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:

"Retroperitoneal liposarcoma (RPLS) is a type of cancer that begins in fat cells and affects soft tissues deep within the body. Recurrence is common because the tumor size and location make complete surgical removal challenging and other treatment strategies are limited due to an incomplete understanding of the factors driving RPLS progression. To gain insight into this process at the molecular level, researchers set out to uncover the role of the cell ion channel TRPM2-S, which allows calcium and other ions to enter the cell and is often associated with cancer. The team showed that high TRPM2-S expression by RPLS cells was associated with higher patient survival than lower levels of TRPM2-S expression. They also found that TRPM2-S can increase the concentration of reactive oxygen species (ROS) within the cell by inhibiting the transcription factor FOXO3a leading to cell proliferation under normal oxygen concentrations but increased cell death under the stress caused by ROS toxicity..."

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:

"Autophagy is a catabolic process in which intracellular components are degraded in lysosomes. Stresses such as nutrient deficiency, hypoxia, and chemotherapy can trigger autophagy, making autophagy relevant to cancer treatment. Autophagy appears to play complex dual roles in cancer immune escape. For example, autophagic degradation of the immune checkpoint protein PD-L1 generally enhances T cell activation and suppresses tumor growth, but cancer cells can encapsulate PD-L1 and another checkpoint protein, CD47, in endosomes to prevent their degradation. In addition, MHC-I/II autophagy enables cancer cell immune escape and inhibits antigen presentation and T cell activation. However, autophagic mitochondrial degradation, termed mitophagy, can improve the antitumor immune response. Therefore, autophagy can positively or negatively affect cancer immune escape, which may depend on the experimental context, and autophagy may synergize with immune cells to regulate cancer immune surveillance..."

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 have taken a significant step towards personalizing the treatment of cancer. Using DNA sequencing, they’ve developed a way to scan blood samples for mutations in circulating tumor DNA -- small bits of genetic material that are released as cancer cells die. The genomic reservoir contained in this DNA is representative of nearly all tumors carried by a patient, providing the foundation needed for comprehensive genetic profiling. Such profiling may help clinicians select the most appropriate therapies for a given patient. The genetic mutations giving rise todrivingthat drive cancer development often differ markedly among individuals. Interventions that match a patient’s unique genetic profile offer great promise, but obtaining tumor tissue for genetic testing can be invasive, and risky and sometimes impossible. To bypass these limitations, the researchers established a way to enrichextract, sequence, and analyze circulating tumor DNA..."

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 (GC) remains a major public health issue, especially in developing countries. However, recently discovered small RNA molecules called tsRNAs hold promise for the treatment of GC and other cancers. In a new study, scientists searched for tsRNAs that are dysregulated in GC and might therefore be targets for therapy. They found that the tsRNA tRF-Val-CAC-016 was downregulated in GC samples from patients. In vitro, upregulation of this tsRNA in GC cell lines suppressed cell proliferation. Mechanistic studies revealed that tRF-Val-CAC-016 normally inhibits the oncogene CACNA1d, thereby regulating the MAPK signaling pathway to limit proliferation, suggesting that the downregulation of tRF-Val-CAC-016 observed in GC allows the cancer cells to replicate. In mice, treatment with a tRF-Val-CAC-016 mimic decreased GC tumor growth, confirming this tsRNA’s therapeutic value..."

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:

"Mutations in the gene tp53 are often detected in the early stages of colitis-associated colorectal cancer (CAC). The development of CAC is facilitated by gut microbiota disruption (dysbiosis) and chronic intestinal inflammation, but whether tp53 mutations are linked to this dysbiosis and inflammation remains unclear. To learn more, a recent study examined zebrafish larvae with a tp53 mutation. The mutant fish exhibited intestinal inflammation that was due to gut microbiota disruption. confirming the link between tp53 and these pathological changes. Overall, gut microbiome diversity was decreased, while pathogenic Aeromonas bacteria were abnormally abundant, aggressively colonizing the gut. Further investigation revealed that the gut dysbiosis in the mutants induced inflammation by disrupting sialic acid metabolism. Supporting this finding, inhibition of the sialic acid-releasing enzyme sialidase alleviated the pathologies in mutant zebrafish larvae..."

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