MedComm – Oncology最新文献

{"title":"VISTA-targeted antibody-drug conjugates exhibit potent antitumor effects on malignant pleural mesothelioma","authors":"Jingyue Kang,&nbsp;Zongliang Zhang,&nbsp;Ruyuan Zhang,&nbsp;Meijun Zheng,&nbsp;Caiying Jiang,&nbsp;Hui Yang,&nbsp;Aiping Tong,&nbsp;Yan Zhang","doi":"10.1002/mog2.78","DOIUrl":"https://doi.org/10.1002/mog2.78","url":null,"abstract":"<p>Malignant pleural mesothelioma (MPM) is a malignant tumor of the pulmonary pleural tissue for which there is a lack of effective targeted therapy. In this study, moderate to high V-domain immunoglobulin T-cell activation suppressor (VISTA) expression levels were observed in most MPM clinical tumor samples. We prepared two high-affinity anti-VISTA monoclonal antibodies (mAbs) and generated two novel VISTA-targeted antibody-drug conjugates (ADCs) by conjugating anti-VISTA mAbs with the potent cytotoxic drug monomethyl auristatin E (MMAE). αV1-MMAE and αV2-MMAE showed potent killing effects to VISTA-positive cell lines in vitro, with half-maximal inhibitory concentration (IC₅₀) of nanomolar levels. αV1-MMAE and αV2-MMAE were also able to significantly induce apoptosis and cause G2/M phase arrest in VISTA-positive cells. In the VISTA-positive human MPM xenograft model, both αV1-MMAE and αV2-MMAE showed significant antitumor activity, led to a significant survival advantage compared to mice in the control group, and effectively induced apoptosis in the tumor tissues of mice. In conclusion, we demonstrated that the novel VISTA-targeted ADCs (αV1-MMAE and αV2-MMAE), especially αV1-MMAE, had potent killing effects against VISTA-positive MPM cells both in vitro and in vivo. Therefore, through further development, they may have the potential to become new drugs for the treatment of MPM.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.78","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141182269","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":"Mechanism and application of acupuncture and electro-acupuncture associated with cancer therapy","authors":"Xinggang Yang,&nbsp;Guangqi Li,&nbsp;Jiaqing Yang,&nbsp;Xuelei Ma","doi":"10.1002/mog2.73","DOIUrl":"https://doi.org/10.1002/mog2.73","url":null,"abstract":"<p>The rapid progress in cancer treatment, along with the increase in cure and control rates, has led to the gradual acceptance of cancer as a chronic disease. Cancer treatment is comprehensive and long-term. However, cancer symptoms and treatment side effects can hinder patients' quality of life and adherence to treatment, ultimately impacrefting their long-term survival. Acupuncture (AC) and electro-acupuncture (EA) have been widely used to treat various diseases. AC and EA have demonstrated their ability to relieve symptoms and side effects related to cancer treatment. The review provides a brief overview of the historical lineage and basic principles of AC treatment, as well as a detailed exploration of the mechanisms and clinical applications of AC and EA to relieve cancer symptoms and treatment side effects. AC and EA can play a therapeutic role by regulating systems of nervous, endocrine, immune and so on. Clinical studies have demonstrated that AC and EA can effectively relieve pain, postoperative ileus, and other symptoms. The safety of AC and EA has been tested worldwide. Furthermore, we discuss the challenges and future research directions for AC and EA in the field of cancer treatment.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.73","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141069065","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":"Pathogenic mechanisms and etiologic aspects of Mycobacterium avium subspecies paratuberculosis as an infectious cause of cutaneous melanoma","authors":"Ellen S. Pierce,&nbsp;Charulata Jindal,&nbsp;Yuk Ming Choi,&nbsp;Kaitlin Cassidy,&nbsp;Jimmy T. Efird","doi":"10.1002/mog2.72","DOIUrl":"https://doi.org/10.1002/mog2.72","url":null,"abstract":"<p>Infectious etiologies have previously been proposed as causes of both melanoma and non-melanoma skin cancer. This exploratory overview explains and presents the evidence for the hypothesis that a microorganism excreted in infected ruminant animal feces, <i>Mycobacterium avium</i> subspecies <i>paratuberculosis</i> (MAP), is the cause of some cases of cutaneous melanoma (CM). Occupational, residential, and recreational contact with MAP-contaminated feces, soil, sand, and natural bodies of water may confer a higher rate of CM. Included in our hypothesis are possible reasons for the differing rates and locations of CM in persons with white versus nonwhite skin, why CM develops underneath nails and in vulvar skin, why canine melanoma is an excellent model for human melanoma, and why the Bacille Calmette-Guérin (BCG) vaccine has demonstrated efficacy in the prevention and treatment of CM. The pathogenic mechanisms and etiologic aspects of MAP, as a transmittable agent underlying CM risk, are carefully deliberated in this paper. Imbalances in gut and skin bacteria, genetic risk factors, and vaccine prevention/therapy are also discussed, while acknowledging that the evidence for a causal association between MAP exposure and CM remains circumstantial.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.72","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140914763","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":"Transpiration of neurological phenomena in cancer: Long-term depression (LTD) abrogates cancer stem cell memory and sensitizes it to metabolic therapy","authors":"Gayathri Ravichandran,&nbsp;Aravind Kumar Rengan","doi":"10.1002/mog2.71","DOIUrl":"https://doi.org/10.1002/mog2.71","url":null,"abstract":"<p>Therapy resistance and recurrence are irrefutably ascribed to the unique attributes of the cancer stem cell (CSC) population. Therefore, discerning the underlying mechanism is imperative in arbitrating a strategic therapeutic approach. In this study, we have observed the coexistence of neuron-like cell (NLC) subpopulations in different cancer cell lines. The NLC subset was further validated by transfection studies and was found to be positive for PSD-95. As a proof of concept, we have also demonstrated the transpiration of neurological phenomena such as long-term potentiation (LTP) and long-term depression (LTD) in cancer. We have utilized PMA drug and IL-13 cytokine to study LTD and LTP, respectively, and observed a correlation between the memory marker (GLUN2B) and stemness markers (CD95 and CD58). Moreover, the transcriptional protein pCREB, which plays a crucial role in memory formation, was found to influence CD44 protein levels. These findings suggest that the instigation of LTD can impair cellular memory and sensitize CSC to the metabolic inhibitor, 3Bromopyruvate. Furthermore, this study interfaces the neurobiology of cancer and nanomedicine, wherein we have used biomimetic nanocarriers for the active targeting of drugs and demonstrate their ability to augment therapeutic efficiency.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.71","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140641900","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":"The biological essence of synthetic lethality: Bringing new opportunities for cancer therapy","authors":"Meiyi Ge,&nbsp;Jian Luo,&nbsp;Yi Wu,&nbsp;Guobo Shen,&nbsp;Xi Kuang","doi":"10.1002/mog2.70","DOIUrl":"https://doi.org/10.1002/mog2.70","url":null,"abstract":"<p>Synthetic lethality (SL), a genetic concept, has revolutionized the development of antitumor therapies by providing avenues to target previously “undruggable” targets with enhanced specificity for tumor cells over normal tissue. The principles of SL have expanded beyond genetic definitions to encompass biological functions, including genome stability, cell cycle regulation, cell death mechanisms, cellular metabolism, cell–cell interactions, and the tumor microenvironment (TME). Tumor cells with inactivated survival pathways are sensitive to therapeutic inhibition of compensatory mechanisms, while normal cells remain unaffected. Exploiting SL based on functional contexts has the potential to significantly improve cancer patient survival by reducing resistance to targeted therapies and enhancing antitumor efficacy when combined with other treatment modalities. This review explores the underlying mechanisms of synthetic lethality interactions (SLI) characterized by biological functions in individual cancer cells and the TME. We also provide a comprehensive summary of strategies for leveraging the dynamic nature of SLI to overcome therapeutic resistance. Additionally, we discuss various approaches and models for screening and designing potent SL agents tailored to the specific needs of cancer patients, as well as strategies for combining SL drugs in tumor treatment. This review offers valuable insights into harnessing SL as a promising avenue for precision cancer therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140321799","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 into Janus kinases specificity: From molecular architecture to cancer therapeutics","authors":"Tian-Hua Wei,&nbsp;Meng-Yi Lu,&nbsp;Si-Hui Yao,&nbsp;Yu-Qi Hong,&nbsp;Jin Yang,&nbsp;Meng-Yuan Zhang,&nbsp;Yu-Qi Yin,&nbsp;Yu-Jie Han,&nbsp;Qing-Qing Li,&nbsp;Zi-Xuan Wang,&nbsp;Yi-Bo Wang,&nbsp;Zhen-Jiang Tong,&nbsp;Yun Zhou,&nbsp;Wei-Chen Dai,&nbsp;Yan-Cheng Yu,&nbsp;Shan-Liang Sun,&nbsp;Ye Yang,&nbsp;Nian-Guang Li,&nbsp;Zhi-Hao Shi","doi":"10.1002/mog2.69","DOIUrl":"https://doi.org/10.1002/mog2.69","url":null,"abstract":"<p>Janus Kinases (JAKs) play a crucial role as therapeutic targets for various cancers. However, the current JAK inhibitors (JAKi) available have limited therapeutic benefits due to their lack of selectivity. This review focuses on the structural analysis to elucidate the molecular determinants of JAKs specificity and the discovery and design of selective JAKi. It includes descriptions and comparison of different JAK structures and their binding sites, a comparative analysis of JAKi and their binding modes, detailed interaction fingerprints (IFPs), and an extensive structure-selectivity relationship (SSRs). Moreover, the review also explores the challenges and possibilities of using computational structure-based methods for discovering and designing selective JAKi. Other structure-based approaches, such as targeting the pseudokinase domain, as well as covalent and allosteric designs, are also covered. Based on this analysis, key determinants corresponding to JAK specificity and rational medicinal chemistry strategies are proposed to facilitate the development of highly selective JAKi. Overall, we aim to enhance the understanding of JAK specificity and explore strategies that can lead to the discovery of effective and selective JAKi in cancer therapy, thus improving the prognosis for cancer patients.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.69","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140291393","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":"Advances and applications of nanoparticles in cancer therapy","authors":"Xianzhou Huang,&nbsp;Tao He,&nbsp;Xiuqi Liang,&nbsp;Zhongzheng Xiang,&nbsp;Chao Liu,&nbsp;Shiyao Zhou,&nbsp;Rui Luo,&nbsp;Liping Bai,&nbsp;Xiaorong Kou,&nbsp;Xinchao Li,&nbsp;Rui Wu,&nbsp;Xinyu Gou,&nbsp;Xinyue Wu,&nbsp;Dongxue Huang,&nbsp;Wangxian Fu,&nbsp;Yingjie Li,&nbsp;Ruhan Chen,&nbsp;Ningyue Xu,&nbsp;Yixi Wang,&nbsp;Hao Le,&nbsp;Tao Chen,&nbsp;Yangsong Xu,&nbsp;Yuting Tang,&nbsp;Changyang Gong","doi":"10.1002/mog2.67","DOIUrl":"https://doi.org/10.1002/mog2.67","url":null,"abstract":"<p>Rapid growth in nanoparticles (NPs) as delivery systems holds vast promise to promote therapeutic approaches for cancer treatment. Presently, a diverse array of NPs with unique properties have been developed to overcome different challenges and to achieve sophisticated delivery routes for enhancement of a series of therapies. Inspiring advances have been achieved in the field of cancer therapy using NPs. In this review, we aim to summarize the up-to-date progression of NPs for addressing various challenges, and expect to elicit novel and potential opportunities alternatively. We first introduce different sorts of NP technologies, illustrate their mechanisms, and present their applications. Then, the achievements made by NPs to break obstacles in delivering cargoes to specific sites through particular routes are highlighted, including long-circulation, tumor targeting, responsive release, and subcellular localization. We subsequently retrospect recent research of NPs in different cancer treatments from single therapy, like chemotherapy, to combination therapy, like chemoradiotherapy, and to integrative therapy. Finally, the challenges and perspectives of NPs in cancer therapy, and their potential impact on the field of oncology are discussed. We believe this review can offer a deeper understanding of the challenges and opportunities of NPs for cancer therapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.67","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140145801","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":"Targets of tumor microenvironment for potential drug development","authors":"Ling Zhang,&nbsp;Ziruoyu Wang,&nbsp;Kailu Liu,&nbsp;Yihang Liu,&nbsp;Shuai Wang,&nbsp;Wei Jiang,&nbsp;Fanghui Lu,&nbsp;Yongjun Dang","doi":"10.1002/mog2.68","DOIUrl":"https://doi.org/10.1002/mog2.68","url":null,"abstract":"<p>The tumor microenvironment (TME) is the ecosystem surrounding a tumor, which usually consists of nontumoral cells or components, and molecules they produce and release. The frequent and continuous interplay between tumor cells and the TME strongly affects tumor development, disease progression, metastasis, and responses to therapeutic interventions. As a hub of potential therapeutic targets, the TME has gained appreciable momentum in cancer research. Here we systematically review the progress in targeting the TME as a strategy to develop novel antitumor drugs from the immunological, stromal and extracellular matrix components of the TME, shedding light on its complex synergies with tumor cells. This exploration highlights the transformative potential these elements hold in refining cancer treatment approaches. This thorough examination not only accentuates the TME's multifaceted nature but also positions it as a formidable avenue for propelling forward the paradigms of cancer therapy. This review aims to foster a deeper understanding of the TME's role in oncogenesis and its potential exploitation in advancing targeted, efficacious cancer treatments, marking a significant stride in the realm of cancer research.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.68","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140015095","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":"The hidden architects of glioblastoma multiforme: Glioma stem cells","authors":"Om S. Sahoo,&nbsp;Rhiti Mitra,&nbsp;Naveen K. H. Nagaiah","doi":"10.1002/mog2.66","DOIUrl":"https://doi.org/10.1002/mog2.66","url":null,"abstract":"<p>Glioblastoma multiforme (GBM), a WHO grade IV diffuse glioma, is a highly aggressive brain tumor with a median survival of less than a year. Characterized by robust proliferation and invasion, recent studies spotlight glioma stem cells (GSCs) within GBM tumors, pivotal in tumor development, progression, and treatment resistance. This review aims to shed light on the critical role of GSCs in the initiation and progression of GBM, emphasizing their contribution to tumor development and resistance to existing treatments. Unlike normal stem cells, GSCs play a pivotal role in GBM pathogenesis. The review delves into the unique characteristics of GSCs, marked by heightened metabolic activities and distinct epigenetic and transcriptional programming. Recognizing the significance of GSCs in recent years, the review examines how their presence amplifies the lethal nature of GBM. The review also critically evaluates recent advancements in glioma and GBM diagnostic methods and treatment therapies, which also include targeting GSCs. Providing a concise yet comprehensive overview, the review contributes insights into GBM's intricate dynamics, offering potential directions for future research and therapeutic strategies.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.66","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139676577","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":"Targeting iron–sulfur cluster assembly scaffold protein as a vulnerability in KRAS-activated pancreatic ductal adenocarcinoma","authors":"Huarui Cai,&nbsp;Hongjuan Cui,&nbsp;Erhu Zhao","doi":"10.1002/mog2.65","DOIUrl":"https://doi.org/10.1002/mog2.65","url":null,"abstract":"<p>In two recent publications in Science<span>¹</span> and Cell Discovery,<span>²</span> researchers have discovered that iron–sulfur cluster assembly scaffold protein (ISCU) plays crucial roles on maintaining glutathione (GSH) homeostasis, α-KG catabolism, DNA methylation and so on. These groundbreaking findings not only establish crucial connections among iron–sulfur (Fe–S) metabolism, GSH homeostasis, alpha-ketoglutarate (α-KG) catabolism, DNA methylation, and tumor growth but also emphasize the significant and integrated regulation of mitochondrial function and gene expression by ISCU (Figure 1).</p><p>Liu et al.<span>¹</span> unveiled the vital role of ISCU in maintaining optimal mitochondrial functions by restoring the balance between iron and GSH. In addition, a previous study<span>³</span> has provided evidence that glutamine, a precursor of GSH, promotes tumor growth through a KRAS-regulated metabolic pathway in pancreatic ductal adenocarcinoma (PDAC), thereby suggesting that ISCU potentially influences tumor development by modulating GSH homeostasis. Ren et al.<span>²</span> uncovered a previously undisclosed association between Fe–S metabolism and tumor growth in kirsten rat sarcoma viral oncogene homolog (KRAS)-activated PDAC. Such findings offer a promising avenue for the treatment of KRAS-activated PDAC, as well as for interventions targeting ISCU-mediated cellular processes.</p><p>PDAC is a highly lethal disease with a mounting incidence and unfavorable prognostic outcomes, underscoring the urgent requirement for the development of efficacious therapeutic approaches. Thus, accurate biomarkers to help stratify risk would greatly improve current diagnostic and decision-making dilemmas. Fe–S clusters are ancient, ubiquitous metal cofactors that possess various physiological functions in antioxidant, iron regulation, the tricarboxylic acid (TCA) cycle, and many other metabolic reactions. Accumulated evidence suggests that abnormal Fe–S clusters assembly pathways lead to mitochondrial dysfunction and cause various diseases, particularly with an impact on tumor development.<span>⁴</span> For instance, nitrogen fixation gene 1 (NFS1) cysteine desulfurase, as an indispensable protein in Fe–S cluster biogenesis, plays a vital role in mitochondrial metabolic reprogramming. In human colorectal cancer, NFS1 can suppress PANoptosis under oxaliplatin chemotherapy, and NFS1 high expression was linked to unfavorable survival outcomes and hyposensitivity to chemotherapy in patients.<span>⁵</span> In addition, succinate dehydrogenase complex iron–sulfur subunit B (SDHB) is also an Fe–S cluster protein consisting of three Fe–S clusters. In SDHB-deficient cancer cells, succinate levels are elevated, resulting in hypermethylation of histones and DNA, and glutamine becomes the primary source of TCA cycle metabolites via reductive carboxylation.<span>⁶</span></p><p>No","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.65","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139655410","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}