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.

An introduction to what cancer is and how it is the by-product of broken DNA replication.

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:

"Resistance to therapy is a major hurdle in current cancer treatments. A major part of the problem is heterogeneity. Tumors, by their nature, have multiple cell lineages with varying characteristics. Among these are cancer stem cells (CSCs). CSCs can regenerate a tumor even after treatment kills many of its other cells. And they can go dormant, transport drugs outside the cell membrane, avoid apoptosis, and express resistance-conferring non-coding RNAs, all of which boost tumors’ resistance to treatment. A new review describes common CSC surface markers, deregulated signaling pathways, and resistance mechanisms as well as the status of research into CSC therapies. Current therapies targeting CSCs do not address tumor heterogeneity or the complexity of the tumor microenvironment..."

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

Cancer is an everyday topic in the news and in most extended families. The types and treatment of cancers can be complex and confusing. Module 2 provides students with knowledge and resources concerning the development of cancers related to environmental factors. It is important for students to realize that the state-of-the-art of cancer treatment prior to 1986 (the year the trial started) is not the current state-of-the-art. Treatment of many types of cancer has progressed enormously due to medical research. Treatment of childhood leukemia is one of the success stories in cancer treatment. Research linking childhood leukemia to environmental factors or a specific environmental factor has progressed more slowly. Several links are provided within the website that students can read to become aware of environmental factors in Woburn that have been studied, including Woburn Chemical Industry, Woburn's Water Supply and Hematology of Leukemia. Several research articles are available for students to read and are cited within the searchable database at Bibliography & References.

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 the most commonly diagnosed cancer in women worldwide. Despite better treatments, metastatic breast cancer remains incurable and is a major cause of cancer-related death. Cancer progression and metastasis involve multiple steps that are dependent on intercellular communication, but much remains to be understood about this process. A recent study examined one aspect of cancer cell communication: exosomes carrying microRNA (miRNA) cargoes. Researchers isolated exosomes from human breast cancer cell lines. Using cell migration and invasion assays, they found that the tumor-promoting capacity of exosomes was positively correlated to their cells of origin. The most differentially expressed miRNA was miR-7641, which could promote tumor cell progression and metastasis. Exosomal miR-7641 could promote tumor growth in a mouse model, and its levels were elevated in the plasma of patients with distant metastasis..."

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 immunosuppressive tumor microenvironment (TME) plays essential roles in cancer development and progression. Exosomes mediate crosstalk between tumor cells and other stromal or immune cells in the TME, but how tumor-derived exosomes promote the progression of bladder cancer, one of the most common types of cancer, remains unclear. To find out, researchers recently examined the effects of exosomes extracted from the conditioned medium (CM) of MB49 bladder cancer cells. The researchers found that the cancer-derived exosomes were ingested by mouse macrophages both in vitro and in vivo and that they induced macrophage polarization toward the immunosuppressive M2 phenotype. Exosome-secreting MB49 cells induced tumor growth in mice, but the exosome inhibitor GW4869 reduced tumor growth, macrophage M2 polarization and immunosuppression, confirming the pro-tumor effects of the cancer-derived exosomes..."

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:

"Viral infection can be devastating. But some viruses are an important part of therapies for fighting diseases like cancer. Adenoviruses are one example – they deliver deadly payloads to cancer cells without harming healthy tissue. Or do they? A recent study suggests that adenovirus infection could promote the formation of glioma stem cells, the self-renewing cells that keep brain tumors alive and spreading. Experiments on glioma cells derived from human patients showed that adenovirus infection promoted the formation of tumorspheres, solid, spherical formations that develop from self-renewing glioma stem cells. When transplanted into mice grafted with glioma tumors, these formations promoted tumor growth. A closer look revealed three signaling molecules that adenoviruses activate during this process: TLR9, a pro-inflammatory receptor, NEAT1, a non-coding RNA frequently overexpressed in human tumors, and STAT3, a protein linked to tumor formation..."

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

The human body is composed of trillions of cells. Each cell has a life cycle, in the same way that all living things do. In this seminar you will explore and reflect on how eukaryotic cells (that is, cells with a nucleus) reproduce and make copies of themselves.Sometimes there can be mistakes in the copying process, which can lead to cancer. Part of this lesson will show how cancers can happen.Additionally, you will be challenged to create a model of the process to demonstrate your learning of this topic.

In this course we will explore how altered metabolism drives cancer progression. Students will learn (1) how to read, discuss, and critically evaluate scientific findings in the primary research literature, (2) how scientists experimentally approach fundamental issues in biology and medicine, (3) how recent findings have challenged the traditional “textbook” understanding of metabolism and given us new insight into cancer, and (4) how a local pharmaceutical company is developing therapeutics to target cancer metabolism in an effort to revolutionize cancer therapy.

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:

"Overexpression of the protein EGFR is associated with various cancers. That’s made EGFR inhibitors a promising class of anti-cancer drugs. Although EGFR targeting of colorectal cancer is well understood, some patients respond unexpectedly well. A pair of studies have studied why cancers with the KRAS G13D mutation respond well to EGFR inhibition. They propose different mechanisms to explain the beneficial response. One study suggests that a tumor-suppressing protein known as NF1 decreases the KRAS activity that drives cancer growth. The other suggests that NF1 actually decreases NRAS and HRAS but not KRAS. Now, a new study appears to provide some clarity in the matter. Using antibodies specific to each RAS protein, researchers showed that an abundance of NF1 downregulates the proteins NRAS and HRAS in colorectal cancer cells, with no effect on KRAS..."

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:

"Angiogenesis, the formation of new blood vessels, is a popular target of various therapies. Some therapies, like those used in tissue engineering, are designed to promote angiogenesis and new tissue growth, while other therapies, such as those designed to fight cancer, aim to suppress angiogenesis— a lifeline for tumor cells. Unfortunately, these therapies aren’t always effective. Now, a new mathematical model could help researchers understand what molecular levers to pull to effectively modulate angiogenesis. Trained on published experimental data, the model predicted the effects of activating two common targets of angiogenesis-based therapies: vascular endothelial growth factor, or VEGF, and fibroblast growth factor, or FGF. Computational experiments showed that the two factors modify both the ERK signaling pathway, which is linked to cell proliferation, and the Akt signaling pathway, which is associated with cell survival and 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:

"Cytotoxic T lymphocytes such as T and NK cells are critically involved in the immune response to cancer development. Their cell-surface receptors coordinate to precisely regulate their function, and dysregulation of these molecules has been linked to immune escape. A recent study identified molecules targeting one of these receptors: T cell immunoglobulin and ITIM domain (TIGIT). TIGIT is a novel immune checkpoint molecule involved in T and NK cell anergy. Binding with its ligand, PVR, can induce immune tolerance, allowing cancer cells to escape immune surveillance. To facilitate the design of inhibitors targeting TIGIT/PVR binding, researchers examined the binding interaction in silico. Their results suggested that the loops of PVR undergo a major rearrangement upon binding to TIGIT. The potential residues critical for the TIGIT/PVR interaction were discovered, and simulation analysis identified four PVR mutants with enhanced affinity to TIGIT..."

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

This open textbook for Concepts of Fitness and Wellness at Georgia Highlands College was created through a Round Seven ALG Textbook Transformation Grant.

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:

"Prostate cancer is the most common cancer and the second most common cause of cancer-related death in men. The standard treatment is androgen deprivation therapy (castration), but prostate cancer becomes resistant to this treatment over time. Targeting the androgen receptor seems logical but has had little effect on patient survival so far. Intriguingly, a chemical related to estrogen, 4-hydroxyestradiol (4-OHE2), also promotes cancer occurrence and progression. A recent study examined the role of 4-OHE2 in castration-resistant prostate cancer (CRPC) cells. The protein CYP1B1 is involved in the production of 4-OHE2, and CYP1B1 was found to be elevated in CRPC cells. In addition, 4-OHE2 promoted ERα transcriptional activity in CRPC cells. 4-OHE2 promoted tumor formation through the IL6-STAT3 pathway, which sends inflammatory signals important in many cancers..."

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, or NSCLC, is the leading cause of cancer-related death worldwide. While radiation therapy can be powerful against NSCLC, lung cancer cells may develop resistance. A new study traces this “radioresistance” to a protein that interacts with estrogen receptor ERβ. ERβ is known to alter the radiation sensitivity of certain breast cancer cells. So researchers wondered: Might ERβ might do the same in cells affected by NSCLC? To find out, they blasted lab-grown cells with gamma rays and tracked ERβ’s behavior. Results showed that radiation indirectly activated ERβ-based defenses through the protein CLPTM1L. CLPTM1L is abnormally expressed in the cytoplasm of many human lung cancer cells, especially in cells affected by NSCLC. A closer look revealed that radiation caused CLPTM1L to migrate to the nucleus of cancer cells, where it gained direct access to ERβ’s genetic machinery and its ability to induce radioresistance..."

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 one of the most prevalent forms of cancer worldwide. Due to its complex pathology, breast cancer is often diagnosed late in its development—when it has already spread to other body parts. STAT3 is one protein known to play an important role in breast cancer, regulating gene expression within tumor cells to drive cancer progression, but growing evidence shows that STAT3 plays an equally important role outside of tumor cells—within the “tumor microenvironment”. Here, STAT3 suppresses immune defenses through interactions with various cells including myeloid-derived suppressor cells (MDSCs), macrophages, and dendritic cells (DCs). Interestingly, STAT3’s capacity to bypass these defenses relies on pathways for both immune suppression and activation. These findings make STAT3 an attractive target for anticancer therapies, which could help patients with breast cancer receive effective treatment as early as possible..."

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

Students learn about biomedical engineering while designing, building and testing prototype surgical tools to treat cancer. Students also learn that if cancer cells are not removed quickly enough during testing, a cancerous tumor may grow exponentially and become more challenging to eliminate. Students practice iterative design as they improve their surgical tools during the activity.

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 eIF6 is involved in ribosome formation and mRNA translation and is essential for the growth and reproduction of cells, including cancer cells. However, eIF6’s role in oral squamous cell carcinoma (OSCC) remains unclear. To learn more, researchers recently analyzed eIF6 in 233 OSCC samples and in OSCC cell lines. They found that cytoplasmic eIF6 expression was abnormally high in OSCC tissues and was associated with tumor size and clinical grade. Upregulating eIF6 promoted OSCC cell growth, migration, and invasion in vitro and enhanced tumor growth in vivo. eIF6 also encouraged epithelial-mesenchymal transition (EMT), a process necessary for cancer cell migration, in OSCC cells, but depletion of eIF6 (with sh-eIF6-2) suppressed the cancer-enhancing effects. Mechanistic studies revealed that eIF6 exerted its tumor progression-promoting effects by activating the AKT signaling pathway, and further experiments confirmed that eIF6 and AKT directly interacted in the cytoplasm..."

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 cells’ behavior depends on their underlying structure – the cytoskeleton. A dynamic network of protein filaments and tubules, the cytoskeleton drives motion. It is also central to cell development – and cancer. One protein at the center of cytoskeletal events is Merlin. Like other FERM-family proteins, Merlin mediates interactions between actin and transmembrane receptors, translating signaling into motion, adhesion, and growth regulation. Because it regulates such essential pathways, Merlin has a dual role in human biology. Its connection to the cytoskeleton is essential for embryonic development. and the signaling pathways it orchestrates are required for cell differentiation in later stages of development. At the same time, Merlin also maintains appropriate cell signaling levels and growth, preventing cancer progression. Further studies will shed light on Merlin's role in different contexts, improving our understanding of therapeutic strategies for disorders of both development and 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:

"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.