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

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 cells are abnormal cells that rapidly proliferate and often find ways to evade the immune system’s attempts to stop them. Such cells often overexpress the genes MYC and ARF6 and have a mutated version of the KRAS gene. These changes are inextricably linked and result in significant resistance to cancer therapies. KRAS activates MYC gene expression and possibly promotes the translation of the messenger RNA for both MYC and ARF6. Then MYC induces expression of genes related to mitochondrial formation and energy production. Meanwhile, ARF6 protects the mitochondria from oxidation-induced injury. ARF6 may also promote cancer invasion, metastasis, and immune evasion. Thus, KRAS, MYC, and ARF6 cooperate to help cancer spread and to avoid the immune system and immune-based treatments. These harmful associations are common in pancreatic cancer and can be strengthened by mutations in other genes like TP53..."

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:

"Pancreatic ductal adenocarcinoma (PDAC) is one of the most common causes of cancer-related death globally and is increasing in incidence. While some cancers can be effectively treated with immune checkpoint blockade (ICB) therapy, no such treatments currently exist for PDAC, and no effective biomarkers of this disease have been identified. Recently, researchers demonstrated the ability to shrink PDAC tumors in mice using the drug silvestrol. PDAC is associated with mutations in the KRAS gene that cause the excessive production of proteins involved in normal cell functioning, such as ARF6, AMAP1, and MYC. Interestingly, while silvestrol tended to promote tumor growth in mice with PDAC when administered alone, when combined with anti-PD-1 therapy, a form of ICB treatment, silvestrol reduced the size of PDAC tumors by disrupting the ARF6-AMAP1 pathway in KRAS-mutated cells..."

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