Release date: 2017-06-28
1. JCI: Scientists are expected to develop new therapies that effectively inhibit the progression of lung cancer
The gene p53 can act as a tumor suppressor under normal conditions, but it will participate in the development and development of nearly half of human cancers when it is mutated. Recently, researchers from the Massachusetts Massia Cancer Research Center revealed lung cancer through research. The molecular mechanisms by which cells are dependent on mutant p53, and related research may provide new ideas and hopes for the development of new and effective lung cancer therapies.
Every year, lung cancer causes many cancer patients to die, including colon cancer, breast cancer, prostate cancer, etc. According to the American Cancer Society, there will be more than 220,000 new lung cancer patients in the United States in 2017. Of course, researchers are needed. Rapidly develop new and effective therapies to deal with. In this study, the researchers revealed a novel strategy to inhibit the development of lung cancer in mouse models and cultured cell lines by blocking the function of a supervised protein called ChK1, which is capable of increasing the success of genome replication.
Researcher Deb said that certain mutant p53 not only relax the function of tumor suppression, but also may cause cancer. In this study, we first elucidated a mechanism for how cancer cells depend on the mutation function of p53 to survive. And growth, based on relevant research results, we may be able to develop new therapies to kill lung cancer cells carrying mutant p53 without damaging healthy tissue.
The key to this study is the replication of the genome during cell growth. All cells undergo DNA replication and cell division through this process, and each stage of the cycle is important for critical processes such as cell genome replication and cell division. By studying the genome of cancer cells, the researchers found that the mutated p53 gene is capable of producing excess ChK1 and cyclin A proteins that help regulate cell cycle progression and ChK1 function, especially to help inhibit replication forks. "collapse"; before cell division, our genome must be replicated from a pre-set replication origin to make a copy of the daughter cells; the newly replicated DNA will begin to replicate along the replication fork of the parental genome, and more A supervised protein (such as ChK1) can also inhibit the newly formed replication fork from "collapse" before DNA replication is completed. When the replication fork "collapses", the cell classification will not be completed and the cell will die.
Inhibition of ChK1 protein is often used to inhibit the growth of cancer cells. However, it is currently rarely successful in clinical trials. The results of this study suggest that ChK1 inhibitors may be effective in blocking cancer cells in patients with acquired p53 function. Reproduction, therefore, ChK1 inhibitors may not currently be able to be used in a suitable cancer population. Finally, researcher Deb said that we plan to develop a new strategy to use this study to block the spread of lung cancer carrying mutant p53. Since p53 can be mutated in many cancers, this study may help guide a variety of Treatment of different types of cancer patients.
2. Nat Genet: Genome-wide association studies elucidate novel susceptibility loci that induce lung cancer
Recently, a research report published in the international journal Nature Genetics, researchers from the University of Toronto and other institutions conducted a large genome-wide association study using genotyping platforms developed by several cancer research institutions. A novel susceptibility locus for lung cancer was identified.
Although smoking is a major risk factor for lung cancer, past studies have shown that the heritability of lung cancer may account for 18%; of course, in the previous genome-wide association study, researchers also identified multiple lung cancer susceptibility sites. However, the researchers cannot explain the hereditary nature of most diseases. In this study, researchers have made major breakthroughs in this research.
In this study, the researchers studied European individuals with existing data (including 14,803 subjects and 12,262 control individuals), and they eventually identified 18 disease susceptibility sites, including 10 novel sites. These novel sites can reveal dramatic changes in risk patterns between lung adenocarcinoma and squamous lung cancer, with four sites associated with overall lung cancer and six sites directly associated with lung adenocarcinoma. The researchers also found that mutations in multiple genes involved in telomere function may play a key role in inducing lung adenocarcinoma risk (not squamous lung cancer risk).
Researcher Amos said that we are very excited that the scale of the study and the genes found to affect lung cancer risk have not been reported by other researchers before; this study may help us clarify the new mechanisms affecting lung cancer risk. In particular, the researchers identified a number of novel mutations that affect cell telomere function, which directly affect the risk of lung adenocarcinoma.
In addition, the researchers also found that mutations around the nicotinic receptor subunits that affect lung cancer risk and smoking seem to have a certain impact on the body's cerebellum, researchers rarely found that the cerebellum can participate in the body's addictive behavior; People also need to conduct more in-depth research to understand the role of targeted genes in influencing lung cancer risk, smoking behavior and smoking effects.
3. Leukocyte-enhancing drugs are safe during concurrent chemotherapy and radiotherapy for lung cancer
Sub-analysis of phase III CONVERT clinical trials confirmed that the blood cell boosting drug is safe during small cell lung cancer (SCLC) synchronized radiotherapy. The results of the relevant subanalysis were published at the European Lung Cancer Conference (ELCC).
Dr. Fabio Gomes, a cancer surgeon at the Christie NHS Foundation Trust in the United Kingdom, said, "The best treatment for limited-term SCLC is synchronized radiotherapy. The efficacy of this intensive treatment is accompanied by greater toxicity (mainly It occurs in the blood, esophagus and lungs. This means that this therapy is not suitable for every patient, and more patients will try to follow the plan."
Granulocyte colony-stimulating factor (G-CSF) is often used as a supporting measure to promote neutrophil survival, proliferation and differentiation. The expected neutropenia is not so severe, and patients recover more quickly, reducing their risk of infectious complications. However, its use during SCLC-synchronized radiation therapy is controversial, and the American Society of Clinical Oncology (ASCO) does not recommend using it regularly. This is because a randomized clinical trial of 215 eligible patients between 1989 and 1991 has shown that when using granulocyte-macrophage colony-stimulating factor (GM-CSF) during synchronized chemotherapy, Significant increases in severe thrombocytopenia, severe anemia, pulmonary complications, and poisoning have occurred.
Gomes said, "Since this clinical trial, which may affect the use of colony stimulating factors in this situation, was released in 1995, two major changes have occurred. First, this clinical trial is for GM-CSF testing. GM-CSF acts on more than one blood cell lineage and is now infrequently used. Second, since then, modern radiotherapy technology has progressed rapidly and become more precise, which reduces the risk of poisoning."
The Phase III CONVERT clinical trial enrolled 547 patients with limited-stage SCLC who underwent concurrent radiotherapy and were randomized to receive once-daily or twice-daily radiation. There was no difference in overall survival between the two patient groups.
This clinical trial allows the use of G-CSF, and at some point in this treatment, approximately 40% of patients receive its use. For the results of the analysis published today at the European Lung Cancer Conference, these researchers compared the poisoning and treatment outcomes of patients who received G-CSF during concurrent chemoradiotherapy and those who did not receive G-CSF.
They confirmed that among patients receiving G-CSF during treatment, the incidence of severe thrombocytopenia and severe anemia almost doubled, 30% and 20%, respectively, however, these odds were lower than previously reported. This was followed by a significant increase in further supportive measures such as platelets and blood transfusions. However, there is no difference in lung complications or survival.
Gomes said, "G-CSF does not have a significant negative impact on the treatment outcomes of these patients, which is very gratifying. A proper supportive measure can balance higher blood poisoning throughout the treatment period. â€
He continued, “We conclude from this analysis that G-CSF is safe during thoracic radiotherapy and should promote patients to receive a planned full course of synchronized radiotherapy to achieve the best possible benefit. These findings should give clinicians confidence to use G-CSF when needed in this situation. We aim to release a complete analysis later this year, which may be helpful in helping to change current guidelines."
Commenting on these findings, Dr. Stefan Zimmermann, Senior Consultant, Medical Oncology, HFR-H?pital Cantonal, Switzerland, said, “Oncologists do need G-CSF to alleviate neutropenia, increase chemotherapy delivery and compliance, but take timely action. The benefits of synchronized therapy outweigh the risk of poisoning."
He continued, "In this study, the use of G-CSF did not lead to an increased risk of pneumonia, but the incidence of severe thrombocytopenia is worrying. The use of G-CSF is beneficial for progression-free survival and overall survival. We can conclude that it is reasonable to use G-CSF for primary or secondary prevention of febrile neutropenia, but patients with a higher risk of thrombocytopenia should be treated with caution."
4. JCI: A prototype drug uses a new mechanism to treat lung cancer
Cells continue to use molecular switches (phosphate molecules) to turn protein expression on and off, and as such, this molecular switch has become a common drug target. In a new study, the researchers found that direct activation of a tumor suppressor protein with a new small molecule prevented lung cancer from growing in mice. The relevant research results were published in the Journal of Clinical Investigation on May 15, 2017, and the title of the paper is "Activation of tumor suppressor protein PP2A inhibits KRAS-driven tumor growth".
Dr. Goutham Narla of Case Western Reserve University in the United States said, "All of the drugs we currently have to treat our cancer patients are targeted kinases, enzymes that attach phosphate molecules to proteins. But, just as important, There is an enzyme that removes the phosphate molecule (ie, phosphatase)."
A phosphatase called PP2A is able to shut down their expression by removing phosphate molecules attached to tumor proteins. However, according to Dr. Narla, "The expression of this tumor suppressor protein is turned off in almost every major cancer. Its inactivation is essential for normal cells to become cancer cells."
Narla and his team decided to adopt an unconventional approach to cancer drug development: look for molecules that directly target PP2A in order to reactivate its tumor suppressive properties.
A total of 54 researchers screened whether a series of drug-like molecules could reactivate PP2A in lung cancer cells and prevent lung cancer tumor growth in mice.
The researchers found that a specific prototype drug can attach to a subunit of the PP2A protein, effectively activating the enzyme. As Dr. Narla explained, this study is the first to use a small molecule to directly activate an enzyme that removes phosphate molecules.
In laboratory models, including preclinical lung cancer cell models and mouse models, this prototype drug also prevents lung cancer cell proliferation. Mice receiving this prototype drug injection have fewer lung cancer tumors and do not experience weight loss or behavioral abnormalities associated with other cancer drugs. In a mouse model, the efficacy of this prototype drug is comparable to the current combination of drugs used to delay lung cancer progression.
To confirm where this prototype drug binds to PP2A, these researchers also developed lung cancer cells that have specific mutations at putative drug binding sites. Mice suffering from tumors produced by these mutant lung cancer cells did not benefit from this prototype drug because the prototype drug was unable to bind and reactivate PP2A.
Narla notes, “About more than 2,000 papers explore the role of PP2A in cancer. In breast cancer, prostate cancer, lung cancer, brain cancer, childhood cancer, ovarian cancer, and endometrial cancer, every major cancer Involving the inactivation of this protein. It allows us to activate the molecules it expresses to have a potential to play a role in a range of cancer patients."
Narla added, “We are testing our prototype drugs in a series of animal models. If things continue to progress well, then we hope to use this prototype drug for clinical trials next year. Our initial clinical trials will be more extensive. It will cover many different types of cancer patients, including lung cancer patients."
The study was conducted in preclinical lung cancer cell models and mouse models, and the results obtained may not be applicable to human lung cancer. Furthermore, mice received lung cancer tumor transplants instead of producing the tumor themselves, and they received this prototype drug treatment for only four weeks. The long-term therapeutic effect of this prototype drug is still unknown.
5. Nature: a key step in revealing the evolution of lung cancer
Lung adenocarcinoma is an invasive lung cancer that accounts for approximately 40% of lung cancer cases in the United States. It is believed to be produced by benign lung adenomas.
Now, in a new study, researchers from the Massachusetts Institute of Technology identified a major molecular switch in the evolution of lung cancer. When a lung adenoma in a lung cancer model mouse is converted to a lung adenocarcinoma, the switch is turned on. They also found that blocking this switch would prevent lung adenomas from becoming more aggressive. Therefore, drugs that interfere with this switch may be suitable for the treatment of early stage lung cancer, they say. The results of the study were published online May 10, 2017 in the journal Nature, entitled "A Wnt-producing niche drives proliferative potential and progression in lung adenocarcinoma".
Tyler Jacks, author of the paper and director of the Koch Comprehensive Cancer Institute at the Massachusetts Institute of Technology, said, "When a tumor changes from a benign state to a malignant state, understanding the molecular pathways that activate it has an important impact on treatment. These findings also help develop prevention or Methods that interfere with the development of advanced disease."
When a small fraction of cells in a lung adenoma begin to become like stem cells, the switch is turned on, allowing them to create new cancer cell populations without restriction.
Tuomas Tammela, the first author of the paper and a postdoctoral researcher at the Koch Comprehensive Cancer Institute at the Massachusetts Institute of Technology, said, "It seems that these stem cells are engines of tumor growth. They are endowed with very strong proliferative potential, they produce other cancer cells, It also produces more stem-like cells."
In this study, the researchers found a focus on the role of a cellular signaling pathway called Wnt. This pathway is usually active during embryonic development, but it is also active in a small population of adult stem cells that are capable of producing specific tissues, such as the intestinal lining.
A major role of the Wnt pathway is to maintain cells in a stem-like state, so these researchers speculate that Wnt may be involved in the rapid proliferation of early lung adenomas that turn into lung adenocarcinoma.
These researchers explored this problem with genetically engineered mice with lung adenomas. These mice usually progress to lung adenocarcinoma. In these mice, they found that Wnt signaling is inactive in lung adenomas, but during this transformation, approximately 5% to 10% of lung adenoma cells activate the Wnt pathway. These cells then produce new cancer cells without restriction.
In addition, approximately 30% to 40% of lung adenoma cells begin to produce a chemical signal that constructs a "niche." This microenvironment is a local environment necessary to maintain cells in a stem cell-like state.
Tammela said, "If you take stem cells out of this microenvironment, then it quickly loses this stem-ness. You have a cell type that forms this microenvironment, and then you have another Accept this microenvironmental signal and behave like a cell type like a stem cell."
Although Wnt has been found to promote tumor formation in some other cancers, including colon cancer, this study suggests that it plays a new role in lung cancer, possibly in other cancers such as pancreatic cancer.
Tammela said, "The novelty of this discovery is that this pathway is not a tumor promoter, but it modifies the characteristics of these cancer cells. It qualitatively changes the way cancer cells behave."
Targeting Wnt
When the researchers asked these mice to take a drug that interferes with Wnt proteins (a Wnt inhibitor), they found that their lung adenomas stopped growing and their survival increased by 50%. Furthermore, when these treated tumor cells are transplanted into another animal, they are not able to produce new tumors.
The researchers also analyzed human lung adenocarcinoma samples and found that 70% of the samples had Wnt activation, and 80% of the samples had microenvironment cells that activated Wnt activity. They say these findings suggest that testing Wnt inhibitors in early lung cancer patients may be worthwhile.
These researchers are also developing methods to deliver Wnt inhibitors in a more targeted manner in order to avoid some of the side effects of these drugs. Another approach that may avoid side effects is to develop more specific inhibitors that only target Wnt proteins that are active in lung adenocarcinoma. The inhibitors they used in this study target all 19 Wnt proteins and are now used in clinical trials for the treatment of other cancers.
6. Cell Rep: Breakthrough! Identify new therapeutic targets that are effective against prostate cancer and lung cancer
Recently, a research report published in the international magazine Cell Reports, researchers from the University of Pennsylvania found that a newly identified molecular chain in a mouse model of prostate cancer may provide treatment for prostate cancer and other cancers. New target.
The researchers said that overexpression of protein PKCε and tumor suppression from Pten deficiency may induce prostate cancer progression, and this lethal combination often induces elevated levels of the cancer-causing molecule CXCL13, when researchers deliberately block CXCL13 or When CXCL5 is expressed, its adsorbed cell surface receptor, mouse prostate cancer cell metastasis, and tumor formation characteristics are impaired.
Researcher Kazanietz said that in addition to providing evidence to reveal the malignant cycle of cancer induced by PKCε, this study also found that blocking CXCL13-CXCL5 molecules may help develop a new type of cancer therapy; researchers plan to identify novel compounds. To block CXCL13 or CXCL5 molecules to help develop potential anti-cancer effects, the researchers also found that levels of CXCL13 in the blood may be used as a biomarker to help determine the accuracy of prostate cancer progression in patients' bodies. status.
In the next step, researchers will clarify how to interfere with CXCR5/CXCL13 from cancer cells and cells in the vicinity of the tumor microenvironment. Cancer growth and development can also be induced in the vicinity of the tumor microenvironment. Nowadays, both chest and lung oncologists and oncologists have found that PKCε protein is overexpressed in lung cancer patients, but they do not understand the exact molecular event results. In general, higher levels of PKCε protein tend to be poorer than patients. Related.
The final researcher Kazanietz said that based on the results of this study, we may have made new discoveries in the field of lung cancer research, and we will conduct in-depth joint research to develop new therapies or pharmaceutical preparations for prostate cancer and lung cancer.
7. Cancer Res: Circulating tumor cells can predict the survival of patients with lung cancer
For non-small cell lung cancer patients with ALK rearrangement, their clinical response duration and drug strength to crizotinib are unpredictable, and almost all patients will eventually develop resistance.
In a new study, researchers from France evaluated whether circulating tumor cells with abnormal ALK-FISH patterns were predictive of progression-free survival in ALK rearrangement patients treated with crizotinib. The relevant research results were published in the international academic journal Cancer Research.
In this study, the researchers enrolled 39 patients with non-small cell lung cancer with ALK rearrangement who were treated with crizotinib as an ALK inhibitor. The researchers collected blood samples from baseline and patients treated with crizotinib for two months, using immunofluorescence staining combined with filtration and concentration to detect abnormal ALK-FISH patterns in circulating tumor cells.
The researchers classified circulating tumor cells into different subpopulations based on ALK rearrangement and ALK-CNG signaling. They found no significant association between baseline number of ALK rearrangement or ALK-CNG circulating tumor cells and progression-free survival. However, they observed a significant association between a decrease in the number of ALK-CNG circulating tumor cells and a longer progression-free survival after receiving crizotinib.
The researchers also found through multivariate analysis that dynamic changes in ALK-CNG circulating tumor cells are the strongest factors associated with progression-free survival. Studies have shown that ALK-CNG is one of the important mechanisms by which tumors acquire resistance to crizotinib.
The results of this study suggest that dynamic changes in the number of circulating tumor cells in ALK-CNG may be a predictive biomarker that can be used to assess the efficacy of crizotinib in patients with ALK rearranged non-small cell lung cancer. A series of molecular analyses of circulating tumor cells suggest that real-time monitoring of patients and prediction of clinical outcomes in patients is expected in the future.
8. White blood cell count predicts the effectiveness of lung cancer immunotherapy
Recently, a study reported at the European Lung Cancer Congress (ELCC) showed that white blood cell counts can be used to predict whether lung cancer patients will benefit from immunotherapy. The ELCC is an important scientific exchange academic conference for medical professionals in the field of lung cancer in Europe. It is organized by the European Society of Medical Oncology (ESMO) and the International Association for the Study of Lung Cancer (IASLC). The ELCC provides a comprehensive multidisciplinary overview of the latest knowledge of breast malignancies, covering prevention, screening, diagnosis, treatment modalities, and the results of basic, clinical, and translational research, with the participation of leading international experts and presentations.
The study's lead author, Dr. Marcello Tiseo, DMT Thoracic Oncology Surgery, University Hospital of Parma, Italy, said: "Immunoside checkpoint inhibitors such as nivolumab and pembrolizumab monoclonal antibodies significantly increase non-small cell lung cancer (NSCLC) Overall survival of patients. Researchers are looking for a predictive biomarker to select patients who will benefit from this treatment to avoid unnecessary drug toxicity and waste of resources in some unresponsive patients."
He continued: "The amount of PD-L1 expression in tumor biopsy is used to select the appropriate patient, but the protocol is not completely accurate, probably because it does not reflect a dynamic immune response. Biomarkers in the blood are easier Obtained, may be a better indicator of immune response."
This study assessed whether white blood cell counts predict whether lung cancer patients respond to nivolumab monoclonal antibody therapy. The study involved 54 patients with NSCLC who received a dose of 3 mg/kg of nivolumab every 14 days. White blood cell counts were performed at baseline, after the second nivolumab cycle and after the fourth nivolumab cycle. The researchers compared white blood cell counts for nivolumab responders and non-responders and found that white blood cell counts predict whether patients will respond to nivolumab mAb treatment during baseline and treatment. At baseline levels, the number and concentration of natural killer cells in the respondent increased, and the number of natural killer cells increased during treatment. Patients who responded to nivolumab mAb also had a greater number and higher concentration of CD8-positive T cells, which expressed PD-1.
Dr. Marcello Tiseo said: "The number and function of natural killer cells and the frequency of PD-1 expression in CD8-positive T cells may be predictive biomarkers of nivolumab treatment in advanced NSCLC. Identifying a set of blood-predicting biomarkers will enable early Identify patients who are most likely to benefit from anti-PD-1 and anti-PD-L1 treatment."
Swiss HFR-H? Dr. Stefan Zimmermann, Senior Consultant, Medical Oncology, pital Cantonal, commented on the findings: "In the current era of precision medicine, we urgently need appropriate predictive biomarkers to select patients who will benefit from specific treatments. It has been found that baseline levels of certain leukocytes do play a role in predicting immunotherapeutic responses in lung cancer patients. We should study these new factors in future clinical trials, along with tumor PD-L1 expression and other markers that make up the cancer immune map. Together, predict whether patients can benefit from treatment."
9. Cell: Identification of immunotherapeutic targets for early stage lung cancer
Immunotherapy has achieved remarkable results in patients with advanced lung cancer. Now, in a new study, researchers from research institutions such as the Icahn School of Medicine at Mount Sinai have found that immunotherapy has great promise in treating newly diagnosed lung cancer patients. This deadly disease has the opportunity to stop it before standing firm, providing a potential cure. The results of the study were published in the May 4, 2017 issue of Cell, titled "Innate Immune Landscape in Early Lung Adenocarcinoma by Paired Single-Cell Analyses."
Researchers at the Tisch Cancer Institute at the Icahn School of Medicine in Mount Sinai have found that some of the same immune cells have just gained a foothold in immune cells that allow immunotherapy to improve the condition of some patients with advanced lung cancer. It also exists. The author of the paper, Dr. Miriam Merad, professor of oncology at the Tisch Cancer Institute and chief physician (hematology and internal medicine oncology) said that before this, little was known about the immune response in early stage lung cancer.
When lung cancer patients undergo surgery to remove cancerous lesions, Dr. Merad and his team obtained lung tumor samples from these patients, surrounding healthy lung tissue samples, and blood samples, and immediately analyzed the samples at the cellular level to map the presence of immunity. System component map.
The Merad team devised a bar code approach: attaching a different metal isotope to the cells in each sample, allowing the samples to be brought together for simultaneous analysis of cells from these three tissue types. They combined this bar code approach with multiscale immune profiling to map a complete immune cell map to find tumor-driven changes. These changes will be susceptible to targeted immunotherapy.
Analysis of these samples indicates that immune system components are already present in stage I lung cancer lesions, and these components may disrupt the ability of anti-tumor T cells to fight cancer. These single-cell analysis results unpredictably reveal tumor-driven immune changes in detail, providing a powerful tool for developing new immunotherapies in the future, such as immunological checkpoint inhibitors, especially those targeted to protect cancer from the immune system. Immunological checkpoint inhibitors of PD-1 and PD-L1 proteins; these immunological checkpoint inhibitors have been shown to have great promise in the treatment of advanced cancer.
Dr. Merad said, "Immune therapy is mainly used to treat advanced or metastatic lung cancer, but its benefits in the treatment of early stage tumors are still unknown. The standard treatment for early stage lung cancer is usually the use of surgical resection of the lesion, sometimes accompanied by chemotherapy and Radiotherapy. Our study reveals that early lung lesions infiltrate a large number of different immune cells, suggesting that immunotherapy may also be used to treat extremely early lesions and potentially develop a cure that is truly Stop the ground before the lungs stand firm."
The new study also identified a number of additional immunotherapeutic targets, thereby increasing the number of patients who benefited significantly from immunotherapy. For the time being, the number of patients benefiting from immunotherapy is still relatively small. Currently, this study is being used to conduct clinical trials of immunotherapy for patients with early stage lung cancer.
Dr. Merad said, "About 50% of patients with small cell lung cancer will relapse. When lung cancer enters advanced stage, chemotherapy does not have a great success rate, so knowing how to attack early lung cancer may be the number of patients who relapse and their overall survival. The period has had a major impact. Our research further confirms that immunotherapeutic agents are the most effective in treating early cancer, especially in patients who have never received chemotherapy.
10. Nat Commun: A major discovery! A subtype of lung cancer can be transformed into another subtype!
Recently, a research report published in the international magazine Nature Communications, researchers from the University of Kentucky found that under certain genetic conditions, a non-small cell lung cancer may be transformed into another lung cancer subtype. .
The lineage switch of lung cancer is resistant to some cancer therapies. In this study, the researchers specifically examined the mechanism by which this lineage switch occurred. In previous studies, the researchers did not know which cells in the adult lungs are the cell origins of the two major subtypes of non-small cell lung cancer, the two major lung cancer subtypes are adenocarcinoma and squamous cell carcinoma; Similarly, researchers are not aware of the differences in DNA assembly between different lung cancer subtypes. The presence of lung adenocarcinoma is clinically defined as the presence of all adenocarcinoma lesions, and there is a marked stratification of squamous lesions in the same tumor, suggesting that lung adenocarcinoma and squamous cell carcinoma may be from the lungs. The same cells in the organization, but the current researchers lack clear evidence to confirm this.
In this study, the researchers found that lung adenocarcinoma cells can be reassembled in a special way to transform into squamous cell carcinoma of the lung. By studying the mouse model of adenocarcinoma lung tumors, the researchers will This is inherited from human adenocarcinoma lung tumors. Human adenocarcinoma lung tumors are genetically identical to mice, including activation of oncogene KRAS and tumor suppression from Lkb1; Subsequently, the researchers conducted a transplant test and found that in the mouse body, the established lung adenocarcinoma tumor can be transformed into lung squamous cell carcinoma.
The researchers then isolated different lung cells, and studies showed that only certain lung cells were able to produce lung tumors with lineage switching properties. Researcher Christine Fillmore Brainson said that the data in this study made us very excited. We found that cells in lung tissue can produce adenocarcinoma tumors, and the technology we use to transform and separate cells can also be applied to the depth of various lung cancers. researching. When EGFR tyrosine kinase inhibitor therapy fails, many oncologists have observed the presence of a lineage switch, which is often clinically performed for a second biopsy, but usually the second biopsy is often not performed after chemotherapy, the investigator It is believed that this practice may revise our understanding of the specific mechanisms of chemotherapy tolerance.
Finally, researcher Brainson pointed out that now that we have elucidated the molecular mechanisms of lineage switches, we will also begin to delve into how to manipulate this mechanism to develop new individualized therapies for the treatment of lung cancer.
Source: Bio Valley
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