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:

"Chemotherapy failure is a devastating problem that frequently results from cancer multidrug resistance (MDR). MDR is often due to overexpression of proteins called ABC transporters, which can pump chemotherapy drugs out of cancer cells. However, there are currently no effective treatments for MDR. A new study tested whether adagrasib (MRTX849), a promising anticancer drug targeting a mutant KRAS protein, can help fight MDR in cancer cell lines overexpressing the ABC transporter ABCB1 and in mice with ABCB1-overexpressing tumors. Both in vitro and in vivo, adagrasib increased the anticancer efficacy of conventional chemotherapy drugs. Adagrasib did not change the expression level or location of ABCB1 in the cells to exert its MDR- reversing effects. Rather, it suppressed the ability of ABCB1 to pump the drugs out of the cancer cells, likely by preventing binding of the energy molecule ATP, which normally powers the transporter’s pumping action..."

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:

"Apoptosis is a form of cell death that occurs as part of normal development. Once considered irreversible, apoptosis might not mark the end for all cells—including cancer cells. Growing evidence suggests that cancer cells can be rescued from the brink of death through a process called anastasis, which could explain how tumors resist anticancer therapies. From the Greek for “resurrection,” anastasis can occur through a variety of mechanisms, such as by arresting the activity of caspases, enzymes in charge of dismantling the cell during apoptosis by activating DNA repair mechanisms and by allowing cell fragments to fuse and continue living even after apoptosis has begun. Further studies are needed to explore how cancer cells cheat death through anastasis and how to adjust anticancer therapies accordingly..."

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 transcription factor Nrf2 plays paradoxical roles in cancer biology. Transient Nrf2 activation can protect against cancer development, but permanent Nrf2 activation promotes progression and treatment resistance. Persistent activation can be triggered by Keap1-inactivating mutations that cause Nrf2 nuclear accumulation and/or by mutations in the ETGE and DLG motifs of Nrf2, which are important regions for Nrf2–Keap1 interaction. Epigenetic silencing of Keap1 and disruption of the Nrf2–Keap1 interaction by other proteins can also aberrantly activate Nrf2. Given the detrimental effects of excessive activation, pharmacologically balancing Nrf2 activity is a promising avenue for cancer treatment. Numerous Nrf2 activators have been discovered or developed, such as the synthetic compound oltipraz (OPZ) and the plant-derived compound curcumin (CUR). In general, Nrf2 activators can promote the functions of antioxidants, phase II detoxification factors, and transducers..."

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:

"Gastrointestinal stromal tumors (GISTs) are the most common malignant tumors in a type of gut tissue called mesenchyme. They’re caused by mutations that activate receptor tyrosine kinase (RTK) enzymes, and treatment with RTK inhibitors is initially successful, but over half of patients develop resistance, indicating a need for better treatments. Researchers recently investigated whether the drug THZ1, an inhibitor of the protein CDK7 that’s effective in other cancers, could help. They first confirmed that CDK7, which helps regulate the cell life cycle and gene transcription, was overexpressed in high-risk human GISTs. They also found that CDK7 overexpression predicted a poor outcome. However, low-dose THZ1 exerted pronounced anticancer effects in GIST cells both in vitro and in a mouse model. THZ1 also synergized with the RTK inhibitor imatinib to increase its efficacy..."

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 most common cancers worldwide and has high rates of recurrence and death. In patients with advanced HCC and poor liver function, surgery and ablation aren’t very effective, so pharmacotherapy is typically used. However, traditional antitumor drugs don’t have ideal properties or efficacy, and they’re highly toxic to normal cells. Recently developed nanotechnologies have shown promise for improving drug kinetics and efficacy against HCC. For example, nanoparticles can deliver drugs to tumor tissues and affect specific cells and molecules in the tumor microenvironment. These nanocarriers can reach their targets passively (due to intrinsic tumor characteristics) or actively (via molecules engineered onto their surfaces). Drug release from the nanoparticles can be induced by conditions common in tumors, such as hypoxia and acidification or by externally applied stimuli, such as light, heat, ultrasound, and magnetic fields..."

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:

"Gallbladder cancer (GBC) is becoming increasingly common, especially in American Indian and Southeast Asian populations. Early GBC can be successfully removed with surgery, but advanced GBC has a poor prognosis . and the existing treatments have many side effects. To explore better therapies, researchers recently investigated the anti-GBC effects of penfluridol, an antipsychotic drug with anticancer activity. In vitro, penfluridol (PF) strongly inhibited the replication and invasion of three GBC cell lines, confirming its anti-GBC potential, but it also dramatically increased glucose consumption via glycolysis, which is a hallmark of cancer. Specifically, penfluridol activated the AMPK/PFKFB3 glycolysis pathway. However, inhibiting glycolysis, particularly the AMPK/PFKFB3 pathway (with Compound C, CC) solved this problem enhancing penfluridol’s GBC-killing effects. The same synergistic effects were observed in mouse tumor models in vivo..."

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:

"Adoptive cell therapy is a powerful anticancer strategy in which patients are administered extra immune cells. Often, the cells are engineered to express chimeric antigen receptors (CARs) that recognize specific cancer cell proteins (antigens), enabling cancer targeting. The strength of the anticancer effect depends on structures within the CARs called costimulatory domains. One such domain, 4-1BB, activates the NFκB signaling pathway, but the relationship between the amount of antigen present and the strength of the elicited response isn’t well described. To help, researchers recently developed a mathematical model of NFκB signaling induced by a 4-1BB-containing CAR. Simulations revealed that the degree of NFκB pathway activation differed in response to different antigen concentrations, but the timing was consistent. The model performed well even when the input parameters were changed, suggesting its reliability under different conditions..."

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 cancer, tumor cells secrete chemicals that suppress immune function by upregulating the expression of immune “brakes”. Immunotherapy with checkpoint inhibitors can release these brakes to effectively treat certain types of cancer. However, other types of cancer are resistant to checkpoint inhibitors, so alternate treatments are needed. In mouse models, infection with the malaria parasite Plasmodium can activate immune defense against cancer. Similarly, global human epidemiological data indicate that malaria occurrence is inversely associated with cancer mortality. In mice, Plasmodium induces proinflammatory molecule production, immune cell activation, and subsequent systemic immune responses while simultaneously upregulating the expression of brake molecules through a feedback mechanism of the immune system to prevent unchecked damage by these immune responses..."

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.

Join Scripps' Bill Gerwick in an exploration of the potential uses of one of the most ancient of all life forms - blue-green algae - as a source for new pharmaceuticals with used ranging from anticancer compounds to drug screening. (54 minutes)

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:

"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:

"Breast cancer is the most common cancer among women, and metastatic breast cancer remains highly lethal. During metastasis, cancer cells migrate from the breast to areas called pre-metastatic niches, which are favorable for cancer growth. These niches are created with the help of small extracellular vesicles (sEVs) released by breast cancer cells. Via their protein and RNA cargoes, sEVs encourage inflammation in the niches and suppress immunity, allowing arriving cancer cells to escape immune detection. By promoting new blood vessel formation and leakage of existing blood vessels, sEVs ensure a supply of nutrients for cancer growth in the niches. They can also transform certain cell types in the niches into cancer-supporting cells called cancer-associated fibroblasts. The expression patterns of proteins called integrins in sEVs help determine exactly where metastatic cancer cells will settle, such as in the lungs, liver, or brain..."

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:

"Prostate cancer is one of the most common and deadliest cancers among men. Reducing the levels of male hormones is the first-line treatment, but many cases become resistant to this “chemical castration”. Immunotherapies that leverage or improve the tumor-killing abilities of immune cells called macrophages might be viable alternatives but so far, there is limited preclinical or clinical evidence as to whether these therapies are effective. Researchers recently used a mouse model to explore whether a macrophage-activating drug called VSSP can successfully treat castration-resistant prostate cancer. VSSP inhibited tumor growth in surgically castrated mice with less-aggressive prostate cancer, but not in those with castration-resistant prostate cancer. The scientists next treated macrophages with VSSP in the laboratory and administered them to mice with castration-resistant cancer. They found that the VSSP-treated macrophages reduced tumor growth in the mice..."

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 an aggressive disease that kills almost 900,000 people each year, but chemotherapy, a common treatment, has toxic side effects and can induce resistance, resulting in treatment failure and relapse. One alternative is to use bacteria to fight cancer directly or to deliver drugs to target tissues. However, many of the bacteria tested so far are pathogenic and therefore carry risks of infection. In a recent study, researchers created an engineered probiotic to treat colorectal cancer orally. They isolated the nontoxic lactic acid bacterium Pediococcus pentosaceus from the Korean food, kimchi, and programmed it to carry P8, a previously identified candidate protein for colorectal cancer treatment. In a mouse colorectal cancer model established with human cancer cells, the engineered probiotic, PP\\*-P8, limited tumor sizes and growth rates. Furthermore, in mice with chemical-induced colitis-associated cancer, the probiotic caused polyp regression and ameliorated gut microbiota disruption..."

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