This series looks at the Oxford Martin School's academics and how their research is making a difference to our global future. The series will be of interest to people who are concerned about the future for the planet, how civilisation will adapt to emerging problems and issues such as climate change, over population, increased urbanisation of populations and the creation of vaccines to fight against future pandemics. The Oxford Martin School academics explain their various research topics in an accessible and thoughtful way and try to find practical solutions to these issues.

This course illustrates how knowledge and principles of biology, biochemistry, and engineering are integrated to create new products for societal benefit. It uses a case study format to examine recently developed products of pharmaceutical and biotechnology industries: how a product evolves from initial idea, through patents, testing, evaluation, production, and marketing. Emphasizes scientific and engineering principles; the responsibility scientists, engineers, and business executives have for the consequences of their technology; and instruction and practice in written and oral communication.
The topic focus of this class will vary from year to year. This version looks at inflammation underlying many diseases, specifically its role in cancer, diabetes, and cardiovascular disease.

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe how changes to gene expression can cause cancerExplain how changes to gene expression at different levels can disrupt the cell cycleDiscuss how understanding regulation of gene expression can lead to better drug design

By the end of this section, you will be able to:Describe how cancer is caused by uncontrolled cell growthUnderstand how proto-oncogenes are normal cell genes that, when mutated, become oncogenesDescribe how tumor suppressors functionExplain how mutant tumor suppressors cause cancer

By the end of this section, you will be able to:Describe how cancer is caused by uncontrolled cell growthUnderstand how proto-oncogenes are normal cell genes that, when mutated, become oncogenesDescribe how tumor suppressors functionExplain how mutant tumor suppressors cause cancer

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer-associated fibroblasts (CAFs) are part of the “soil” in which tumors grow. These cells have diverse origins and can interact with tumor cells in various ways, making it difficult to determine whether they’re friends or foes in cancer treatment. Detecting biomarkers can help address this challenge by allowing researchers to identify different CAF subsets. Several CAF biomarkers are associated with cancer promotion, such as FAP, vimentin, galectin 1, and osteopontin. For example, FAP increases cancer cell invasiveness and leads to immunotherapy resistance. Other CAF biomarkers are associated with cancer inhibition, like meflin, which is linked to a good prognosis in pancreatic and lung cancers. However, some biomarkers can either encourage or suppress cancer depending on the context..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Chronic myeloid leukemia, or CML, is a rare, slow-growing cancer of the bone marrow. It’s caused by the protein Bcr-Abl, which builds up and causes cells to grow and divide out of control. Now, researchers have identified one of Bcr-Abl’s close molecular partners and figured out how it might be forced to abandon Bcr-Abl and stop its deadly buildup. Experiments revealed that Bcr-Abl interacts with the heat shock protein HSP90AB1. HSP90AB1 supports Bcr-Abl’s rampant and deadly buildup in cells by blocking its entry into the nucleus. By deactivating HSP90AB1 in cultured cells with the antibiotic tanespimycin (17AAG), the researchers discovered that they could lock Bcr-Abl in the nucleus, reducing the spread of CML and programming CML cells for death. While more work is needed to understand how these processes play out in humans, these findings support the development of heat shock protein inhibitors as viable treatments for CML and other Bcr-Abl-associated malignancies..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

In this video segment, adapted from NOVA, Dr. Judah Folkman uses the scientific method to discover how cancer cells induce the formation of new blood vessels, which in turn nourish those cancer cells.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Leukemia relapse after conventional treatments is difficult to treat and has high patient mortality. Relapse is driven by the reawakening of previously quiescent cancer cells. Traditional treatments are ineffective against quiescent cells, as they instead target rapidly dividing cells. A new study investigated a potential dual-target treatment, C212, in cell culture. C212 is a derivative of curcumin, a compound that has shown anticancer properties in previous research. C212 was effective against both growing and quiescent leukemia cells. C212 drives quiescent leukemia cells deeper into dormancy by increasing their exit threshold, and then kills these deep-quiescent cells. This differs from previous strategies that awaken quiescent cells to kill, which runs the risk of wakening treatment-resistant subpopulation of cells. Molecular docking and experimental analyses showed that C212 could bind to Hsp90 and interferes with its function..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer cell growth depends on the production of new blood vessels by tumor endothelial cells in a process called angiogenesis. But the growing cancer cells produce large amounts of lactic acid as a byproduct of glucose breakdown. How tumor endothelial cells are able to survive in this toxic environment is unclear. In a recent study, researchers sought to uncover the mechanism of tumor endothelial cell survival in a lactic acid-rich tumor microenvironment. Using genetics and proteomics, they compared the RNA and protein levels of pH-regulating proteins in tumor endothelial cells to those in normal endothelial cells. They found that carbonic anhydrase 2 (CAII), an important pH regulator, was elevated in tumor endothelial cells, which was induced through the VEGF signaling pathway. Blocking CAII in tumor endothelial cells decreased cell survival in lactic acid conditions, and treating tumor-bearing mice with a CAII inhibitor had decreased lung metastasis..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Cancer is one of the most common diseases. According to some sources, every third person will eventually develop cancer. This Mini Lecture deals with the causes and therapeutic options of cancer with direct quotes by Nobel Laureates Renato Dulbecco, Howard Temin, and Aaron Ciechanover.

Le monde doit faire face à de nombreuses difficultés, sur le plan médical, notamment. Le cancer en fait partie.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Gastrointestinal stromal tumors (GISTs) are the most common malignant tumors in a type of gut tissue called mesenchyme. They’re caused by mutations that activate receptor tyrosine kinase (RTK) enzymes, and treatment with RTK inhibitors is initially successful, but over half of patients develop resistance, indicating a need for better treatments. Researchers recently investigated whether the drug THZ1, an inhibitor of the protein CDK7 that’s effective in other cancers, could help. They first confirmed that CDK7, which helps regulate the cell life cycle and gene transcription, was overexpressed in high-risk human GISTs. They also found that CDK7 overexpression predicted a poor outcome. However, low-dose THZ1 exerted pronounced anticancer effects in GIST cells both in vitro and in a mouse model. THZ1 also synergized with the RTK inhibitor imatinib to increase its efficacy..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Non-small cell lung cancer (NSCLC), the most common lung cancer, is also the most lethal cancer worldwide. The protein CPNE1 has been found to promote NSCLC, but it’s not clear how. To find out, researchers recently manipulated CPNE1 expression in NSCLC cells in vitro. CPNE1 overexpression activated cancer progression processes, such as proliferation, migration, invasion, and MET signaling, while CPNE1 silencing produced the opposite effects. Silencing RACK1, another cancer-driving protein, suppressed the tumor formation and MET signaling activation caused by CPNE1 overexpression, confirming that RACK1 mediates CPNE1-induced cancer progression and suggesting that MET is involved. Since CPNE1 is also believed to activate EGFR signaling, the researchers tested the effects of both MET and EGFR inhibition on NSCLC tumors in mice..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.