Several articles focus on new advances in the field of lung adenocarcinoma!

"Lung adenocarcinoma is a kind of non-small cell lung cancer which is more likely to occur metastasis In recent years, the incidence of lung adenocarcinoma in the population has continued to rise In this paper on the achievements of scientists in the field of lung adenocarcinoma research to organize and learn with you! Photo Credit: :: Heavyweight! Chinese scientists have successfully mapped a comprehensive proteomic map of human lung adenocarcinoma! : A recent study published in the international journal, scientists from the Shanghai Institute of Pharmaceutical Research of the Chinese Academy of Sciences and other institutions through a comprehensive study of Chinese lung adenocarcinoma patients () comprehensive protein cellanalysis analysis of lung adenocarcinoma is the leading cause of death in all cancers in the worldIn the article, the researchers revealed the molecular characteristics associated with lung adenocarcinoma and the association between these molecular characteristics and patient clinical prognosis, potential prognostic biomarkers, and drug targets; Sub-journal: Blocking the efficacy of improved anti-drugs on mutant lung adenocarcinoma: Lung cancer is one of the leading causes of cancer-related deaths worldwideAbout some cases of lung cancer are classified as non-small cell lung cancer ()Several changes in the cancer-causing driving gene have been reported in the program, including epidermal growth factor receptors () coding genes and interstitial lymphoma kinase () coding genesIn a new study, researchers from Japan's National Cancer Center and Nagoya University and other research institutions studied immunothitypes in tumor microenvironments of mutant lung adenocarcinoma, which are largely ineffective in the case of mutated lung adenocarcinomas, i.esudden-mutationed lung adenocarcinomaHowever, mutant lung adenocarcinoma has an inflamed immunosuppressive tumor microenvironment and the effect-regulating cells () usually present in the inflamed tumor microenvironment show higher immersion thereSignal activation (end kinase) and reduced interferon regulatory factors (): the former increases in the recruitment of regulatory cells; :: Genome rearrangement of non-smoking lung adenocarcinoma predates cancer diagnosis: Researchers from the Korea Institute of Advanced Science and Technology and Seoul University found in a new study that researchers found that catastrophic genome rearrangement early in childhood and adolescence can lead to lung cancer in late childhood for non-smokersThe findings could help explain how some non-smoking-related lung cancers are producedThe findings were recently published in the journalThe researchers confirmed that gene fusion in non-smokers mostly occurs earlier, sometimes early in childhood or adolescence on average, 30 years before lung cancer is diagnosedThis study showed that these mutant lung cells carrying cancer-causing seeds () have been dormant for decades until further and many other mutations accumulate sufficiently before progressing into lung cancerThis is the first study to reveal the landscape of genomic structural variation of lung adenocarcinomaLung cancer is the most common type of lung cancer, the leading cause of cancer-related deaths worldwideMost lung adenocarcinomas are associated with long-term smoking, but about a quarter of lung adenocarcinomas occur in non-smokersIt's not clear exactly what makes non-smokers develop the cancerNew research shows that mutant lung adenocarcinoma requires alpha participation: signaling pathways closely related to important physiological activities such as cell proliferation, inflammation, and survival enter the nucleus can promote gene transcription and promote cell growth and tumor evolution The most common regulatory methods of signaling pathways include the promotering and binding of kinase activity of upstream signaling alpha to promote target gene transcription released from the complex by the occurrence of phosphoryeandization and ubiquitation degradation Activation sexist in many tumors but the kinases involved in the activation of the event are still less understood in a recent study published in the International Academic Journal by researchers from Greece studied regulated kinases involved in signaling pathway activation in mutated lung adenocarcinoma In this study, researchers identified the role of alpha and beta in a mouse model of chemical drug-induced and expressed mutant lung adenocarcinoma They used reported gene mice and alpha-beta conditions to knock out mice and found that activation during the development of chemically induced and genetically induced lung adenocarcinoma was present in two different stages of early and late stages in which beta and alpha occurred in cancer stem cells Breakthrough! Scientists have succeeded in analyzing the molecular mechanisms that induce human lung adenocarcinoma": Nearly half of human lung adenocarcinoma cancer cancer events are not clear to researchers who often complicate the development of selective targeted therapies, but these tumors appear to contain inactive mutations, including some mutations without significant carcinogenic function; a recent study published in the international journal from the National Cancer Research Center of Spain (a study)
The researchers found that the expression of endogenous () kinase inactivation subtypes (equivalent to human mutations) in the mouse body may induce the onset of lung adenocarcinoma in the body, which indicates inactive mutations or can trigger the event of lung adenocarcinoma The researchers point out that the signalstrength of the pathway is important not only in the development of tumors but also in the cells that induce the initiation of cancer, but also in determining tumor subtypes Cascading signals can act as a central node to transduce signals from membrane receptors into the nucleus of the cell, which are often abnormally active in most human cancers and a large number of studies have shown that rising signal levels or lead to cytotoxicity that in turn act as a natural barrier to the early development of cancer; SOURCE: Scientists reveal new targets for lung adenocarcinoma treatment Candidate drugs are in clinical trials: Researchers at the Mayo Clinic in the United States have discovered that a cancer gene can promote lung cancer The findings, published in the international academic journal the Mayo Clinic, provide evidence that it can drive the formation of lung adenocarcinoma tumors; About one of the patients with lung cancer has been diagnosed with lung adenocarcinoma The most common driver of this cancer is a genetic mutation Mediamediated lung adenocarcinoma is a particularly deadly type of lung cancer, in part because direct-target treatments have not been clinically successful In normal cells, the last step in cell division can be directed - cytoplasmic division "But it's very surprising that we found that in lung gland cancer cells it's not a necessary molecule for the cytoplasmic division process, and this suggests that cancer cells must also be playing the other functions needed by cancer cells." In this article, the researchers report that synthetic ribosomes that promote ribosomes in lung gland cancer cells are protein synthesis machines within cells responsible for translating them into proteins Revealing the transpolarity of lung adenocarcinoma and its molecular mechanism: Recently, the latest research results of Ji Hongbin Research Group of the Institute of Biochemistry and Cell Biology of the Shanghai Institute of Life Sciences of the Chinese Academy of Sciences were published online The study was the first to confirm the translposal differentiation of lung adenocarcinoma in the body and reveal its molecular mechanism The existence of genealogical conversion between lung adenocarcinoma and lung scale cancer is a long-standing and important scientific issue in the field of lung cancer Lung adenocarcinoma and lung scale cancer are the two main pathological subtypes of non-small cell lung cancer with different gene expression spectrums and biological markers, so the classical theory is that they originate from different lung epithelial cells: lung adenocarcinoma originates mainly from alveolar epithelial cells, while lung scale cancer comes from base cells But studies have found that at least non-small cell lung cancer in the same tumor can contain both adenocarcinoma and scale cancer two completely different types of pathology clinically called lung adenocarcinoma; it is interesting to note that adenocarcinoma in lung scale cancer and scale cancer parts often have the same genetic mutation spectrum based on tumor cloning theory that there may be spectral transformation between these two different pathological types but the difficulty of the study has remained at the level of hypothesis : Positive feedback loops in human lung adenocarcinoma: It is well known that tumor cells need to provide a stable supply of sufficient nutrients to grow In order to ensure the supply of nutrients they must secrete messenger compounds to stimulate the proliferation and germination of adjacent blood vessels Recently, scientists in the field of neurology at the German Institute of Research discovered a new positive feedback loop between vascular endothelial growth factor () and its receptors in human lung adenocarcinoma When combined, it stimulates tumor cells to secrete growth factors, which accelerates tumor growth In experiments in mice with lung cancer, scientists turned off growth factors and proteins that regulate the signal to slow tumor growth The size of the tumor shrinks even more significantly when used with other inhibitors Researchers have demonstrated that vascular endothelial cell growth factor receptors exist in tumor cells that describe a new signal transduction pathway in lung cancer cells that trigger new vascular growth They also learned that these inhibitor treatments make sense only when cancer cells are expressing a large number Gene mutations are associated with shorter survival in patients with advanced lung adenocarcinoma: In a study published in the journal, genetic mutations can predict shorter survival times in patients with advanced lung adenocarcinoma Ph.D and colleagues from Northwestern University in the United States evaluated women with advanced lung adenocarcinoma over the year, studying the prognosis of mutations for genetic and mutation states in people who had never smoked The researchers found that the average age of these patients was old and that the Kardashians had a performance status score or higher After multivariate analysis, the researchers also found that mutations were associated with a longer overall lifetime risk ratio, and associated with a shorter survival risk ratio : Three articles of research directly refer to genes that cause lung adenocarcinoma: : In three studies published in the journal, researchers from abroad announced that they have found abnormal genes that cause lung adenocarcinoma; The abnormal gene, called the fusion gene, is formed by the fusion of two genes for some reason Researchers believe that lung adenocarcinoma accounts for about the total number of lung cancers The fusion gene was found in the patient's body during the team's investigation of the patient's tissue The team found that the fusion gene has cancer-inducing properties and confirmed that therapeutic drugs such as thyroid cancer can kill the resulting cancerous cells () More wonderful counts! Stay tuned!