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 signaling pathways direct protein expression, cellular metabolism, and cell growthIdentify the function of PKC in signal transduction pathwaysRecognize the role of apoptosis in the development and maintenance of a healthy organism

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:

"Researchers have identified a gene important to the growth and spread of gastric cancer, opening the door to new understanding of this deadly disease. The gene, known as SIX1, has been implicated in disease progression in several cancers, but its link to gastric cancer wasn’t clear. This ambiguity prompted researchers at China Medical University to take a closer look at the role of SIX1 in gastric cancer cells. The team started by measuring SIX1 protein expression in gastric tumors and adjacent non-tumor tissue collected from 208 patients. They found high levels of SIX1 in nearly half the tumor samples and virtually none in the non-cancerous tissue – a pattern suggesting that SIX1 is an important biomarker for gastric cancer. This notion was supported by the finding that patients with higher levels of SIX1 had more advanced disease than those with moderate SIX1 expression..."

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:

"Acute lymphoblastic leukemia (ALL) is the most common cancer in children, and 85% of cases are B-cell ALL (B-ALL). Although the prognosis is usually good, 10–15% of patients have relapsing or refractory disease, which can lead to poor outcomes. To aid in the development of better treatments for these patients, a new study investigated the role of netrin-1 in B-ALL, as this axon guidance protein has been linked to tumorigenesis in many cancers. In the study, serum netrin-1 levels were higher in children with B-ALL than in children without cancer, and when the children with B-ALL were grouped by risk stratification, the high- and intermediate-risk groups had higher netrin-1 levels than the low-risk group. In vitro, recombinant netrin-1 prevented apoptosis of B-ALL cells, thus supporting cancer cell survival by interacting with the receptor Unc5b to activate the FAK-MAPK pathway. However, netrin-1 did not affect B-ALL cell migration..."

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:

"Colorectal cancer is the third most common form of cancer in the world and one of the most lethal. Fortunately, researchers are beginning to find weaknesses in how it operates. One team from Korea is focusing on specialized cells known as cancer stem cells, or CSCs. Like normal stem cells, CSCs possess the ability to self-renew and differentiate into multiple cell types, making them an engine for the spread or recurrence of colorectal cancer. Disrupting CSC activity, therefore, could be one way to shut down colorectal cancer. To do that, the Korean team targeted the Wnt/β-catenin and RAS/MAPK signaling pathways. These pathways control CSC properties and tend to be over activated in patients with colorectal cancer. Administering KYA1797K, a small molecule that destabilizes β-catenin and RAS proved effective in mice and in lab-grown human cells. KYA1797K suppressed CSCs’ capacity to regenerate and therefore limited tumor growth..."

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:

"Tumor cells create an environment that fosters growth by communicating with surrounding tumor and non-tumor cells. Understanding and ultimately disrupting this communication is the goal of many emerging anticancer strategies. A recent study recently examined how the oncogene YAP orchestrates cellular communication during the formation of liver tumors. Researchers identified several secreted factors that are induced by YAP to adjust cell-cell communication in support of tumor growth. One of these, a protein known as PAI-1, regulates the expression of factors associated with cellular senescence and was found to be linked to poor clinical outcomes in patients with liver cancer. Experiments showed that YAP, with the help of a separate protein (TEAD4), controls PAI-1 expression and secretion ultimately generating a tumor-supportive microenvironment..."

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:

"New genes involved in tumorigenesis are constantly being discovered. Potassium Channel Tetramerization Domain (KCTD)-containing proteins have historically been involved in neurodevelopmental and neuropsychiatric disorders, obesity, or signal transduction pathway modulation. Recently, this diverse group of proteins has been shown to be linked to cancer. KCTD proteins share a conserved BTB domain that allows for protein-protein interactions. Ever-growing evidence suggests that these proteins are involved in protein degradation as well as a multitude of other biological functions in different cancers. Through their BTB domain, most KCTD proteins act as adapters to selectively recruit proteins for ubiquitination and degradation. But non-protein-degradation roles in DNA replication and repair, transcription, cell cycle control, tumor suppression, and tumorigenesis have also been found..."

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:

"Gastric cancer (GC) remains a major public health issue, especially in developing countries. However, recently discovered small RNA molecules called tsRNAs hold promise for the treatment of GC and other cancers. In a new study, scientists searched for tsRNAs that are dysregulated in GC and might therefore be targets for therapy. They found that the tsRNA tRF-Val-CAC-016 was downregulated in GC samples from patients. In vitro, upregulation of this tsRNA in GC cell lines suppressed cell proliferation. Mechanistic studies revealed that tRF-Val-CAC-016 normally inhibits the oncogene CACNA1d, thereby regulating the MAPK signaling pathway to limit proliferation, suggesting that the downregulation of tRF-Val-CAC-016 observed in GC allows the cancer cells to replicate. In mice, treatment with a tRF-Val-CAC-016 mimic decreased GC tumor growth, confirming this tsRNA’s therapeutic value..."

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