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 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:

"Epigenetic DNA modifications, like methylation, heritably alter gene expression without changing the genetic code. Aberrant epigenetic alterations and dysregulated methylation often drive cancer development. Identifying such alterations could lead to new cancer biomarkers or treatment targets. Colorectal cancer in particular could benefit from epigenetic biomarkers, as it is the third deadliest cancer globally and has limited early detection methods. In a recent study, researchers screened methylation databases of colorectal cancer patients, and they honed in on HAND2, a transcription factor whose promotor region was frequently methylated in these patients. In the lab, experiments demethylating HAND2 reverted its expression in cultured colorectal cancer cells. Demethylation of HAND2 inhibited pro-cancer behavior — proliferation, invasion, and migration — in these cells. HAND2 demethylation also suppressed tumor growth relative to controls in tumor xenograft experiments..."

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:

"Breast cancer is a leading cause of cancer-related death among women worldwide. One process that fuels the proliferation, survival, and migration of breast cancer cells is aerobic glycolysis. In normal cells, this conversion of glucose into lactate is normally reserved for low-oxygen conditions. Researchers have now identified a tumor-suppressing protein that helps regulate aerobic glycolysis in breast tumors. HRD1 is an enzyme known to suppress breast cancer proliferation and invasion. Experiments on human breast cancer cells clearly showed that upregulation of HRD1 decreased aerobic glycolysis. and subsequently inhibited breast cancer proliferation and invasion. This effect was found to be mediated by the enzyme PFKP. PFKP downregulation allowed HRD1 to inhibit the aerobic glycolysis and spread of breast cancer cells. These findings point to a new regulatory role for HRD1 and offer a possible target for future breast cancer therapies..."

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 frequently diagnosed cancer and the second leading cause of cancer-related death in the world. Understanding the associated mechanisms is critical to the development of strategies to treat patients with colorectal cancer. Emerging evidence suggests that LOXL1, a lysyl oxidase, is a promising drug candidate for its effects on malignant cancer progression. Now, a molecular-level study could indicate why. Researchers examined the effects of LOXL1 on tumorigenicity and metastasis ability in lab-grown colorectal tumor cells and mouse xenografts. In vitro, LOXL1 overexpression dramatically reduced migration, invasion, and colony formation. In mice, LOXL1 overexpression drastically inhibited metastatic progression and tumor growth. Further experiments showed that LOXL1 exerted its effects by inhibiting the transcriptional activity of Yes-associated protein (YAP). by interacting with MST1/2 and increasing the phosphorylation of MST1/2 thereby activating the Hippo signaling pathway..."

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) remains deadly, indicating a need for better diagnosis and treatment strategies. The protein OVOL2 is known to suppress tumor development in NSCLC and other cancers. However, it’s unclear whether OVOL2 exerts its anticancer effects by disrupting aerobic glycolysis, the main energy pathway in tumor cells. To find out, researchers recently investigated OVOL2 signaling in NSCLC. OVOL2 was downregulated in NSCLC cells and mouse NSCLC tissues compared to normal lung (NL) samples. Specifically, OVOL2 was negatively regulated by NF-κB signaling via the ubiquitin–proteasome degradation pathway. However, lentivirus (LV)-mediated overexpression of OVOL2 reduced NSCLC cell survival in vitro, and OVOL2 impaired aerobic glycolysis in NSCLC cell lines and mouse xenograft models. OVOL2 exerted its beneficial effects by binding to P65 and inhibiting P300 recruitment while facilitating HDAC1–P65 binding..."

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:

"Oncogenic PIM kinases and the tumor suppressor LKB1 regulate cell growth and metabolism in different directions. LKB1 suppresses tumorigenesis largely by phosphorylating and activating the energy sensing kinase AMPK. Anti-oncogenic PIM inhibitors also increase AMPK phosphorylation. However, the exact mechanism by which PIM inhibition affects AMPK remains unclear. A recent study explored the potential PIM-LKB1 interaction related to AMPK phosphorylation in prostate (PC3) and breast (MCF7) cancer cells. Inhibition of activity (by DHPCC9 or AZD1208) or expression (by triple knockout, TKO) of all three PIM kinases increases AMPK phosphorylation. These effects are LKB1-dependent, suggesting that PIM kinases regulate AMPK via LKB1. Additional assays confirmed that PIM kinases phosphorylate LKB1 to inactivate it, identifying LKB1 as a novel PIM substrate. In a chick embryo xenograft model, LKB1 knockout increased tumorigenic growth of prostate cancer cells..."

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:

"The protein IFNα can reduce growth and promote apoptosis of cancer cells by stimulating genes such as PML, whose deficiency is linked to tumorigenesis, but the contributions of different PML isoforms to the anticancer effects remain unclear. Given that PML-II positively regulates genes that are induced during the type I IFN response, researchers recently investigated whether and how PML-II participates in IFNα-induced cell death using a cervical cancer cell line. In cells with PML-II deletion (siPML-II), death during IFNα stimulation was reduced, and IFNα-induced ISG54 mRNA expression was attenuated. In addition, silencing PML-II decreased the expression of TRAIL and PUMA during IFNα stimulation, indicating that the extrinsic and intrinsic apoptosis pathways were blunted..."

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:

"Breast cancer remains one of the most common cancers among women, indicating that better treatments are needed. The drug THZ1 is effective against triple-negative breast cancer, which frequently features overexpression-inducing mutations in the protein p53. However, THZ1 is ineffective against breast cancer cells with nonmutated (wild-type, WT) p53. To improve treatment options, researchers recently tried to increase the THZ1 sensitivity of WT p53 breast cancer cells. Treating the cells with nutlin-3, a molecule that indirectly prevents p53 degradation, enhanced the killing ability of THZ1, and overexpression experiments confirmed that this sensitization was due to upregulation of functional p53. Further investigation into the mechanism revealed that p53 accumulated in the nuclei and mitochondria of the dying cells after nutlin-3 and THZ1 treatment..."

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:

"Peptide hormones are important signaling molecules within the body. One such peptide is the secreted protein augurin, which is encoded by the gene Ecrg4, whose expression has been reported in a wide range of human tissues. The product of the gene Ecrg4, the augurin precursor ECRG4, has been predicted to be cleaved to originate different peptides. Augurin is implicated in a variety of processes, including tumorigenesis, inflammation, and infection. It is also involved in the regulation of the hypothalamo-pituitary adrenal axis and in osteoblast differentiation. Augurin is implicated in the modulation of well-known signaling cascades, including NF-kB, PI3K/Akt/mTor, Wnt-beta catenin, and apoptosis pathways, however, the molecular mechanisms underlying its action remain largely unexplored. Given its involvement in health and disease, augurin is an attractive target for the discovery of new therapeutic agents for human pathologies..."

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