• Adenovirus Service • AAV Service • Lentivirus Service • Retrovirus Service
In the field of cancer treatment, immunotherapy is like a brave warrior, which can use the body's own immune system to fight cancer cells. Among them, immune checkpoint inhibitors (ICBs), as an important branch of immunotherapy, can activate immune cells by blocking specific proteins so that they can more effectively eliminate cancer cells. However, reality is not always as people wish. Many patients do not respond well to ICBs, and even gradually develop drug resistance during treatment. This problem has been plaguing the medical community.
In clinical research, scientists have been looking for new ways to overcome type 1 diabetes. This disease plagues millions of patients worldwide. The patient's insulin-producing cells are mistakenly attacked by the immune system, causing blood sugar to soar, requiring lifelong dependence on insulin treatment.
In the world of cancer, colorectal cancer (CRC) is undoubtedly a warning name. It is not only the second leading cause of cancer-related death in the world, but also a complex molecular maze. Although scientists have revealed some molecular changes associated with colorectal cancer, how these changes drive the development of cancer remains an unsolved mystery.
In a new study, researchers from the Georgia Institute of Technology have created a two-pronged approach that marks tumor cells so they can be recognized and destroyed by specially enhanced T cells from the patient's immune system. This approach could one day become a universal strategy for treating some of the most difficult-to-treat cancers, such as brain, breast and colon cancers, by teaching the immune system to find cancers it would normally miss. Their approach worked against these cancers in laboratory tests and did not harm healthy tissue. Importantly, it also prevented the cancer from coming back.
In the battlefield of cancer treatment, the RAS gene family has always been a fortress that is difficult to conquer. The KRAS and NRAS genes in the RAS gene family are like commanders of cell growth and division, regulating the normal growth of cells through signaling pathways. However, when these genes mutate, they become traitors, causing disordered cell proliferation and leading to cancer. Although scientists have developed targeted therapies for KRAS (G12C) and KRAS (G12D) mutations, NRAS-mutated cancers, especially NRAS (Q61*)-mutated melanomas, have always lacked effective treatment strategies. There are about 50,000 new cases of NRAS-mutated melanoma in the United States and Europe alone each year, which is undoubtedly a huge clinical demand gap.
Melanoma is the most dangerous type of human skin cancer, especially NRAS mutant melanoma, which has become a difficult problem in the medical community due to its extremely high invasiveness and poor prognosis. At present, this cancer is mostly indifferent to existing immunotherapy and targeted drugs, leaving patients and doctors helpless.
Recently, researchers published a research paper titled "Cross-species tropism of AAV.CPP.16 in the respiratory tract and its gene therapies against pulmonary fibrosis and viral infection" in Cell Reports Medicine, a subsidiary of Cell. The study showed that AAV.CPP.16 has a high tropism for respiratory tissues across species (including mice and non-human primates), and verified the gene supplementation and gene editing therapy delivered by nasal administration of AAV.CPP.16 for the treatment of idiopathic pulmonary fibrosis and viral infection. This study shows that AAV.CPP.16 is a promising vector for gene therapy and gene editing in the respiratory system and lungs.
In the frontier field of medical research, skin wound healing has always been the focus of scientists. Whether it is accidental trauma, surgical incision, or skin ulcer caused by chronic disease, the speed and quality of wound healing directly affect the patient's recovery process. However, there are many complex molecular mechanisms in the skin repair process, some of which have not yet been fully revealed.
What is mycoplasma?
Low transfection efficiency
