The multidisciplinary study of cancer biology, including carcinogenesis, tumor progression, metastasis, cancer genetics, immunology, and the development of diagnostic, preventive, and therapeutic strategies
10 papersThis paper utilized advanced proteomics to identify 418 proteins interacting with c-Myc, a pivotal protein linked to cancer, in immortalized human and rat fibroblast cells, revealing 389 previously unknown interactors. The findings underscore c-Myc's diverse involvement in cellular processes, including transcription and cytoskeletal organization, by forming various large protein complexes.
This study in mice and in vitro models found that inhibiting ALK7, a protein involved in cell signaling, could reduce the spread of pancreatic cancer by preventing tumor cells from entering blood vessels. ALK7 appears to promote cancer spread by increasing tumor cell movement and breaking down the material surrounding blood vessels, making it easier for cancer cells to invade.
This study explored how lung fibroblast cells (MRC-5) affect liver cancer cells in a lab setting, finding that MRC-5 changed the expression of cancer stem cell markers and inflammation-related molecules on the surface of the liver cancer cells. The specific effects varied depending on the type of liver cancer cell line used.
This study used a 3D imaging technique called chromatin tracing to examine genome organization in mouse models of lung and pancreatic cancer. They identified non-monotonic, stage-specific changes in 3D genome structure during cancer progression, as well as specific genes whose altered 3D organization and expression were linked to prognosis and drug sensitivity.
Some inherited gene mutations increase the risk of clonal hematopoiesis (CH), where abnormal blood cells multiply. Certain combinations of inherited mutations and CH further increase the risk of developing blood cancer. These findings suggest that screening for CH in people with these inherited mutations could help predict their blood cancer risk.
Researchers developed a new photosensitizer molecule, superphane 1 or "singzyme", that effectively kills cancer cells in vitro by generating reactive oxygen species and disrupting redox homeostasis, leading to both apoptosis and ferroptosis. Superphane 1 mimics the activity of natural enzymes, such as NADH oxidase and GSH oxidase, showing enhanced photosensitivity and photocatalytic activity compared to control molecules due to the "super cage effect".
This study, primarily conducted in cancer cell lines, suggests that peroxisomes play a role in maintaining mitochondrial redox homeostasis by transferring reactive oxygen species (ROS) through a contact site mediated by the proteins ACBD5 and PTPIP51. This contact appears to increase during mitochondrial oxidative stress, facilitating ROS transfer and protecting mitochondrial health.
Cancer development and its response to therapy are significantly influenced by inflammation, which can either promote or suppress tumor progression. Chronic inflammation often aids tumor progression and resistance to treatment, whereas acute inflammatory responses can stimulate anti-tumor immunity.
By analyzing gene expression data from thousands of breast cancer samples, this study identified and ranked the genes with the highest prognostic power in two clinically relevant cohorts: estrogen receptor-positive/ERBB2-negative patients treated with chemotherapy and basal breast tumors receiving chemotherapy. This ranking helps prioritize promising biomarker candidates for future research and clinical validation.
This study identifies a novel mechanism by which the oxygen sensor PHD1 regulates muscle protein synthesis. PHD1 stabilizes leucyl tRNA synthetase (LRS), a leucine sensor, enhancing mTORC1 activation and protein synthesis in response to leucine. This interaction is amplified during periods of low oxygen and amino acids, ensuring a robust response when nutrients are restored. The relevance of this pathway is highlighted by the observation of reduced PHD1 and LRS activity in older adults with anabolic resistance.