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 remains the second leading cause of death worldwide, partly because cancer cells can resist chemotherapy. In one resistance mechanism, the Nrf2 signaling pathway helps cancer cells survive the oxidative stress induced by chemotherapy drugs. Therefore, compounds that inhibit Nrf2, like phenolic compounds, might be promising anticancer agents. Phenolic compounds are abundant in traditional herbal products known for their anticancer effects, such as ginger, turmeric, and green tea. Some phenolic compounds, like those in Chinese cinnamon, keep Nrf2 from entering the nucleus, where it normally exerts its activity, while others, like those in yellow azalea, prevent Nrf2 expression. These changes in turn block Nrf2-mediated antioxidant systems, making the cancer cells susceptible to drug-induced oxidative stress or even inducing cell death without the help of other cancer-fighting drugs..."

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:

"In breast cancer cells, malignant behaviors such as migration depend on calcium release from intracellular storage sites. This process is mediated by phospholipase C (PLC)-γ1, which is typically activated by receptor tyrosine kinases. However, PLC-γ1 can also be activated by phosphatidic acid, a product of phospholipase D (PLD). PLD expression and activity are associated with breast cancer cell invasion and migration, but it is unknown whether PLD is needed for PLC-γ1-mediated calcium release. A recent study investigated this possibility in two human breast cancer cell lines. The researchers found that treating the cells with the PLD inhibitor FIPI prevented PLC-γ1-mediated calcium release and cell migration without affecting PLC-γ1 directly, indicating that PLD is indeed connected to migration-related calcium release in breast cancer cells. Silencing of a specific form of PLD, PLD1, also inhibited PLC-γ1-specific calcium release, demonstrating that PLD1 was important for FIPI’s effects..."

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:

"Phospholipid scramblase 1 (PLSCR1) is the most studied member of its protein family and has a complex array of suggested functions. While PLSCR1 was first described as a plasma membrane protein, it has subsequently been found in other cellular compartments and implicated in numerous cellular pathways including apoptosis, intracellular trafficking of membrane proteins, and pro-inflammatory events. PLSCR1 interacts with various effectors, mediators, and regulators that then contribute to distinct cellular processes. While most PLSCR1 interactors are thought to be cell-type specific, the mechanisms of PLSCR1's regulatory functions are often shared. But not all PLSCR1 interactors are endogenous in origin; PLSCR1 also interacts with exogenous viral proteins. These interactions regulate viral uptake and spread in both pro- and anti-viral ways..."

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:

"A recent study published in the British Journal of Nutrition suggests that enterolactone, an estrogen-like compound formed by the breakdown of whole grains and other plant-based foods by gut bacteria, could protect against the risk of death due to colorectal cancer—at least, for women. For men, just the opposite could be true: high concentrations of the compound might actually increase that risk. The findings, published as part of a special issue on nutrition and cancer, point to a potentially significant link between diet and survival after colorectal cancer that warrants a much closer look by researchers. The authors of the study reached those conclusions by examining data from the “Diet, Cancer and Health” study, an ongoing cohort study of older men and women in Denmark. Specifically, they compared the death outcomes of people with varying levels of enterolactone in their blood plasma, before being diagnosed with colorectal cancer..."

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:

"Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Treatments for HCC are limited, and the survival rate remains low. Now, a new study suggests a novel treatment that relies on a unique method of preventing tumor growth. The study focuses on Plasmodium, the parasite that causes malaria. Interestingly, infection with Plasmodium can boost immune cell function, and Plasmodium infection is known to have an antitumor effect. Researchers used a mouse model of HCC to examine the effect of Plasmodium infection on HCC progression. Their results showed that Plasmodium infection efficiently inhibited tumor progression and prolonged survival. Plasmodium infection suppressed tumor angiogenesis, cutting off the tumor’s blood supply. Plasmodium infection also reduces the number of tumor-associated macrophages through malarial pigment. These macrophages help to build blood vessels within tumors..."

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 growth relies upon the production of new blood vessels, also known as angiogenesis, to supply adequate oxygen and nutrients to the cells. Angiogenesis blockade therapy was thus developed to impair blood vessel growth and cut off this supply. This is accomplished with the use of medicines targeting pro-angiogenic factors such as vascular-endothelium growth factor (VEGF), fibroblast growth factor (FGF), and stem cell factor (SCF). For example, bevacizumab is a monoclonal antibody that targets VEGF and has shown promise in combating non-small-cell lung cancer, but the use of angiogenesis inhibitors has also been linked to an increase in local tumor invasiveness and the spread of cancer to other parts of the body. New evidence suggests that these issues can be diminished by administering anti-angiogenic agents in combination with other strategies..."

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:

"Glioblastoma multiforme (GBM) is a deadly brain cancer that affects both adults and children. GBM remains mostly incurable because of the nonuniform nature of GBM cells and the numerous mechanisms involved. However, noncoding RNA molecules called circular RNAs (circRNAs) may be valuable targets for GBM treatment, because these molecules can promote or suppress cancer-related processes like cell proliferation, cell death, invasion, and chemoresistance. For example, various circRNAs can regulate pathways that are dysregulated in GBM, such as the PI3K/Akt/mTOR, Wnt/β-catenin, and MAPK pathways. Other circRNAs can positively or negatively regulate tumor blood supply establishment and metastasis to influence GBM progression. CircRNAs are stable and present in numerous body fluids, and some are associated with tumor grade and outcomes, making them promising biomarkers. In addition, silencing or overexpressing certain circRNAs in patients may help treat GBM or improve patients’ responses to other treatments..."

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:

"Alzheimer’s disease and glioblastoma are the most common and devastating diseases in neurology and neurosurgery departments. In glioblastoma, the Alzheimer’s disease-related protein Presenilin1 limits cell proliferation by inhibiting the Wnt/β-catenin pathway. However, the function of this protein and the underlying mechanism are unclear. To learn more, researchers recently examined Presenilin1’s effects on glioblastoma in vitro and in vivo. Presenilin1 repressed glioblastoma cell migration, invasion, and mesenchymal transition in vitro. Interestingly, its expression was positively correlated with that of Sortilin, a pro-invasion molecule in glioma. Presenilin1 interacted with Sortilin at the transmembrane domain and inhibited its expression via cleavage, enabling β-catenin phosphorylation and repressing invasion in glioblastoma cells. In mouse subcutaneous and intracranial transplantation models, Presenilin1 stimulation dramatically reduced glioblastoma invasion and mesenchymal transition..."

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

This lesson culminates the unit with the Go Public phase of the legacy cycle. In the associated activity, students depict a tumor amidst healthy body tissue using a Microsoft Excel® graph. In addition, students design a brochure for both patients and doctors advertising a new form of painless yet reliable breast cancer detection. Together, the in-class activity and the take-home assignment function as an assessment of what students have learned throughout the unit.

This course covers current understanding of, and modern approaches to human disease, emphasizing the molecular and cellular basis of both genetic disease and cancer. Topics include: The Genetics of Simple and Complex Traits; Karyotypic Analysis and Positional Cloning; Genetic Diagnosis; The Roles of Oncogenes and Tumor Suppressors in Tumor Initiation, Progression, and Treatment; The Interaction between Genetics and Environment; Animal Models of Human Disease; Cancer; and Conventional and Gene Therapy Treatment Strategies.

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:

"(Pro)renin receptor, or (P)RR, is a cell receptor expressed throughout the body. Historically, knowledge about (P)RR has been limited to its functions in the heart and kidneys. But now, growing evidence suggests (P)RR plays a major role in various cancers. Over the last 5 years, researchers have discovered that certain cancers produce abnormally high amounts of (P)RR . which can trigger the formation of tumors in the pancreas, colon, and brain. A recently published review outlines the numerous newly recognized roles of (P)RR in cancer. as well as ways that (P)RR can be used against cancer. including as a target for monoclonal antibody therapy. To read the full review, visit biosignaling.biomedcentral..."

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:

"A major turning point for tumor immunotherapy was the discovery of immune checkpoint proteins, which suppress immunity to facilitate tumor growth. The discovery prompted the development of immune checkpoint inhibitors (ICIs) that can help fight even metastatic and chemoresistant cancers. ICIs that target the proteins CTLA-4, PD-1, and PD-L1 are particularly promising for cancer treatment. These drugs can be used either alone or with other therapies to enhance treatment efficacy. For example, they can be combined with traditional chemotherapy, radiotherapy, antiangiogenic therapy, and cancer vaccines to improve outcomes. In addition, combinations of CTLA-4- and PD-1-blocking ICIs can be used to treat cancers like melanoma. However, despite the encouraging results in some studies, many patients fail to respond to ICIs. ICIs can also exert various immune-related adverse effects on the skin, colon, liver, lungs, kidneys, and heart, and some tumors can become resistant to the drugs..."

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:

"Epithelial cells form continuous coverings over all surfaces in the human body and have distinct top and bottom sides, but they can sometimes transform to function more like mesenchymal cells, losing their tight connections to adjacent cells and gaining mobility. This process, known as epithelial–mesenchymal transition (EMT), can be beneficial for wound healing and embryonic development but can also promote the progression of cancer. Research suggests that acetylation, or the addition of an acetyl group to another molecule, may play an important role in EMT and that this process is controlled by the activity of lysine acetyltransferase enzymes. In particular, the acetylation of specific histones, proteins that provide structural support to chromosomes and can regulate gene activity, could promote EMT. But recent studies have also shown that the acetylation of non-histone proteins could also be involved. For example, the acetylation of the protein E-cadherin has been found to accelerate EMT in 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 human protein Tid-1 sits at the nexus of many key cellular processes and signaling pathways. These processes include cellular proliferation, growth, survival, aging, apoptosis, and even movement. Tid-1 is a member of the heat shock protein 40 family and helps other proteins fold correctly after translation or refold after a damaging stress event. Dysregulated Tid-1 behavior is involved in numerous human diseases including cancers, cardiomyopathies, and neurodegenerative disorders. Given its wide influence within the cell, Tid-1 could be a key biomarker or even therapeutic target for these diseases, but to leverage Tid-1 effectively, researchers need to understand its functionality in detail. To this end, a team of scientists consolidated the current research on human Tid-1. They found that Tid-1’s protein-protein interactions corresponded to its roles in various diseases and provide insight into how Tid-1 affects pathogenic developments..."

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:

"herapeutic monoclonal antibodies bind proteins on tumors, which can enable the killing of cancer cells. However, there can be collateral damage to healthy tissues that also express those proteins. At CytomX , researchers are exploring the use of a new class of antibodies called Probody™ therapeutics. Masks attached to the ends of a Probody therapeutic can “blindfold” the antibody and reduce its binding to healthy tissues. However, when the antibody encounters a tumor, proteases —enzymes in the tumor microenvironment—can remove these masks to activate the antibody. In this way, Probody therapeutics are designed to maximize anti-cancer activity while minimizing harm to healthy tissue. In a new study, researchers used computer modeling to predict how Probody therapeutics can be tuned to achieve this effect. This model, comprising thousands of equations, estimates the amount of both masked and unmasked (or activated) forms of the antibody in the tumor and in the rest of the body after dosing..."

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

Students are introduced to the physical concept of the colors of rainbows as light energy in the form of waves with distinct wavelengths, but in a different manner than traditional kaleidoscopes. Looking at different quantum dot solutions, they make observations and measurements, and graph their data. They come to understand how nanoparticles interact with absorbing photons to produce colors. They learn the dependence of particle size and color wavelength and learn about real-world applications for using these colorful liquids.

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:

"Radiation therapy is a powerful way to kill cancer cells or slow their growth, but radiation can have unintended effects on surrounding cells. In a new study, researchers report that X-rays could actually help cancer cells gain a foothold in otherwise healthy tissue. The team blasted breast cancer cells cultured in the lab with different doses of X-rays. The cells released a cocktail of molecules in response including VEGF-A, a protein that triggers blood vessel formation. The team then transferred that molecular cocktail to healthy endothelial cells. Over time, those healthy cells showed a significantly enhanced ability to form the building blocks of blood vessels. This so-called “bystander effect” points to one way that cancer cells can cling to life even when zapped with radiation, and although the results are constrained to cells cultured in the lab, they could help inform researchers on how radiation therapy might do more harm than good..."

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:

"Ras is a key signaling protein that controls cell fates, including proliferation, differentiation, migration, and apoptosis, and Ras effectors are proteins that influence Ras-regulated signaling pathways. Because mutations in Ras have been found to play a key role in cancer initiation and progression, scientists hope that obtaining a clearer understanding of Ras–Ras effector interactions will improve the development of effective cancer treatments. To meet this need, a team of researchers recently constructed a comprehensive Ras–Ras effector network with information obtained from public pathway and protein interaction databases. The network was composed of 2290 proteins, including 12 classes of Ras effectors, connected through 19,080 protein–protein interactions, with an increasing number of interactions occurring in each layer of the 3-layer signaling network..."

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:

"Esophageal cancers are common globally but are difficult to treat and have a poor prognosis. Esophageal squamous cell carcinoma (ESCC) is especially dangerous and has poorly understood molecular mechanisms. A recent study took a comprehensive look at the kappa opioid receptor (KOR), a protein that has been shown to influence the progression of other cancers. First, researchers examined existing patient datasets and found that ESCC tumors had reduced KOR expression and that lower expression of KOR was correlated with reduced patient survival. In the lab, they found that reducing KOR expression in cultured ESCC cells led to increased proliferation, invasion, and metastasis. When looking for potential mechanisms, they found that down-regulation of KOR activated the PDK1-AKT signaling pathway. It also led to invasion-related changes in cells, including invadopodia formation and cytoskeletal rearrangement. Reducing expression of KOR in mice led to increased metastasis and phosphorylation of the AKT enzyme..."

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:

"Our bodies must undergo tissue self-renewal in order to remain healthy, and cell death is an important part of self-renewal. Apoptosis is a mechanism of programmed cell death that maintains homeostasis without inflammation. As dying cells begin to dismantle, they signal to phagocytes to engulf them, a process called efferocytosis. The balance between these “find-me,” “eat-me,” and “don’t-eat-me” signals is critical. Unfortunately, because efferocytosis prevents inflammatory responses, these signaling pathways are often hijacked by cancer cells to facilitate immune escape. Although traditional cancer therapies, such as chemotherapy and radiation, kill cancer cells directly, the resulting apoptosis can increase efferocytosis and suppress the immune response, allowing for progression of residual cancer. A new strategy is to combine traditional therapies with those that inhibit efferocytosis, killing tumor cells while blocking the pathways that allow them to proliferate..."

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