon the activity level of a gene encoding a protein involved in DNA repair. This "flipped" case study requires students to prepare in advance outside of class by watching several short videos that have been selected to teach the basics of how cancer forms as well as the role of epigenetics in gene silencing. Inside of class, the case is delivered using progressive disclosure format in which students gradually receive additional information to answer a series of directed questions. To determine a treatment plan for Jordan, students analyze data from a research study involving patients treated for his specific type of cancer. The case is designed for advanced high school biology classes as well as lower-level undergraduate general biology courses for non-majors and majors.

Cancer cells are hungry. To feed their rapid growth and division, their metabolism changes. Moreover, they use sugar (glucose) in a different way to normal cells. This animation, created by Nature Reviews Drug Discovery, explores the key aspects of the altered metabolism in cancer cells and explains how these can be exploited for the development of new anticancer strategies.

In the study, published Monday (May 1) in Nature Biotechnology,  Luo and colleagues set their sights on two fusions genes they had previously found to be associated with prostate cancer and various forms of rapid and invasive cancer, including liver tumors. Using a modified CRISPR-Cas9 tool that creates a single- rather than double-stranded break in DNA, they targeted the chromosomal breakpoints that form these fusion genes and replaced fusion DNA with a gene encoding the enzyme HSV1-tk. This enzyme effectively kills tumor cells by converting the drug ganciclovir into its active form, which then blocks DNA synthesis and leads to cell death. (Ganciclovir is used to treat cytomegalovirus in humans.)

She wanted to understand the effects of mutations that the gene for p53 is prone to. In dozens of simulations, she and her colleagues tracked how common p53 mutations further destabilize the already floppy protein, distorting it and preventing it from binding to DNA. Some simulations also revealed something else: a fingerhold for a potential drug. Once in a while, a small cleft forms in the mutated protein's core. When Amaro added virtual drug molecules into her models, the compounds lodged in that cleft, stabilizing p53 just enough to allow it to resume its normal functions.

A new treatment for pancreatic cancer could significantly increase survival rates, Ulster University has claimed. It said the treatment could lead to a five-fold reduction in tumour size. It involves injecting tumours with oxygen micro bubbles that are coated with a drug which is then activated by ultrasound.

" An anti-cancer drug reverses memory deficits in an Alzheimer's disease mouse model, University of Pittsburgh Graduate School of Public Health researchers confirm in the journal Science."

In this case study, we'll follow the process of developing an edible vaccine for the hepatitis B virus and explore practical details of genetic engineering techniques. 

Scientists may debate the accuracy of this equivalency, but most people agree that humans live many times longer than their furry friends. And, as it happens, these friends have features that uniquely qualify them to help us speed biomedical research.