This animation shows how a growing tumor can recruit nearby blood vessels in order to gain a supply of blood.
This animation demonstrates how cancerous cells could be destroyed using a modified virus.
A 3D animation showing the molecule p53 binds to DNA and initiates the transcription of mRNA.
A cancer tumor forms in a bed of healthy cells. The animation goes on to show how the tumor recruits blood vessels and how metastasis occurs.
Chronic myeloid leukemia (CML) is caused by a mutation that leads to an abnormal protein that is always active. The drug Gleevec has a shape that fits into the active site of the abnormal protein and stops its harmful effects.
Gleevec is a drug designed to interfere with the stimulation of growth in leukemia cells. This 3D animation shows how this is achieved.
Dr. Vogelstein shows video taken during a colonoscopy and the removal of a polyp.
As part of the 2003 Holiday Lectures on Science, Dr. Bert Vogelstein and Dr. Huda Y. Zoghbi discuss how their patients have led to a deeper understanding of the genetic and molecular bases of neurological disorders and cancer. Thanks to these patients, researchers can now apply the knowledge...
Although there are numerous kinds of cancer, all stem from alterations that allow cell division to outstrip cell demise.
The identification of hundreds of genes involved in the formation and spread of cancer is leading to promising new methods for diagnosis, prevention, and treatment.
Learn about what p53 does, and how interfering with its function can lead to cancer.
Cancer occurs when a single cell acquires the ability to reproduce aggressively and to invade other tissues. Left unchecked, this anarchy destroys the cellular society. It interferes with the body's normal function, destroys organs, and eventually kills the organism.
Cancers grow and spread by a process akin to evolution.
A text transcript of the 2003 Holiday Lectures on Science, Learning From Patients: The Science of Medicine.
A chapter list to accompany the DVD.
In the 2013 Holiday Lectures on Science, leading medical researchers explain how advances in genomics are revolutionizing their work, leading to a better understanding of disease and to improved treatments.
A brochure from the 2013 Holiday Lectures on Science.
The poster for the 2013 Holiday Lectures on Science, Medicine in the Genomic Era, illustrates the difference between germline and somatic cell mutations.
Dr. Sawyers is an HHMI investigator who has contributed to the development of drugs that target leukemia and prostate cancer.
The drug Gleevec binds to and inactivates BCR-ABL, a mutant kinase that causes chronic myeloid leukemia.
Mutations in the BCR-ABL gene can cause resistance to Gleevec, but another drug, dasatinib, can be used instead.
Understanding that cancer is caused by mutations in genes that regulate cell proliferation has led to the development of targeted drug therapies.
Genetic data from a large number of tumor types reveal commonly mutated genes and uncover connections between different types of cancer.
A student discussion with the lecturers of the 2013 Holiday Lectures on Science.
Dr. Sawyers describes how he became interested in science during medical school, and offers advice to science students.
Ms. Balbas discusses her early interest in medicine, her path to becoming a researcher, and her best day in the lab.
Disrupting the normal processes of differentiation and maturation of the intestinal epithelial cells can lead to cancer.
Dr. Charles Sawyers discusses how the identification of most cancer genes could transform cancer into a chronic disease.
A 3D model of BCR-ABL, an unregulated kinase that causes cancer.
A 3D model of gleevec-resistant BCR-ABL, a mutated form of BCR-ABL.
A 3D model of adenosine triphosphate, or ATP.
A 3D model of imatinib (Gleevec), a drug that mimics ATP and inhibits BCR-ABL.
A 3D model of dasatinib, a drug that can inhibit BCR-ABL and Gleevec-resistant BCR-ABL.