MedComm – Oncology最新文献

{"title":"Immune checkpoint inhibitor-related myocarditis in thymic epithelial tumors: Recent progress and perspectives","authors":"Jianqiong Yin,&nbsp;Zhuoran Yao,&nbsp;Jing Pan,&nbsp;Lu Gan,&nbsp;Jianxin Xue","doi":"10.1002/mog2.31","DOIUrl":"https://doi.org/10.1002/mog2.31","url":null,"abstract":"<p>Thymic epithelial tumors (TETs) are rare anterior mediastinal malignancies originating in the thymus with poor outcomes, and standard platinum-based chemotherapy shows limited efficacy for treating metastatic or recurrent disease. In this setting, further improved novel treatment strategies are needed. Immune checkpoint inhibitors (ICIs) are widely applied in clinical practice for cancer therapy and early results of clinical trials have brought notable objective responses and lasting survival benefits to patients with TETs. However, the incidences of immune-related adverse events (irAEs), especially cardiac adverse events, are higher than those of other tumor types. Myocarditis is a rapidly progressive and life-threatening irAE in patients treated with ICIs, thereby hindering the further utilization of ICI in TETs patients. Therefore, this article aims to review the results of case series and clinical trials that evaluated ICIs for the treatment of TETs and to provide an overview of the clinical features of fatal ICI-related myocarditis in TETs. Furthermore, we approach insights into the immunobiology of thymic tumors and focus on revealing the mechanisms of cardiotoxicity in patients with TETs, hoping to provide several valuable insights for maximizing the therapeutic potential of ICIs in TETs.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.31","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50136174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new synthetic lethal strategy expands the application of PARP inhibitors/cisplatin","authors":"Jinrui Wang,&nbsp;Daniel D. Billadeau,&nbsp;Ying Zheng,&nbsp;Da Jia","doi":"10.1002/mog2.28","DOIUrl":"https://doi.org/10.1002/mog2.28","url":null,"abstract":"<p>In a recent study published in <i>Signal Transduction and Targeted Therapy</i>, <i>Zhang</i> et al.<span>¹</span> identified a panel of genes that served as a novel predictor of response to poly adenosine diphosphate-ribose polymerase (PARP) inhibitors/cisplatin in HR proficient patients, which could guide a broader application of PARP inhibitors/cisplatin in cancer therapy.</p><p>Cancer cells differ from normal cells in their ability to repair damaged DNA—most cancer cells lose one or more DNA repair pathways, resulting in greater reliance on the remaining pathways.<span>²</span> Thus, small molecules that can induce DNA damage have been used to treat various cancers. Among them, cisplatin/PARP inhibitors are well established cancer drugs and are used to target tumor cells with homologous recombination (HR) defects.<span>²</span> Platinum salts (carboplatin, cisplatin, and oxaliplatin) are the commonly-used chemotherapeutic agents, which were historically thought to cause cell death by inducing DNA damage.<span>²</span> Recent studies suggest that the mechanisms of action of platinum salts are more diverse<span>³</span> (Figure 1A). Zhang et al.<span>¹</span> further showed that cisplatin promotes cell death through DNA damage-induced ribosomal stress, rather than failed DNA repair, in certain tumor cells. PARP inhibitors are approved for the treatment of ovarian and breast cancers with BRCA1/2 mutations, and act through synthetic lethality in DNA repair-deficient tumors.<span>^3-5</span> However, it is known that some HR-proficient patients also respond well to PARP inhibitors and cisplatin therapy.<span>³</span> Consistently, Zhang et al.<span>¹</span> also identified patients who benefited from the treatment of PARP inhibitors, despite their normal HR functions. Therefore, it is necessary to identify biomarkers that can help to stratify the patients so they will benefit most from PARP inhibitors and cisplatin therapy.</p><p>To identify these biomarkers, the authors analyzed RNA-Seq data from the Cancer Cell Line Encyclopedia and drug sensitivity data (GDSC) from the extensive and Sanger cell line databases<span>¹</span> (Figure 1B). They used weighted gene co-expression network analysis to negatively correlate drug signatures with co-expressed gene modules.<span>¹</span> Through these analyses, the authors found that expression of genes in the ribosome biogenesis pathway could be used to predict cellular drug response to PARP inhibition or cisplatin-based chemotherapy.<span>¹</span> Ultimately, they obtained a panel of 8 genes involved in ribosome biogenesis for further analysis.<span>¹</span></p><p>In the following studies, the authors provided multiple lines of evidence suggesting that these eight genes could be used to predict PARP inhibitors/cisplatin sensitivity.<span>¹</span> First, ","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.28","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50144503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of DAPK1 and Beclin1 under oxygen and glucose deprivation conditions promotes excessive autophagy and apoptosis in A549 cells","authors":"Linlin Wu,&nbsp;Wenxue Sun,&nbsp;Dehua Liao,&nbsp;Yujin Guo,&nbsp;Qingying Si,&nbsp;Dadi Xie,&nbsp;Pei Jiang","doi":"10.1002/mog2.30","DOIUrl":"https://doi.org/10.1002/mog2.30","url":null,"abstract":"<p>In this study, we aimed to determine the specific roles of death-associated protein kinase 1 (DAPK1) and Beclin1 in non-small cell lung cancer (NSCLC) under oxygen and glucose deprivation (OGD). We found that OGD caused most cells to shrink, aggregate, and produce many vacuoles in the cytoplasm. Transmission electron microscopy revealed the presence of autophagic vesicles in the OGD group but not in the Control group. Moreover, the cell counting kit-8 assay showed that cell proliferation was reduced in the OGD group. Quantitative reverse transcription-polymerase chain reaction, western blot, and cell function assays showed that DAPK1 overexpression under OGD promoted apoptosis and autophagy in A549 cells. The coimmunoprecipitation assay confirmed the interaction between DAPK1 and Beclin1 protein. Moreover, knockdown of Beclin1 inhibited autophagy, but its overexpression promoted apoptosis in A549 cells. In vivo tumorigenesis experiment revealed that overexpression of DAPK1 promoted A549 cell apoptosis. Collectively, overexpression of DAPK1 and Beclin1 under OGD promoted excessive autophagy and apoptosis in A549 cells. Our study may provide a novel therapeutic target and theoretical basis for NSCLC treatment.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.30","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50143946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NKT cells contribute to alleviating lung metastasis in adenoid cystic carcinoma","authors":"Ge-xuan Feng,&nbsp;Meng-jiao Zhou,&nbsp;Lin Cao,&nbsp;Ting-yao Ma,&nbsp;Xue-lian Wang,&nbsp;Ran Gao,&nbsp;Xiao-hong Chen,&nbsp;Lu Kong","doi":"10.1002/mog2.29","DOIUrl":"https://doi.org/10.1002/mog2.29","url":null,"abstract":"<p>Salivary adenoid cystic carcinoma (SACC) with a unique <i>MYB-NFIB</i> fusion has been considered an “immune-cold” tumor, but the mechanisms behind this remain unclear. In this study, we analyzed the immune status of 29 SACC patients and found that most lung metastases exhibited an immunoinflammatory state, in contrast to the primary SACC tissues. Single-cell sequencing data showed that anergic T-cell types were low in primary inflammatory tissues, while inflammatory metastatic lung tissues had elevated levels of anergic CD8⁺ natural killer T (NKT)-like cells and low levels of memory T cells. Primary exclusive tissues had high levels of myeloid-derived suppressor cells (MDSCs) and low levels of activated CD8⁺ NKT-like cells. These data support the fact that metastatic SACC cells might induce a stronger immune response in the lung. Additionally, an in vivo experiment showed that a minimally invasive SACC cell line with higher expression of human leukocyte antigens -B and -C induced NKT cell activation in mice and effectively attenuated the incidence of lung metastases caused by a highly invasive SACC cell line. This suggests that NKT therapy may be active in treating SACC lung metastasis. Conclusively, this study sheds light on the immune microenvironment of SACC and highlights the potential of NKT-based therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.29","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50133264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of pyroptosis-related clusters for prediction of overall survival and characterization of tumor microenvironment infiltration in laryngeal squamous cell carcinoma","authors":"Wei Du,&nbsp;Xueming Xia,&nbsp;Jiayun Yu,&nbsp;Bin Shao","doi":"10.1002/mog2.26","DOIUrl":"https://doi.org/10.1002/mog2.26","url":null,"abstract":"<p>Laryngeal squamous cell carcinoma (LSCC) accounts for one-third of head and neck squamous carcinoma (HNSCC). Although improvements have been made in treatments, the prognosis of patients with LSCC is unsatisfactory. Pyroptosis creates an environment that inhibits tumor growth in various cancers, but pyroptosis regulation in the tumor immune microenvironment in LSCC remains little known. The Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to collect clinical traits and gene expression data of LSCC patients. We present a systematic overview of the immune microenvironment of LSCC based on genetics and transcriptional profiles of pyroptosis-related genes (PRGs) and divide 220 LSCC into three distinct PRGclusters. Based on the three survival-related PRGs identified in Lasso-penalized Cox regression, samples from the training and validation cohorts were divided into two discrete geneClusters. We construct a prognostic model based on Risk score, quantify pyroptosis level and link it with patient outcome. Furthermore, we verified the expression level of one prognostic gene Basic Leucine Zipper ATF-Like Transcription Factor at the tissue level in the validation experiment. These findings reveal the crucial role of pyroptosis and can assist in predicting patient prognosis, guiding optimal treatment choices, and developing new immunotherapies for LSCC.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.26","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50141289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision gas therapy by ultrasound-triggered for anticancer therapeutics","authors":"Fangxue Du,&nbsp;Ruiqian Guo,&nbsp;Ziyan Feng,&nbsp;Ziyao Wang,&nbsp;Xi Xiang,&nbsp;Bihui Zhu,&nbsp;Raul D. Rodriguez,&nbsp;Li Qiu","doi":"10.1002/mog2.27","DOIUrl":"https://doi.org/10.1002/mog2.27","url":null,"abstract":"<p>In recent years, ultrasound, as an external stimuli that can activate different types of naonocatalysts for therapy, has attracted extensive attention. One characteristic that makes ultrasound a particularly attractive trigger stimulus for nanomedicine is that it can be applied to the deep regions of the body noninvasively in a focused way. Different biological effects can be achieved by integrating ultrasound with nanocatalysts, and nanodroplets. Gas therapy, as a green antitumor treatment, has attracted substantial attention. The development of nanotechnology and nanomedicine has made gas therapy more precious by controlled release under internal, and outside factors and targeted delivery. In this article, an overview of ultrasound-based gas therapy on antitumor therapy has been provided. First, we explored the mechanism of ultrasound-triggered gas release. Second, we list the common gas release pathways and their mechanism in response to ultrasound activity. Third, exemplary instances of gas-generating facilities under ultrasound controllable are explored, with an emphasis on their originality and guiding principles. The impact of the gas-generating platform as a tumor therapy has also been considered. Finally, the difficulties and future prospects for this effective therapeutic approach are examined.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.27","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50139143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty acids in cancer: Metabolic functions and potential treatment","authors":"Ao Du,&nbsp;Zhen Wang,&nbsp;Tengda Huang,&nbsp;Shuai Xue,&nbsp;Chuang Jiang,&nbsp;Guoteng Qiu,&nbsp;Kefei Yuan","doi":"10.1002/mog2.25","DOIUrl":"https://doi.org/10.1002/mog2.25","url":null,"abstract":"<p>Lipid metabolic reprogramming is one of the important metabolic characteristics of cancer cells. As major components of lipids, fatty acids provide energy and material basis for cancer cell survival. Abnormal fatty acid metabolism has been found in many cancers. Fatty acid uptake, transport, and synthesis are closely related to the pathogenesis of cancer. Meanwhile, fatty acid changes in the membrane structure of cancer cells and signal transduction mediated by signaling lipids are also helping cancer cells survive in the changing microenvironment. Some of these enzymes and metabolites involved in fatty acid metabolism are emerging as unique cancer biomarkers. Multiple studies have shown that disordered fatty acids can regulate tumor cell proliferation, metastasis, and drug resistance. Therefore, targeting fatty acid metabolism has become a promising treatment strategy. Here, we mainly present metabolic alterations of fatty acids, the basic components of lipids, in cancer. We discuss the cancer treatment based on fatty acid and fatty acid metabolism. These may provide a basis for a better understanding of lipid metabolic reprogramming in cancer, and also provide new ideas for cancer biomarker search, drug development, and combination therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.25","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50127649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morus alba derived Kuwanon-A combined with 5-fluorouracil reduce tumor progression via synergistic activation of GADD153 in gastric cancer","authors":"Jingjing Su,&nbsp;Abhimanyu Thakur,&nbsp;Guangzhao Pan,&nbsp;Jianglong Yan,&nbsp;Isha Gaurav,&nbsp;Sudha Thakur,&nbsp;Zhijun Yang,&nbsp;Alma Cili,&nbsp;Kui Zhang","doi":"10.1002/mog2.24","DOIUrl":"https://doi.org/10.1002/mog2.24","url":null,"abstract":"<p>Despite the application of conventional strategies including chemotherapy, radiotherapy, surgery, or immunotherapy, the mortality of gastric cancer (GC) patients remains high. Often, GC is not diagnosed until it has reached late stage, resulting in a missed surgical window. Therefore, a new therapeutic intervention for GC is necessary. Here, the combined application of Kuwanon-A (KA) and 5-fluorouracil (5-FU) was evaluated for its potential to combat GC for the first time. To determine the anticancer activity of KA (from <i>Morus alba</i>) along with 5-FU against GC, and their mechanism via GADD153, we examained anticancer potential of KA along with 5-FU via in vitro assays with GC cells, namely MKN-45, SGC-7901, HGC-27, and BGC-823, and in vivo assays with mouse xenograft of GC. KA alone could induce G2/M phase arrest and apoptosis in GC cells by activating GADD153 through the PERK/elF2α/ATF4 and IRE1/XBP1 signaling pathways, suggesting a critical role of increased endoplasmic reticulum stress in KA-induced apoptosis of GC cells. Moreover, the combination of KA and 5-FU showed an enhanced synergistic anticancer effect against GC both in vitro and in vivo. Conclusively, the combination of KA and 5-FU can act as an effective anticancer regimen in combating GC.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.24","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50137825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insight on the cellular and molecular basis of blood vessel formation: A specific focus on tumor targets and therapy","authors":"Nimish Mol Stephen,&nbsp;Udayawara Rudresh Deepika,&nbsp;Tehreem Maradagi,&nbsp;Tatsuya Sugawara,&nbsp;Takashi Hirata,&nbsp;Ponesakki Ganesan","doi":"10.1002/mog2.22","DOIUrl":"https://doi.org/10.1002/mog2.22","url":null,"abstract":"<p>The cellular and molecular switches that govern angiogenesis are considered therapeutic targets for several diseases like tumors and atherosclerosis. Thus, understanding the detailed molecular mechanisms underlying the formation of the new blood vessel is essential for developing novel therapeutic strategies. The formation of a new blood vessel (angiogenesis) is tightly regulated by balancing pro- and antiangiogenic molecules. Dysregulated angiogenesis contributes to the pathogenicity of several diseases, including tumors associated with uncontrolled vessel growth. Experimental and clinical studies emphasize that angiogenesis is a critical step for the transition of the tumor to a life-threatening malignancy. In recent years, angiogenesis has been targeted as one of the primary therapeutic goals for treating tumors, and rapid progress has been made by modulating its molecular regulators. Hence, the mechanisms of how blood vessel formation occurs could provide molecular insight into future angiogenic therapy. This review summarizes briefly the molecular players of blood vessel formation comprising vasculogenesis and angiogenesis and their role in tumor progression alongside antiangiogenic therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.22","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50124915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic virotherapy using neural stem cells as a novel treatment option for glioblastoma multiforme","authors":"Tanvir Ahmed","doi":"10.1002/mog2.23","DOIUrl":"https://doi.org/10.1002/mog2.23","url":null,"abstract":"<p>The most deadly and aggressive form of brain cancer is called a glioblastoma multiforme. Following diagnosis, the median duration of survival is only 14 months. It is imperative to develop cutting-edge therapeutic options because the results of conventional treatments are so poor. Replication-competent oncolytic viruses and replication-deficient viral vectors can be used to treat malignant tumors, an idea that has been around for more than a century. Cancer cells can be eliminated by any class. Oncolytic viruses are created with the specific purpose of locating, attacking, and multiplying in cancerous cells while bypassing normal brain tissue. Because of this, the viruses can kill tumors while protecting healthy brain cells. Getting the oncolytic virus reach tumor locations where it is needed is the biggest challenge. If neural stem cells were used as carrier cells to deliver oncolytic viruses to the right tumor locations, glioblastoma multiforme virotherapy will be significantly more efficient. The most recent advancements in the field of utilizing neural stem cells to deliver oncolytic viruses into glioblastoma tumors are the main focus of this review.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.23","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50156065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}