Pancreatic ductal adenocarcinoma is the most common type of pancreatic cancer, which is very lethal and has a 5-year survival rate of only 6%. The poor efficacy of chemotherapy is due in part to the high resistance to current treatment regimens.
In a new study published in the June 6 issue of Nature, researchers at the University of California, San Diego School of Medicine and the Moores Cancer Center, and Keio University in Japan, the University of Nebraska, and Colleagues at Ionis Pharmaceuticals have described an innovative new model that not only enables them to track resistance in vivo, but also reveals a new therapeutic target that early tests have suggested could block pancreatic cancer The growth provides a new strategy.
Combining scientific and clinical expertise in collaboration, Dr. Tannishtha Reya, Professor of the Department of Pharmacology and Medicine, University of California San Diego School of Medicine, Dr. Andrew Lowy, Professor of Surgery Oncology, Department of Surgery, Health and Moores Cancer Center, developed with colleagues A new "report" mouse model has emerged that makes it possible to image, non-invasively track stem cell signals in living animals.
Using this strategy, the team confirmed that the stem cell gene Musashi (Msi) is a key component in the progression of pancreatic cancer. In particular, the work reveals that Msi expression increases with the progression of cancer, and cells expressing Msi are key drivers of cancer growth, drug resistance, and lethality.
Given the role of Msi in promoting invasive disease, the researchers worked with Dr. Robert MacLeod, vice president of oncology discovery at Ionis Pharmaceuticals, to develop a new generation of antisense oligonucleotide (ASO) inhibitors against Msi. These inhibitors effectively target and block cells expressing Msi, resulting in tumor growth arrest in animal models and patient-derived cancer cells.
An antisense inhibitor refers to a synthetic nucleic acid drug designed to selectively bind to a disease-associated target gene messenger RNA and inactivate it.
Reya said that these findings can be widely used to study cancer. “Because live imaging can visualize Msi reporter protein activity, these models can be used to track cancer stem cells in the tumor environment, observe cancer growth and metastasis in real time, and provide a platform for testing new drugs that can better destroy resistant cells. ."
Reya also pointed out that targeting Msi in primary tumors can "significantly change the path of cancer development by inhibiting cancer stem cells and other tumor cells, stopping pancreatic cancer growth and increasing survival. This actually highlights the ability to transform these studies." The ability of the results suggests that Msi antagonists may be a new strategy for targeting chemotherapy resistance."
Recently, researchers at the Massachusetts General Hospital (MGH) have discovered the first potential molecular therapeutic target for the most common form of pancreatic cancer that kills more than 90% of patients. The tumor suppressor protein SIRT6 was found to be inactivated in approximately 30% of pancreatic ductal adenocarcinoma (PDAC), and the team determined the exact signaling pathway that SIRT6 inhibits PDAC formation, a mechanism different from its pathway to inhibit colorectal cancer. The research paper was published online in the April 2016 issue of Cell (Cell reveals the king of cancer treatment targets).
Jeremy Sanford, an associate professor of molecular, cellular and developmental biology at the University of California, Santa Cruz, found that a protein he has been working on seems to play an important role in driving the spread and metastasis of pancreatic cancer cells. This protein is called IGF2BP3 and represents "insulin-like growth factor 2 mRNA binding protein 3". The study, published in the May 19 issue of Cell Reports (Cell Rep: How a protein drives tumor metastasis).
Researchers at the Chinese Academy of Medical Sciences Peking Union Medical College have revealed in a new study that a pancreatic cancer risk variant in the intergenic long-chain non-coding RNA (lincRNA) LINC00673 constructs a binding site that interferes with PTPN11 degradation. . This important study was published in the May 23, 2016 issue of Nature Genetics (Nature Genetics, an academician of Lin Dongxi, reveals a tumor suppressing lincRNA).
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