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In a study published in an international journal, scientists at duke university medical center found that treating multiple types of drugs as a chemical may have great potential for treating stomach cancer. In addition to being known to block the growth of cancer cells, the researchers found that a drug called DFMO directly reduces the virulence of helicobacter pylori, an infection that is a major cause of stomach cancer.
Gastric cancer is the third leading cause of cancer death. Researchers further studied how DFMO can prevent gastric cancer. Helicobacter pylori infects the stomach tissue of half the population, but only about 1 percent of those infected develop stomach cancer, and while it is possible to prevent stomach cancer by treating the infection, researchers don't know who to treat.
Researcher Dr Keith says, helicobacter pylori with common human evolution at least 60000 years, and possibly longer, widespread use of antibiotics is used to eliminate the bacteria infections to prevent gastric cancer seems to be difficult to achieve, researchers say, may by reducing bacterial virulence to effectively prevent the occurrence of cancer of the stomach, after when the researchers of helicobacter pylori infection animal model for research found that promote cell growth more compound amine or there is a certain correlation with the incidence of gastric cancer, and the use of DFMO to treat animals or can effectively prevent the occurrence of cancer of the stomach, DFMO inhibits the function of enzymes that are critical to the production of polyamines.
In order to clarify the mechanism of action of DFMO, researchers from DFMO treated or untreated infection animal collection of helicobacter pylori in the body, using in vitro testing means, the researchers assessed the main virulence factors of helicobacter pylori CagA protein activity, the CagA protein can "injection" promote the generation of carcinogenic signaling pathway in gastric epithelial cells. ......

New molecular mechanism of pancreatic repair

Posted by star on 2019-04-22 19:08:25

    The Wilms tumor suppressor gene (Wt1) encodes a zinc finger transcription factor. The factor is important in the development of gonads, kidneys, adrenals, spleen, and heart. Recent studies suggest that WT1 could also be playing physiological roles in adults.
    Latest findings have shown that under normal conditions, the Wtl gene is activated in stellate cells (a special type of repair cell present in the pancreas and kidney) after pancreatic injury, responsible for the repair process.
    Systemic deletion of WT1 in mice provokes a severe deterioration of the exocrine pancreas, with mesothelial disruption, E-cadherin downregulation, disorganization of acinar architecture and accumulation of ascitic transudate. Despite this extensive damage, pancreatic stellate cells do not become activated and lose their canonical markers.
    The researchers also observed that pharmacological induction of pancreatitis in normal mice provokes de novo expression of WT1 in pancreatic stellate cells, concomitant with their activation. When pancreatitis was induced in mice after WT1 ablation, pancreatic stellate cells expressed WT1 and became activated, leading to a partial rescue of the acinar structure and the quiescent pancreatic stellate cell population after recovery from pancreatitis.
    "If Wt1 is not activated, these cells will not be able to perform their functions," the researcher said, further pointing out that these cells play a key role in the progression of pancreatic cancer because they form alliances with tumor cells. Therefore, the results of this study indicate that the Wt1 gene is essential not only for the normal maintenance of the pancreas, but also for repair after pancreatic injury.”

Short telomere syndromes leads to primary T cell immunodeficiency

Posted by star on 2019-04-21 19:04:50

    Telomeres contain genetic information of chromosome. The telomeres of all cells wear and shrink with age, which limits cell division and proliferation. Researchers at Johns Hopkins University found people’s immune systems cells age and die prematurely, who are born with abnormally short telomeres (ST).
    The mechanisms that drive T cell aging are not understood. The research shows that children and adult telomerase mutation carriers with short telomere length (TL) develop a T cell immunodeficiency that can manifest in the absence of bone marrow failure and causes life-threatening opportunistic infections. Mutation carriers shared T cell–aging phenotypes seen in adults 5 decades older, including depleted naive T cells, increased apoptosis, and restricted T cell repertoire. T cell receptor excision circles (TRECs) were also undetectable or low, suggesting that newborn screening may identify individuals with germline telomere maintenance defects.
    The researchers examined the transcriptional programs of T cells from telomerase mutation carriers; finding that they diverged from older adults with normal TL. Short telomere T cells upregulated DNA damage and intrinsic apoptosis pathways, while older adult T cells upregulated extrinsic apoptosis pathways and programmed cell death 1 (PD-1) expression.
    The mouse study showed telomerase-null mice with short TL showed defects throughout T cell development, including increased apoptosis of stimulated thymocyte, their intrathymic precursors, in addition to depleted hematopoietic reserves.
    T cells from mice with short TL also showed an active DNA-damage response, in contrast with old WT mice, despite their shared propensity to apoptosis. The data suggest there are TL-dependent and TL-independent mechanisms that differentially contribute to distinct molecular programs of T cell apoptosis with aging.

Research reveals why cancer most often spreads to the liver

Posted by star on 2019-04-18 19:31:25

    Ductal adenocarcinoma of the pancreas (PDAC) is the most common form of pancreatic cancer and currently the third leading cause of cancer death in the world. When cancer spreads to another organ, it most often metastasizes to the liver.
    In a new study, researchers from Harvard University in the United States found that liver parenchymal cells, the major functional cells of the liver, are at the center of a continuous response that makes the liver especially sensitive to cancer cells. These cells respond to inflammation by activating STAT3, a protein that increases the production of SAA, which in turn reshapes the liver and creates the "soil" needed for cancer cells to grow.
    "The soil hypothesis is widely accepted, but our research now shows that liver cells are the primary coordinators of this process," said Dr. Gregory Beatty, professor of oncology at the university of Pennsylvania's perelman school of medicine.
    For the new study, Beatty and his team first used the PDAC rat model. They found that almost all liver cells in PDAC rats showed STAT3 activation, compared with less than 2 percent of liver cells in tumor-free rats. They then found that the same biological characteristics could be observed in patients with pancreatic cancer as well as those with caecum and lung cancer. The increased susceptibility of liver to cancer inoculation in rats was effectively prevented by removing only STAT3 from liver cells. They further found that il-6 controls STAT3 signaling in these cells and instructs liver cells to produce SAA, which ACTS as an alarm that attracts inflammatory cells and triggers a fibrotic response, building the "soil" needed for cancer vaccination.
    The study also found that il-6 promoted liver changes regardless of tumor presence, suggesting that any disease associated with elevated il-6 levels, such as obesity or cardiovascular disease may ......

628 cancer therapeutic targets are screened by CRISPR–Cas9

Posted by star on 2019-04-18 19:15:05

    Targeted therapy can selectively kill cancer cells without affecting healthy tissue. Choosing good drug targets is an important part of the successful development of such therapies. In recent years, CRISPR has become a unique tool for the discovery of tumor drug targets, which can be used to mutate, inhibit or activate any target human gene.
    Recently, scientists from UK reported a major achievement: Using genome-scale CRISPR-Cas9 screens 18,009 genes in 324 human cancer cell lines from 30 cancer types. They also developed a genetic score calculation framework that prioritizes cancer drug targets, the team finalized 628 priority targets, including pan-cancer target genes and cancer-type specific genes.
    They divided the 628 most promising targets into three groups based on tractability. One group contains 40 promising targets which are approved in anticancer drugs or a target of some drug candidates in clinical or preclinical development stages. Group 2 contains 277 priority targets, and there are currently no drugs targeting these targets in the clinical development phase, but there is evidence to support the operability of these targets. The third group contains 311 priority targets and there is currently no information or lack of information to support their operability.
    Among these targets, WRN (Wernersyndrome RecQ helicase, a helicase that assists cells to replicate or read DNA by unwinding the double helix structure of the genome) has higher operability scores in many different cancer types.
    The study used CRISPR and RNAi technology to investigate nearly a thousand cancer cell lines. It found that 73% of MSI cancer cells are dependent on WRN; in contrast, the effect of MRN deletions on non-MSI cancer cells is minimal. Studies have also found that inhibition of WRN expression can significantly delay the growth of MSI cancer in mice.

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