Recent advances in the field of cancer research by scientists!
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Last Update: 2020-08-01
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Source: Internet
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Author: User
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this article, the small compilation of scientists in the field of anti-cancer research achievements, to share with you!
Picture Source: UCI School of Medicine. 1.
Nat Commun: Monitoring RNA hot spots or susceptible targets that can reveal cancer cells is expected to help develop a new type of targeted anti-cancer therapy doi: 10.1038/s41467-020-168 , a study published in the international journal Nature Communications, scientists from the University of California and other institutions revealed a special protein responsible for
genetic
changes or can lead to multiple cancers, and the results may help develop effective targeted cancer therapies. In the article, the researchers reveal how genomic instability induced by the APOBEC3A protein provides an unknown susceptibility in cancer cells.in human cells, where thousands of DNA damage occurs every day, and in cancer cells, the expression of the protein APOBEC3A is one of the most common sources of DNA damage and mutations that cause tumors to evolve when they occur in cancer cells, or cause DNA to break, resulting in an susceptibility/vulnerability. Researcher Dr Remi Buisson said that targeting cancer cells with high levels of APOBEC3A protein activity while interfering with THE DNA damage that is necessary to repair damage caused by the APOBEC3A protein may be key to developing more effective cancer therapies; Cancer Res: Scientists identify potential new cancer targets doi: 10.1158/0008-5472.CAN-19-3954 a recent study published in the international journal Cancer Research, scientists from the University of Vanderbilt and others have identified a potential new cancer target. Because of the associated biological mechanisms, researchers do not yet know the key role of conversion growth factor beta (TGF-beta) in cancer progression; for many years, researcher Sergey Novitskiy and others have been studying how nucleotides promote TGF-beta activity, including its
tumor
-driven effects, which are essential for a variety of cell functions;this study, the researchers found that the expression of adenosine receptors is closely related to the production of collagen, but also with the lower mortality rate of patients
with triple-negative
breast cancer, and that adenosine itself has no effect on collagen production, but it weakens the normal TGF-beta response in fibroblasts, thus promoting the atypical formation of extracellular matrix, which in turn supports the growth and metastasis of
tumors. Trends in Cancer: Cancer drugs make cancer cells resistant, and scientists are developing new ways to stop the process! doi: 10.1016/j.trecan.2020.03.009 Cancer treatment can shrink the patient's
tumor
, the patient may feel better, but what is not visible on the CT scan or MR image is that some cells are experiencing ominous changes. These abnormal cells become very large and have two to four times as many chromosomes as healthy cells as a result of new genetic changes caused by cancer treatment itself. Some cells can grow to the correct number of 8 times, 16 times or even 32 times. Soon, they become aggressive and resistant to treatment, and eventually lead to cancer recurrence.researchers say that when you're treated, some cells don't die, they don't die because they get a combination of normal chromosomes and other genetic changes. Many types of chemotherapy actually contribute to this; two cancer-causing genes, c-Myc and BCL2, play a role in the "double blow" of high-level lymphoma, a cancer that is almost incurable. These genes are part of the problem because when they exist, they help lymphoma cells live longer and treat them to become large cells. Cancer Cell: Scientists have successfully transformed autoimmune drugs into anti-cancer drugs doi: 10.1016/j.ccell.2020.04.013 scientists at the University of Southampton's Antibody and VaccineS team have discovered a method that can be developed with a simple molecular "switch" to convert previously developed antibody drugs used to treat
autoimmune
into antibody with strong anti-cancer activity. The work, published in the journal Cancer Cell, focuses on a molecule called CD40, which is present on the surface of immune cells and controls
autoimmune
and cancer. In
autoimmune
diseases, CD40 is considered to be overactive, increasing the chances of the immune system attacking healthy tissue. In cancer, CD40 is thought to be less stimulated, allowing
tumors
cells to evade the immune system. Work is under way to target CD40 with antibody drugs to develop drugs for autoimmune and cancer treatments.have developed antibody drugs to activate (agonists) or inhibit (antagonists) CD40 immune pathways. Researchers at the Southampton Cancer
Immunology
Centre, led by Professor Mark Cragg and Professor Martin Glennie, have now revealed that simply modifying the "constant" domain of antibodies can be converted into an agonizing agent. For three different antagonists, an agonisant "trick" is shown for the transition from anantagonist, which is driven by the hinge portion of the constant domain, which controls the flexibility of the antibody. One of these antibodies has proven to be a "super" agonist that can stimulate the immune system and cure cancer more effectively than the best target CD40 antibodies in current
clinical trials
.
Sci Rep: Scientists found a new anti-cancer compound in willows doi: 10.1038/s41598-020-63349-1found another potential drug in the stems and leaves of willows more than a century after providing aspirin to the world -- this time with anti-cancer properties. Scientists from the Lausanne Institute, in collaboration with cancer biologists at the University of Kent, have discovered a chemical called miyabeacin, which kills a variety of cancer cells, including those that are resistant to other drugs. Particularly exciting is its activity against neuroblastoma, a common childhood cancer that is difficult to treat, with an overall survival rate of less than 50%. In laboratory tests, miyabeacin was also found to be effective in several cell lines of breast, throat and ovarian cancer.researchers say that while the pharmacological activity of the active ingredient salicylic acid in aspirin is well known, the pharmacological properties of miyabeacin may be stronger, and because resistance to treatment is an important problem in cancers such as neuroblastoma, new drugs with new modes of action are needed, and miyabeacin may offer a new opportunity in this regard. Structurally, it contains two groups of salicylic acid, which gives it a potential 'double dose' of anti-inflammatory and anticoagulant ability, which we associate with aspirin. However, our findings report the activity of miyabeacin on many cancer cell lines, including acquired drug-resistant cell lines, providing further evidence for the polypharmacological effects of willows.
Photo Source: EMBO Reports, 2020, doi: 10.15252/embr.201948904.
EMBO Rep: Discovering a new immune brake --- EGR4, is expected to develop a new type of anti-cancer immunotherapy doi: 10.15252/embr.201948904 immune system is like a carefully regulated machine with its own built-in "brake" that prevents it from overreacting and causing excessive inflammation in otherwise healthy tissues. However, this preventive safety net is very fragile, especially in cancer, where tumor cells constantly brake, allowing
tumors
cells to evade immunotherapy. Scientists have identified several molecules that naturally inhibit immune activity, opening the door to immunotherapy, a potentially effective way to use the immune system to attack cancer cells. In order for immunotherapy to fulfil its full potential in human patients, it is also important to learn more about the factors that contribute to anti-cancer immunity.now, in a new study, researchers at the Lewis-Katz School of Medicine at Trump University in the United States and fox Chase Cancer Center have found for the first time that a molecule called EGR4, which plays a major role in male fertility, can act as a key brake on immune activation. They also found that removing EGR4, the key brake that effectively releases, promotes the activation of lethal T-cells, which soak and attack
tumors to enhance anti-cancer immunity, and the findings were recently published in the journal EMBO Reports.7:
Nature Sub-Journal: A New Breakthrough in Cancer! Kill cancer cells by swollen the lysosome! doi: 10.1038/s41565-020-0639-z nano
medicine shows great potential in promoting the diagnosis and treatment of diseases. To this end, therapeutic
diagnostic
reagents are loaded onto
nano-
particles and/or into
nano-
particles to increase their solubility while prolonging blood circulation in order to deliver the drug more effectively to the diseasesite. In addition, the pharmacokinetics and targeting efficiency of the drug can be improved by optimizing the size, shape and surface properties of the
of the
carrier. Currently, many nanoparticle-based administration systems have been approved for tumor treatment, and many more are under way
clinical trials
or preclinical evaluations. However, the challenges of clinical transformation remain, for example, off-target toxicity. Despite extensive research, only a small percentage (usually less than 1%) of the nanoparticles administered by the system can enter the
of solid
tumors. The rest carry toxic drugs into healthy tissues and organs, causing off-target toxicity and harmful side effects.therefore, there is an urgent need to explore new strategies that show better targeting or do not contain toxic drugs at all. Writing in the journal Nature Nanotechnology, Borkowska et al. proposed a "drug-free" strategy to kill cancer cells by controlling the aggregation of inert gold nanoparticles in the lysosomes. A lysozyme is a waste-treated organelle that receives and digests goods from inside and outside the cell. The accumulation of undigested substances causes the lysosome to expand, which increases the permeability of the lysosome membrane and eventually leads to cell death. Thus, lysosomes provide a target for cancer treatment by manipulating the aggregation state of the cargo, such as inert nanoparticles. According to Derjaguin, Landau, Verwey, and Overbeek (DLVO), the aggregation state of nanoparticles is strongly dependent on long-distance electrostatic repulsion, which is very sensitive to the charge on the particle surface and the ion strength and pH of the medium. These parameters can be used to control the aggregation state of nanoparticles. Because
tumor
tissue acidic (pH s 6.5-6.9) is stronger than healthy tissue (pH-7.4), and the lysosome is more acidic (pH-4.8), it provides activation for manipulating the polymerization behavior of reasonably engineered nanoparticles when their surface charge interacts with cells. Science: A study published in the journal Scienceto develop anticancer drugs to kill cancer cells : 10.1126/science.aax6367, researchers from the University of Montreal reported key structural and biochemical differences in a class of anticancer drugs called PARP inhibitors. These significant structural differences are accompanied by differences in the ability of the above-mentioned PARP inhibitors to kill cancer cells. The study addressed long-standing confusion about differences in efficacy of PARP inhibitors used in cancer clinics. In addition, the researchers used their structural and biochemical insights to modify an existing PARP inhibitor to improve their ability to kill cancer cells. "This principle of modifying PARP inhibitor molecules is also used in addition to cancer treatment, such as other indications such as cardiovascular disease and inflammation." John Pascal, senior author of the study, said.. PARP inhibitors are able to target the PARP-1 enzyme, which is involved in the repair of damage to DNA fractures, a chronic form of genomic damage that needs constant monitoring and repair to maintain cell survival. PARP-1 has two main activities: binding to DNA fractures, and producing a molecule called polyADP-ribose. PARP inhibitors can bind to the same region as PARP-1, preventing PARP-1 from producing poly (ADP-ribose), which is such a work.
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