-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
October 29, 2020 // -- An An Integrative Gene Gene Gene and Mathematical Flux Balance Analysis Designs Targeted Red, published in the international magazine Cansr Research In a study by Ox Possibilities in Melanoma Cells, scientists from Vanderburg University and others identified a specific enzyme that may still keep tumor cells growing while cancer drugs are being treated, and the findings may provide scientists with new ideas and hope for developing new ways to block cancer cell growth.
About a decade ago, many cancer researchers focused on studying mutations in cancer cells and how to turn them off, and that focus paid off in the form of treatments that essentially shut down genes that mutate in about half of skin cancers and regulate tumor cell growth. Unfortunately, however, this expensive and painstaking treatment has its limitations, with only half of cancer patients' tumors disappearing for a month to a year, while surviving cancer cells contribute to the recurrence of the cancer patient's disease, which is resistant to the drug.
Photo Source: Pixabay/CC0 Public Domain researcher Vito Quaranta said: 'Then we started studying at a single tumor cell level to explain why some tumors were eliminated while others were unscathed during BRAF inhibitor treatment;
After analyzing the mechanisms by which to-patient cells survive and continue to grow in cancer therapy, the researchers analyzed which baseline metabolic characteristics promote melanoma cells to become drug- resistant cells in a different way than genetics-centric, and they hope to study cancer therapy as a dynamic change because tumors often change their esophysiosis.
The researchers speculate that the logical place to look for differences lies in the nutrients and energy received by cells during and after the suppression of the BRAF gene, using metabolomics and machine learning to classify cells, and the researchers found that the energy sources of drug-resistant cells revolve primarily around redox balance and NOX5, a special enzyme that increases levels in melanomas that are resistant to therapy.
researcher Quranta says drug-resistant cells rely on NOX5 and redox balance, just as people turn on a generator when a power outage, and the enzyme produces waste, like the exhaust gas from a generator, while the enhanced antioxidant ability supported by the cysteine transporter SLC7A11 helps to get rid of the cells, and now researchers understand the mechanism, which is the enzyme's weakness and a refined pathway balance mechanism.
By using a single cell's gene expression pattern, researchers can use machine learning techniques to understand how the metabolism of different cell types is routed, and can help predict whether the specific substances needed for drug-resistant cell metabolism are higher than drug-sensitive cancer cells;
researcher McLean says metabolomics has grown rapidly over the past decade, and researchers who apply it to related studies can now get very influential results.
Now that we've identified NOX5 and Redox balance as key players in the survival and progress of melanoma, it may change the way the entire cancer research community thinks about how to cure cancer.
Since NOX5 does not exist in all tumors, and the redox balance framework in drug-resistant cells may be known in other cancer types, and specifically in melanoma-related studies, the next step for researchers will be to look deeper into finding more effective strategies to track NOX5, or look for One way to destroy NOX5 itself is to find a way to suppress the antioxidant properties of cells, and for other cancer researchers, the findings may help them identify specific enzymes that promote cancer cells that are resistant to other cancer drugs, revealing the weaknesses of these cancers.
In another study published in the international journal Frontiers in Oncology, researchers analyzed the metabolic composition of drug-resistant cancer cells worldwide, revealing a reprogramming process that promotes the continued survival of cancer cells during drug therapy, and speculated that cancer cells that are resistant to the drug may enter a metabolic "blank" state.
researchers will continue to delve into other molecular mechanisms that reveal cancer cell tolerance to cancer drug therapies, providing new ideas and research foundations for the development of effective therapies.
() References: B. Bishal Paudel, Joshua E. Lewis, Keisha N. Hardeman, et al. An Integrative Gene Expression and Mathematical Flux Balance Analysis Identifies Targetable Redox Solutions in Melanoma Cells, Cancer Research (2020). doi:10.1158/0008-5472.CAN-19-3588.2" Dongya Jia, B. Bishal Paudel, Corey E. Hayford, et al. Drug-Tolerant Idling Melanoma Cells Exhibit Theory-Predicted Metabolic Low-Low Phenotype, Frontiers in Oncology (2020). DOI: 10.3389/fonc.2020.01426(3) Research brings understanding of the cellular resistance to cancer treatment, opening doors to new curesby Marissa Shapiro, Vanderbilt University <!--/ewebeditor:page->