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 ATF5 plays a vital role in the formation of several cancers, including breast, lung, ovarian, pancreatic, rectal, and liver cancer. But ATF5’s function in esophageal cancer—one of the most common forms of cancer worldwide—remains unclear. To find out, researchers monitored the activity of ATF5 in esophageal cancer tissues. Much like in other cancers, ATF5 was upregulated in esophageal cancer tissues cultured in the lab, and ATF5 overexpression promoted the proliferation, migration, and invasiveness of esophageal cancer cells. Silencing ATF5, however, inhibited these abilities. In fact, in mice, silencing ATF5 hampered tumor growth. ATF5’s role as a lever that triggers tumor growth is believed to occur through an interaction with HIF1, a protein complex also known to promote the growth and spread of tumors. These findings suggest that the known anti-cancer effects of silencing ATF5 might also be powerful against esophageal 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:

"Many patients undergoing chemotherapy for cancer develop a serious side effect called chemotherapy-induced peripheral neuropathy (CIPN). CIPN involves pain, tingling, burning, or numbness in the hands and feet and is caused by neuroinflammation triggered by the protein HMGB1, but the exact mechanisms aren’t clear. To learn more and help find a treatment, researchers recently examined the plasma of human patients and mice with oxaliplatin-induced CIPN. They found that the levels of HMGB1 and its target enzyme MMP-9 (a pain marker) were elevated in CIPN plasma and that a higher dose of oxaliplatin was associated with higher HMGB1 levels and worse pain. In cell experiments, HMGB1 was degraded—and inflammatory molecule expression was suppressed—when the enzyme AMPK was activated suggesting that AMPK activation might be beneficial for CIPN. These effects were dependent on the protein SR-A1..."

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:

"Chronic myeloid leukemia, or CML, is a rare, slow-growing cancer of the bone marrow. It’s caused by the protein Bcr-Abl, which builds up and causes cells to grow and divide out of control. Now, researchers have identified one of Bcr-Abl’s close molecular partners and figured out how it might be forced to abandon Bcr-Abl and stop its deadly buildup. Experiments revealed that Bcr-Abl interacts with the heat shock protein HSP90AB1. HSP90AB1 supports Bcr-Abl’s rampant and deadly buildup in cells by blocking its entry into the nucleus. By deactivating HSP90AB1 in cultured cells with the antibiotic tanespimycin (17AAG), the researchers discovered that they could lock Bcr-Abl in the nucleus, reducing the spread of CML and programming CML cells for death. While more work is needed to understand how these processes play out in humans, these findings support the development of heat shock protein inhibitors as viable treatments for CML and other Bcr-Abl-associated malignancies..."

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:

"Bone morphogenetic proteins (BMPs) regulate cell-fate decisions during embryonic development. But after birth, dysfunctional BMP expression is linked to some human diseases, like carcinomas. In lung cancer, BMPs are reactivated and suppress AMPK signaling. Mitochondrial stress activates AMPK to a ‘normal’ level, where it promotes cancer cell survival, but AMPK can induce cell death if ‘hyperactivated.' BMPs inhibit LKB1, a kinase that can hyperactivate AMPK, making BMPs a potential therapeutic target. So, researchers tested two BMP inhibitors as a combination treatment with mitochondrial targeting agents. In lung cancer cell lines that express LKB1, the combination treatment activated AMPK and suppressed cell growth. The combination treatment was increasing nuclear localization of the aptly named apoptosis inducing factor (AIF) in these cells, an effect that depended on LKB1 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:

"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:

"Researchers from Japan have discovered a new method for using the immune system to attack liver cancer, the sixth most common cancer in the world. The researchers previously reported that patients with hepatitis had a higher risk of developing liver cancer when they expressed low levels of a gene called MICA. Building on this discovery, they set out to identify whether increasing the expression of this gene offers a way to treat the disease. MICA’s normal function is to alert the immune system to cells that are potentially dangerous, including those on their way to becoming cancerous. But if MICA levels drop, the immune system no longer recognizes these cells, allowing them to multiply. To find ways of turning MICA expression back on, the researchers screened a library of over 600 FDA-approved drugs on liver cancer cells and identified a single drug, vorinostat, that greatly increased MICA levels..."

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:

"Glioblastomas are deadly, malignant brain tumors. Even with current treatment methods, the median life expectancy after diagnosis is only 15 months. This extreme treatment resistance is primarily due to changes in the tumor microenvironment (TME). Glioblastomas sometimes recruit normal cells to aid growth, and neural progenitor cells (NPCs) have been observed migrating toward glioblastomas. Understanding the interaction between tumor and non-tumor cells in the TME is critical to developing new treatments. Recently, researchers examined the effects of extracellular vesicles (EVs) from glioblastoma cell lines on the cell lines themselves and mouse NPCs (mNPCs). In both glioblastoma cell lines and mNPCs, glioblastoma-derived EVs promoted proliferation and migration. Using a combination of proteomic profiling and laboratory assays, researchers examined the potential mechanisms of this effect and identified the PI3K-Akt-mTOR pathway as a key mediator..."

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:

"Organoids are 3-dimensional structures built in the laboratory from human pluripotent stem cells (hPSCs) to mimic human tissues and organs and have paved the way for research into new disease treatments that would never have been possible with traditional approaches. One field that is notably benefiting from the use of organoids is cancer research, particularly the study of glioma, the most common type of tumor originating in the brain. Poor outcomes are often associated with glioma because of its rapid growth and resistance to chemotherapy, but cerebral organoids hold promise for the development of novel treatments for this type of cancer, as they can be used as valuable tools to track tumor development and screen new drugs. Human cerebral organoids can also be grown from a patient’s own tissues for the creation of personalized cancer treatments, and they can be genetically engineered to study how common gene mutations affect tumor 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:

"A new study shows that abnormal production of nitric oxide in the body leads to the progression of breast cancer in mice. This finding could open the door to new treatments for early-stage breast cancer that stabilize the production of this pivotal molecule. Nearly one-third of newly diagnosed breast cancers in the US are early-stage lesions. Though technically pre-cancerous, about 40% of these lesions could progress to invasive cancers. Researchers don’t yet fully understand what drives these insidious formations. But various studies have reported a common link between cancer risk factors related to lifestyle—such as a high-fat diet, high alcohol consumption, and low physical activity—and abnormal production of nitric oxide. Normally, physiological stress triggers the production of large amounts of nitric oxide. This activates tissue-specific functions of neurons, muscles, immune cells, blood vessels and other specialized 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:

"Despite being the standard treatment for lung cancers, immune checkpoint inhibitors (ICIs) are often less effective for patients with EGFR mutations. And these mutations are far from uncommon; 40% of lung adenocarcinoma (LUAD) patients have them, but one protein that might play a role in this process is ARID1A. A recent study examined ARID1A expression in a cohort of LUAD patients with or without EGFR mutations. Overall, low ARID1A expression corresponded to increased immune cell infiltration and longer survival times. The data also suggested that ICIs were more effective for LUAD patients with EGFR mutations if they had low ARID1A expression. Mechanistic experiments in cultured EGFR-mutated LUAD cells suggested that reducing ARID1A expression inhibited autophagy. Autophagy is a normal process in healthy cells, but it helps cancer cells evade the immune system. Specifically, reduced ARID1A expression decreased autophagy by activating the EGFR/PI3K/Akt/mTOR 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:

"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.

A PowerPoint about a teacher going through breast cancer for a high beginning level ESOL class. Worksheets and suggested exercises are also on the PowerPoint.

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.

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:

"Phosphatidylserine (PS) is a lipid found in the cell membrane. When exposed on the outside of a cell during stress or during cell death, PS can trigger immune suppression. PS also engages PS receptors on immune cells, resulting in clearance of the cell and production of immune suppressive factors. One way tumors evade the host immune system is by engaging PS signaling. Therefore, inhibiting PS signaling suppression is a promising option for treating cancer. A recent review highlights the contributions of the TIM and TAM family of receptors to PS signaling and immune suppression in tumors. and some of the immunotherapy strategies targeting these receptors that are being investigated in preclinical and clinical trials. Due to the complexity of PS-induced immune suppression, there are still many unknowns. such as the detailed mechanisms and signaling pathways that are involved. or the consequences of interrupting these signaling pathways..."

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 is the third leading cause of cancer-related mortality worldwide. Treatment of metastatic gastric cancer typically aims to prolong overall survival and maximize health-related quality of life. For patients who have failed previous gastric cancer treatments, the oral, fixed-dose tablet trifluridine/tipiracil, appears to do just that. Adding tipiracil slows trifluridine metabolism, boosting the anti-cancer effect at a manageable level of drug toxicity by increasing trifluridine bioavailability in the body. Once inside the cancer cell, trifluridine inhibits cell proliferation by interfering with DNA synthesis. The pivotal phase 3 TAGS trial examined trifluridine/tipiracil’s efficacy and tolerability in previously treated patients with metastatic gastric cancer or adenocarcinoma of the gastroesophageal junction..."

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:

"Craniopharyngiomas are among the most common calcified tumors in the central nervous system. Although calcification is known to complicate tumor removal, especially in the delicate central nervous system, the underlying mechanism is poorly understood. A recent study examined the calcification of adamantinomatous craniopharyngiomas. Using cultured primary cells, the researchers induced calcification with the protein Bmp2. Calcified cells had elevated expression of the histone deacetylase HDAC3. Paradoxically, however, inhibiting HDAC3 activity increased calcification and differentiation into osteoblasts. Researchers discovered that this disconnect between HDAC3 expression and its activity came down to its cellular location. Bmp2, it turned out, was blocking HDAC3 from relocating to the nucleus. Bmp2 blocked relocation indirectly by increasing the expression of the microRNA miR-181b. miR-181b decreased the expression of the protein CBX4, which normally stabilizes the nuclear localization of HDAC3..."

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