MedComm – Oncology最新文献

{"title":"Enhancing cancer immunotherapy and antiangiogenic therapy by regulating gut microbes: Opportunities and challenges","authors":"Jie Xu,&nbsp;Yaomei Tian,&nbsp;Die Hu,&nbsp;Xi Yan,&nbsp;Li Yang","doi":"10.1002/mog2.85","DOIUrl":"10.1002/mog2.85","url":null,"abstract":"<p>As the largest microecosystem in the human body, gut microbes (GMs) and their metabolites play an important role in regulating human health. In recent years, immune checkpoint therapy (ICT) combined with antiangiogenic agents is an emerging combination therapy for cancer. There is growing evidence that GMs can affect the effectiveness of drugs to treat cancer. GMs not only regulate angiogenesis in the tumor microenvironment, but also influence the efficacy of immune checkpoint inhibitors. Many studies show that <i>Bifidobacterium</i> can upregulate the anticancer function of immune checkpoint blockers. In addition, GMs have been found to be involved in the formation of blood vessels and other developmental processes. Clinically, GMs are believed to play a key role in patients receiving antiangiogenic therapy and ICT. In this perspective, we provide an overview of the composition and function of the gut microbiome, and discuss the role of the GMs against the conditioning of angiogenic therapy and ICT. We also summarize new approaches and clinical translational trials using GMs for cancer therapy, and present opportunities and challenges for targeting GMs for cancer therapy in the future.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.85","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141926024","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":"Early prediction of neoadjuvant chemotherapy efficacy for mass breast cancer based on dynamic contrast-enhanced magnetic resonance imaging radiomics","authors":"Pei-Wei Cao,&nbsp;Xue-Ying Deng,&nbsp;Yue-Peng Pan,&nbsp;Shuai-Ming Nan,&nbsp;Chang Yu","doi":"10.1002/mog2.84","DOIUrl":"https://doi.org/10.1002/mog2.84","url":null,"abstract":"<p>Radiomics uses automated algorithms to extract high-order features from images, which can contribute to clinical decisions such as therapeutic efficacy evaluation. We assessed the value of a dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI)-based radiomics model for predicting pathological complete response (pCR) after a second cycle of neoadjuvant chemotherapy (NAC) in patients with mass breast cancer. We retrospectively analyzed data from 149 patients with mass breast cancer who underwent NAC between January 2017 and December 2022. Using DCE-MRI, before NAC and after a second cycle of NAC, the least absolute shrinkage and selection operator and logistic regression (LR) algorithms were applied for feature selection and radiomics modeling. We found significant differences in two clinical imaging features (molecular subtypes, background parenchymal enhancement changes) and two radiomics features. Clinical and radiomics features were employed to build clinical, radiomics, and combined models to predict pCR. The LR model that combined clinical and radiomics features had an area under the curve of 0.811, higher than that for the imaging or radiomics model. Our findings suggest that a combined model based on imaging and radiomics features can improve early prediction of NAC efficacy for patients with mass breast cancer.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.84","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141968284","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":"Alanyl-tRNA synthetase AARS1: A novel lactate sensor and lactyltransferase mediating p53 lactylation and tumorigenesis","authors":"Qiqing Yang,&nbsp;Heyu Li,&nbsp;Long Zhang","doi":"10.1002/mog2.83","DOIUrl":"10.1002/mog2.83","url":null,"abstract":"<p>In a recent study published in <i>Cell</i>, Zong et al. discovered that alanyl-tRNA synthetase 1 (AARS1) senses the accumulated lactate and subsequently facilitates global lysine lactylation in tumor cells.<span>¹</span> Furthermore, they found that p53 is a crucial target protein of AARS1-mediated lactylation. Due to the structural similarity between lactate and <span>l</span>-alanine, AARS1 has the capability to directly bind to lactate and transfer it to the K120 and K139 residues of p53 under conditions involving ATP consumption. The lactylation of p53 impairs its DNA binding, liquid–liquid phase separation (LLPS), and transcriptional activation ability, ultimately promoting cancer progression. Additionally, the study revealed that β-alanine inhibits the binding of AARS1 to lactate, suggesting potential implications for cancer treatment. This study identified a novel lactate sensor and lactyltransferase, opening new avenues for furture research on lactylation.</p><p>In 2019, Zhang et al. reported that lactate, which is a byproduct of glycolysis, can modify histones by lactylation.<span>²</span> The Warburg effect explains how the tumor cells rely on glycolysis as the primary energy source, causing accumulation of high lactate levels. Besides, the acidic intratumoral environment causes protein lactylation, ultimately altering the functions of many proteins, promoting cancer progression. As our understanding of lactylation has increased, numerous “readers” and “erasers” of lactylation have been identified.<span>^{3, 4}</span> However, few “writers” of lactylation have been reported. In an effort to fill this gap in knowledge, Zong et al. discovered AARS1 as a novel lactyltransferase responsible for mediating global lactylation in cancer cells. Their findings highlight how AARS1 links cell metabolism with proteome alteration and plays a role in regulating carcinogenesis. Overall, this study shed light on the intricate relationship between energy metabolism and protein lactylation in cancer cells and provide valuable insights into potential targets for cancer therapeutic intervention.</p><p>When evaluating the TCGA breast cancer data set, Zong et al. found that intratumoral lactate may inhibit p53 functions. Furthermore, intratumoral lactate accumulation was closely associated with cancer progression in a mouse model of mammary tumor virus-polyoma middle T antigen transgenic breast cancer. To investigate the role of lactate in vivo, Zong et al. injected mice intraperitoneally with sodium lactate and observed that p53 activity was significantly inhibited in cancer cells. Moreover, knocking out lactate dehydrogenase A in mice resulted in reduced levels of intratumoral lactate and increased p53 activity. To determine whether lactate directly antagonized p53 functions in vitro, Zong et al. used a cell-free system based on luciferase fragment complementation assay to measure p53 activity. They found that tumor cells co","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.83","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141807227","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":"Next-generation sequencing identifies that protein tyrosine phosphatase receptor type D mutation is favorable to immunotherapy in human cancer","authors":"Yongsheng Huang,&nbsp;Jianwei Liao,&nbsp;Ming Gao,&nbsp;Sha Fu,&nbsp;Faya Liang,&nbsp;Yuanling Jiang,&nbsp;Jiahuan Luo,&nbsp;Jinghua Huang,&nbsp;Ni Tan,&nbsp;Danlan Wang,&nbsp;Xinke Yin,&nbsp;Shuwei Ren,&nbsp;Peiliang Lin,&nbsp;Renhui Chen,&nbsp;Ping Han,&nbsp;Xiaoming Huang,&nbsp;Nengtai Ouyang","doi":"10.1002/mog2.80","DOIUrl":"https://doi.org/10.1002/mog2.80","url":null,"abstract":"<p>Protein tyrosine phosphatase receptors (PTPRs) play a crucial part in numerous tumor processes. However, the effect of PTPR mutations on the immune checkpoint inhibitor (ICI) response needs to be further clarified. Next-generation sequencing was performed on 453 cancer patients in our internal cohort. The genomic alterations, tumor mutation burden (TMB), neoantigens, and immune-related features/pathways of other cohorts were analyzed. Here, protein tyrosine phosphatase receptor type D (PTPRD) has a high mutation frequency and an intensified co-occurrence with other PTPRs. Patients who responded to ICI therapy were enriched with the PTPRD mutation (PTPRD-MUT). PTPRD-MUT patients had a higher objective response rate (44.1% vs. 29.1%), TMB/neoantigens, and longer overall survival time than PTPRD-wild-type (PTPRD-WT) patients. Genomic alterations with a higher mutation frequency of genes (such as LRP1B) were enriched in PTPRD-MUT patients. More abundant immune cells (including CD8⁺ T cells and macrophages) and upregulated immune-related genes were found in PTPRD-MUT patients. Moreover, Gene sets enrichment analyses showed that multiple antitumor immune pathways are activated in PTPRD-MUT patients. Therefore, PTPRD-MUT is beneficial for immunotherapy of multiple cancer types and may be a predictive biomarker of patient clinical outcomes.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.80","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141565746","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":"Clinical homologous recombination repair gene reversion analysis identifies mechanisms of resistance to PARP inhibitors and platinum-chemotherapy","authors":"Yan Jia,&nbsp;Qiong Yang,&nbsp;Yutong Ma,&nbsp;Miaofang Wu,&nbsp;Qiuxiang Ou,&nbsp;Zhongqiu Lin,&nbsp;Yunyu Wu,&nbsp;Jing Li","doi":"10.1002/mog2.79","DOIUrl":"https://doi.org/10.1002/mog2.79","url":null,"abstract":"<p>Identifying mechanisms underlying cancer resistance to therapy is vital for advancing treatment strategies. Pathogenic mutations of homologous recombination repair (HRR) genes are known biomarkers for platinum (Pt)-based chemotherapy and poly ADP ribose polymerase inhibitors (PARPi) effectiveness. Yet, the dynamics of HRR reversion mutations, which may herald therapy resistance, are not fully elucidated. Addressing this gap, our study analyzed secondary HRR gene mutations in a comprehensive pan-cancer data set of approximately 13,000 patients who underwent targeted next-generation sequencing. We identified a subset of patients harboring secondary mutations, which were further categorized into three tiers based on their nature, and occur in the presence of a primary pathogenic mutation, notably in <i>BRCA1</i>, <i>BRCA2</i>, <i>PALB2</i>, and <i>RAD51D</i> genes. Here we show that secondary <i>BRCA2</i> mutations, indicative of adaptive resistance, emerge post-Pt/Olaparib treatment. This challenges the prevailing notion that pathogenic HRR mutations uniformly predict therapeutic sensitivity, highlighting a nuanced genetic interplay that impacts treatment success. This investigation enriches our understanding of cancer's adaptive mechanisms against therapy, suggesting a pivotal shift towards more personalized, dynamic treatment strategies. It underscores the imperative of adapting to cancer's genetic evolution, aiming for a step ahead in the ongoing battle against this disease.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.79","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141488702","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 werner helicase with synthetic lethality in microsatellite instability cancers: Promising therapeutic approaches","authors":"Huanzhang Xie,&nbsp;Jing Zhang","doi":"10.1002/mog2.82","DOIUrl":"https://doi.org/10.1002/mog2.82","url":null,"abstract":"<p>Two recent companion papers published in Nature have reported two promising drug candidates, HRO761<span>¹</span> and VVD-133214,<span>²</span> for microsatellite instability (MSI) cancers targeting the werner syndrome RecQ helicase (WRN), a synthetic lethal target in cancer cells with MSI. Currently, both candidates are undergoing clinical trials to evaluate their safety, tolerability, and preliminary antitumor activity in MSI patients.</p><p>Microsatellites, also known as short tandem repeats, are susceptible to slippage errors during replication, rendering them heavily reliant on the DNA mismatch repair (MMR) system. MMR deficiency results in widespread MSI by failing to correct replication errors, thus initiating cancer via aberrant tumor suppressor gene function. The prevalence of MSI ranges from 10% to 30% across multiple cancer types, such as colorectal, endometrial, ovarian, and gastric cancers.<span>^1-3</span> In MSI tumors, deficiencies in MMR mechanisms heighten genomic instability, prompting the activation of alternative DNA repair pathways, including those implicating WRN. Inhibitors targeting WRN in MSI cancer cells, which already possess compromised DNA repair mechanisms, may induce synthetic lethality, thereby triggering DNA damage and subsequent cancer cell death. This targeted approach is ineffective against normal or microsatellite instability (MSS) cells, as their MMR mechanisms remain intact. Hence, WRN inhibitors emerge as a highly promising synthetic lethal agent, with the potential to selectively eradicate tumor cells while sparing normal cells (Figure 1A).</p><p>Novartis researchers reported HRO761,<span>¹</span> a novel WRN helicase inhibitor (Figure 1B) which targets the ATPase of WRN as a noncovalent inhibitor. Cocrystal structures of HRO761 with WRN helicase revealed its binding to a nonconserved site at the D1–D2 interface, immobilizing WRN in an inactive conformation with an approximate 180° rotation relative to the adenosine triphosphate (ATP)-bound conformation (Figure 1C). Despite its 702 Da molecular weight, HRO761 displayed favorable physicochemical properties and pharmacokinetics (PK), with a clean off-target profile. In vitro cellular assays showed that HRO761 exhibits an IC₅₀ of 100 nM in ATPase assays at high ATP concentration, effectively impairing the viability of MSI cancer cells, while showing no effect in MSS cells. Furthermore, characterization of HRO761 treatment effects on MSI cells revealed time- and dose-dependent cell cycle arrest and DNA damage, regardless of p53 mutation status. In the SW48 cell-derived xenografts (CDX) model, oral administration of 15–60 mg/kg HRO761 resulted in significant tumor regression without observed toxicity. Additionally, combination therapy involving HRO761 with other antitumor drugs may enhance treatment efficacy and reduce side effects and resistance. In vivo studies show complete tumor regression with combi","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.82","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141315451","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":"Self-oxygenating hydrogel: Regulation of postsurgical tumor recurrence/metastasis and wound healing","authors":"Xinyi Yan,&nbsp;Qi Chen","doi":"10.1002/mog2.81","DOIUrl":"https://doi.org/10.1002/mog2.81","url":null,"abstract":"<p>In a recent study published in Nature Communications, Zhou et al. reported a sprayable, self-oxygenating hydrogel (HIL@Z/P/H), encapsulating photosynthetic cyanobacteria (PCC 7942), and tumor-targeted nanomedicine (HIL@Z), which could rapidly crosslink at the melanoma resection site, not only effectively inhibited tumor recurrence or metastasis but also aided in wound healing postsurgery.<span>¹</span></p><p>Melanoma, a highly aggressive and metastatic cancer, predominantly relies on surgical intervention as its primary treatment modality. Despite surgical resection, the challenge persists in completely eradicating all malignant tissue, especially residual cells along the operative margins, which are particularly prone to triggering local recurrence.<span>²</span> As has been demonstrated, the hypoxic conditions at the surgical site promote the dissemination and distant metastasis of residual melanoma cells while perpetuating a chronic inflammatory state within the wound. This not only hampers the healing process but also constitutes a profound risk to the patient's survival and diminishes the quality of their postsurgical life.<span>³</span> To minimize risks and accelerate wound recovery following surgery, radiotherapy, chemotherapy, and immunotherapy therapy are frequently employed as adjunctive treatments.<span>^{4, 5}</span> However, the therapeutic outcomes of these strategies often fall short of expectations and are accompanied by notable toxic side effects. Hence, the pursuit of efficacious strategies to alleviate the hypoxic microenvironment has emerged as a crucial goal.</p><p>Therefore, addressing the fundamental issue of the deteriorative hypoxic microenvironment after surgery that leads to tumor recurrence/metastasis and delayed wound healing, Zhou's group employed nanotechnology to design a therapeutic hydrogel (Figure 1A). Specifically, they noticed PCC 7942, microorganisms that harness a primitive photosynthetic system to produce oxygen in a lasting and controllable manner, making them a promising candidate to explore as an oxygen generator for alleviating hypoxia. Besides, they fabricated HIL@Z, which was composed of hyaluronic acid (HA), indocyanine green (ICG), L-arginine (<span>L</span>-Arg), and zeolite imidazole framework (ZIF-8). Next, they proceeded to encapsulate the PCC 7942 along with HIL@Z in situ at the surgical wound site by spraying a calcium alginate hydrogel. Noteworthy, the porous channels of the hydrogel facilitated nutrient and gas transport (Figure 1B), which can provide an ideal environment for PCC 7942 to support their long-term survival and thereby maintain consistent photosynthetic oxygenation. The photosynthetic oxygenation capability of HIL@Z/P/H did not show significant changes during 15 days of storage, demonstrating excellent stability in oxygenation efficiency (Figure 1C). After obtaining HIL@Z/P/H, Zhou and colleagues proceeded to further validate its func","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.81","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141264619","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":"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}