Cancer letters最新文献

{"title":"LncRNA SNHG1 facilitates colorectal cancer cells metastasis by recruiting HNRNPD protein to stabilize SERPINA3 mRNA","authors":"Huan Yang ,&nbsp;Chunli Gong ,&nbsp;Yuyun Wu ,&nbsp;Xia Xie ,&nbsp;Yang Chen ,&nbsp;Zhibin Li ,&nbsp;Qiuyue Shi ,&nbsp;Jiao Liu ,&nbsp;Nannan Gao ,&nbsp;Bing He ,&nbsp;Chao Wang ,&nbsp;Qiushi Liao ,&nbsp;Jianying Bai ,&nbsp;Yufeng Xiao","doi":"10.1016/j.canlet.2024.217217","DOIUrl":"10.1016/j.canlet.2024.217217","url":null,"abstract":"<div><p>Metastasis continues to negatively impact individuals diagnosed with colorectal cancer (CRC). Research has revealed the important role of long noncoding RNAs (lncRNAs) in CRC metastasis, but the underlying mechanisms remain unclear. Here, we revealed that the lncRNA small nucleolar RNA host gene 1 (SNHG1) is expressed at higher levels in metastatic CRC tissues than in primary CRC tissues, and that high lncRNA SNHG1 expression indicates poor patient outcomes. We found that lncRNA SNHG1 promotes the migration and invasion of tumor cells both in vivo and in vitro. Moreover, lncRNA SNHG1 increases serpin family A member 3 (SERPINA3) mRNA stability by interacting with the heterogeneous nuclear ribonucleoprotein D (HNRNPD) protein, and subsequently upregulates SERPINA3 expression. Moreover, HNRNPD and SERPINA3 reversed the effects of lncRNA SNHG1 knockdown on CRC cell metastasis. In conclusion, we report that the lncRNA SNHG1 recruits HNRNPD, in turn upregulating SERPINA3 expression and ultimately facilitating CRC cell migration and invasion. Targeting the lncRNA SNHG1/HNRNPD/SERPINA3 signaling pathway might be a therapeutic option for preventing CRC metastasis.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217217"},"PeriodicalIF":9.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation and integration of cell-free DNA signatures for detection of lung cancer","authors":"Ruyue Xue ,&nbsp;Xiaomin Li ,&nbsp;Lu Yang ,&nbsp;Meijia Yang ,&nbsp;Bei Zhang ,&nbsp;Xu Zhang ,&nbsp;Lifeng Li ,&nbsp;Xiaoran Duan ,&nbsp;Rui Yan ,&nbsp;Xianying He ,&nbsp;Fangfang Cui ,&nbsp;Linlin Wang ,&nbsp;Xiaoqiang Wang ,&nbsp;Mengsi Wu ,&nbsp;Chao Zhang ,&nbsp;Jie Zhao","doi":"10.1016/j.canlet.2024.217216","DOIUrl":"10.1016/j.canlet.2024.217216","url":null,"abstract":"<div><p>Cell-free DNA (cfDNA) analysis has shown potential in detecting early-stage lung cancer based on non-genetic features. To distinguish patients with lung cancer from healthy individuals, peripheral blood were collected from 926 lung cancer patients and 611 healthy individuals followed by cfDNA extraction. Low-pass whole genome sequencing and targeted methylation sequencing were conducted and various features of cfDNA were evaluated. With our customized algorithm using the most optimal features, the ensemble stacked model was constructed, called ESim-seq (<strong>E</strong>arly <strong>S</strong>creening tech with <strong>I</strong>ntegrated <strong>M</strong>odel). In the independent validation cohort, the ESim-seq model achieved an area under the curve (AUC) of 0.948 (95 % CI: 0.915–0.981), with a sensitivity of 79.3 % (95 % CI: 71.5–87.0 %) across all stages at a specificity of 96.0 % (95 % CI: 90.6–100.0 %). Specifically, the sensitivity of the ESim-seq model was 76.5 % (95 % CI: 67.3–85.8 %) in stage I patients, 100 % (95 % CI: 100.0–100.0 %) in stage II patients, 100 % (95 % CI: 100.0–100.0 %) in stage III patients and 87.5 % (95 % CI: 64.6%–100.0 %) in stage IV patients in the independent validation cohort. Besides, we constructed LCSC model (<strong>L</strong>ung <strong>C</strong>ancer <strong>S</strong>ubtype multiple <strong>C</strong>lassification), which was able to accurately distinguish patients with small cell lung cancer from those with non-small cell lung cancer, achieving an AUC of 0.961 (95 % CI: 0.949–0.957). The present study has established a framework for assessing cfDNA features and demonstrated the benefits of integrating multiple features for early detection of lung cancer.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217216"},"PeriodicalIF":9.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524006116/pdfft?md5=06ace2b3f890936c86eab90af08d98da&pid=1-s2.0-S0304383524006116-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Nrf2 aggravates ionizing radiation-induced intestinal injury by activating the cGAS/STING pathway via Pirin","authors":"Yiqing Xu ,&nbsp;Lei Wang ,&nbsp;Hong Liao ,&nbsp;Xueyan Li ,&nbsp;Yingzi Zhang ,&nbsp;Xuming Chen ,&nbsp;Bing Xu ,&nbsp;Yi Liu ,&nbsp;Wenzhi Tu ,&nbsp;Yong Liu","doi":"10.1016/j.canlet.2024.217218","DOIUrl":"10.1016/j.canlet.2024.217218","url":null,"abstract":"<div><p>Ionizing radiation (IR)-induced intestinal injury remains a major limiting factor in abdominal radiation therapy, and its pathogenesis remains unclear. In this study, mouse models of IR-induced intestinal injury were established, and the effect of IR on nuclear factor erythroid 2-related factor 2 (Nrf2) was determined. More severe IR-induced intestinal damage was observed in Nrf2 knockout (KO) mice than in wild-type mice. Then, the negative regulation of cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) signaling by Nrf2 was examined both <em>in vivo</em> and <em>in vitro</em> after IR. This was accompanied by alterations in the intestinal neutrophil and macrophage populations in mice. Subsequently, the effect of the cGAS/STING pathway on the intestinal toxicity of IR was also investigated. Moreover, the downregulation of cGAS/STING by Nrf2 via its target gene, <em>Pirin</em>, was confirmed using transfection assays. A rescue experiment with Pirin was also conducted using adeno-associated virus in Nrf2 KO mice. Finally, the protective effect of calcitriol against IR-induced intestinal injury, along with increased Nrf2 and Pirin levels and decreased cGAS, pSTING, and interferon-beta levels, were observed. Taken together, our results suggest that Nrf2 alleviates IR-induced intestinal injury through Pirin-mediated inhibition of the innate immunity-related cGAS/STING pathway.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217218"},"PeriodicalIF":9.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protease activated receptor-1 regulates mixed lineage kinase-3 to drive triple-negative breast cancer tumorigenesis","authors":"Piush Srivastava ,&nbsp;Saket Jha ,&nbsp;Sunil Kumar Singh ,&nbsp;Harsh Vyas ,&nbsp;Periannan Sethupathi ,&nbsp;Rakesh Sathish Nair ,&nbsp;Kheerthivasan Ramachandran ,&nbsp;Basabi Rana ,&nbsp;Sandeep Kumar ,&nbsp;Ajay Rana","doi":"10.1016/j.canlet.2024.217200","DOIUrl":"10.1016/j.canlet.2024.217200","url":null,"abstract":"<div><p>Triple-negative breast cancer (TNBC) is difficult to treat breast cancer subtype due to lack or insignificant expressions of targetable estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2). Therefore, finding a targetable protein or signaling pathway in TNBC would impact patient care. Here, we report that a member of the Mixed Lineage Kinase (MLK) family, MLK3, is an effector of G-protein-coupled protease-activated receptors 1 (PAR1) and targeting MLK3 by a small-molecule inhibitor prevented PAR1-mediated TNBC tumorigenesis. <em>In silico</em> and immunohistochemistry analysis of human breast tumors showed overexpression of PAR1 and MLK3 in TNBC tumors. Treating α-thrombin and PAR1 agonist increased MLK3 and JNK activities and induced cell migration in TNBC cells. The PAR1 positive/high (PAR1^+/hi) population of TNBC cells showed aggressive tumor phenotype with increased MLK3 signaling. Moreover, combined inhibition of the PAR1 and MLK3 mitigated the TNBC tumor burden in preclinical TNBC models. Our data suggests that activation of the PAR1-MLK3 axis promotes TNBC tumorigenesis. Therefore, combinatorial therapy targeting MLK3 and PAR1 could effectively reduce TNBC tumor burden.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"603 ","pages":"Article 217200"},"PeriodicalIF":9.1,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524005950/pdfft?md5=299a2332d1aeebafeadf30b49e521baa&pid=1-s2.0-S0304383524005950-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte growth factor promotes melanoma metastasis through ubiquitin-specific peptidase 22-mediated integrins upregulation","authors":"Qiong Gao ,&nbsp;Na Li ,&nbsp;Yujie Pan ,&nbsp;Peng Chu ,&nbsp;Yuanzhang Zhou ,&nbsp;Huijun Jia ,&nbsp;Yang Cheng ,&nbsp;Guoqing Xue ,&nbsp;Jiankun Song ,&nbsp;Yue Zhang ,&nbsp;Houyu Zhu ,&nbsp;Jia Sun ,&nbsp;Bin Zhang ,&nbsp;Zhaolin Sun ,&nbsp;Deyu Fang","doi":"10.1016/j.canlet.2024.217196","DOIUrl":"10.1016/j.canlet.2024.217196","url":null,"abstract":"<div><p>Hepatocyte growth factor (HGF) plays a critical role in promoting tumor migration, invasion, and metastasis, partly by upregulating integrins. The molecular mechanisms behind how HGF facilitates integrin-mediated tumorigenesis are not fully understood. In this study, we demonstrate that the ubiquitin-specific peptidase 22 (USP22) is essential for HGF-induced melanoma metastasis. HGF treatment dramatically increased the expression of both USP22 and multiple integrin family members in particular ITGAV, ITGB3, and ITGA1. An unbiased analysis of the TCGA database reveals integrins as common downstream targets of both USP22 and HGF across multiple human cancer types. Notably, CRISPR-mediated deletion of USP22 completely eliminates HGF-induced integrin expression in melanoma cells. At the molecular level, USP22 acts as a bona fide deubiquitinase for Sp1, a transcription factor for the ITGAV, ITGB3, and ITGA1 genes. USP22 interacts with and inhibits Sp1 ubiquitination, protecting against Sp1 proteasomal degradation. Supporting this, immunohistology analysis detects a positive correlation among USP22, Sp1, and integrin αv in human melanoma tissues. This study identifies the death from the signature gene USP22 as a critical positive regulator for HGF-induced integrin expression by deubiquitinating the Sp1 transcription factor during melanoma metastasis.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217196"},"PeriodicalIF":9.1,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of PRMT5 moderately suppresses prostate cancer growth in vivo but enhances its response to immunotherapy","authors":"Qinju He ,&nbsp;Yuanzhen Zhang ,&nbsp;Wenchao Li ,&nbsp;Saisai Chen ,&nbsp;Jiangling Xiong ,&nbsp;Ruizhe Zhao ,&nbsp;Kai Yuan ,&nbsp;Qiang Hu ,&nbsp;Song Liu ,&nbsp;Guozhen Gao ,&nbsp;Mark T. Bedford ,&nbsp;Dean G. Tang ,&nbsp;Bin Xu ,&nbsp;Cheng Zou ,&nbsp;Dingxiao Zhang","doi":"10.1016/j.canlet.2024.217214","DOIUrl":"10.1016/j.canlet.2024.217214","url":null,"abstract":"<div><p>Protein arginine methylation is a common post-translational modification (PTM) catalyzed by nine protein arginine methyltransferases (PRMTs). As the major symmetric arginine methyltransferase that methylates both histone and non-histone substrates, PRMT5 plays key roles in a number of biological processes critical for development and tumorigenesis. PRMT5 overexpression has been reported in multiple cancer types including prostate cancer (PCa), but the exact biological and mechanistic understanding of PRMT5 in aggressive PCa remains ill-defined. Here, we show that PRMT5 is upregulated in PCa, correlates with worse patient survival, promotes corrupted RNA splicing, and functionally cooperates with an array of pro-tumorigenic pathways to enhance oncogenesis. PRMT5 inhibition via either genetic knockdown or pharmacological inhibition reduces stemness with paralleled differentiation and arrests cell cycle progression without causing appreciable apoptosis. Strikingly, the severity of antitumor effect of PRMT5 inhibition correlates with disease aggressiveness, with AR⁺ PCa being less affected. Molecular characterization pinpoints MYC, but not (or at least to a lesser degree) AR, as the main partner of PRMT5 to form a positive feedback loop to exacerbate malignancy in both AR⁺ and AR^— PCa cells. Inspired by the surprising finding that PRMT5 negatively correlates with tumor immune infiltration and transcriptionally suppresses an immune-gene program, we further show that although PRMT5 inhibitor (PRMT5i) EPZ015666 or anti-PD-1 immunotherapy alone exhibits limited antitumor effects, combination of PRMT5i with anti-PD-1 displays superior efficacy in inhibiting castration-resistant PCa (CRPC) <em>in vivo</em>. Finally, to expand the potential use of PRMT5i through a synthetic lethality concept, we also perform a global CRISPR/Cas9 knockout screen to unravel that many clinical-grade drugs of known oncogenic pathways can be repurposed to target CRPC when used in combination with PRMT5i at low doses. Collectively, our findings establish a rationale to exploit PRMT5i in combination with immunotherapy or other targeted therapies to treat aggressive PCa.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"602 ","pages":"Article 217214"},"PeriodicalIF":9.1,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-STAT5B interaction facilitates the co-transcriptional m6A modification of mRNA to promote breast tumorigenesis","authors":"Poshan Yugal Bhattarai ,&nbsp;Garam Kim ,&nbsp;Sung-Chul Lim ,&nbsp;Hong Seok Choi","doi":"10.1016/j.canlet.2024.217215","DOIUrl":"10.1016/j.canlet.2024.217215","url":null,"abstract":"<div><p>Enhanced expression of methyltransferase-like 3 (METTL3) promotes the m⁶A modification of specific mRNAs, contributing to breast tumorigenesis. While the mRNA substrates targeted by METTL3 are well characterized, the factors dictating the selection of these specific mRNA remain elusive. This study aimed to examine the regulatory role of the transcription factor STAT5B in METTL3-induced m⁶A modification. METTL3 specifically interacts with STAT5B in response to mitogenic stimulation by epidermal growth factor (EGF). Chromatin immunoprecipitation and CRISPR/Cas9 mutagenesis showed that STAT5B recruits METTL3 to gene promoters like <em>CCND1</em>, where METTL3 interacts with RPB1, dependent on CDK9-mediated RPB1 (Ser2) phosphorylation during transcription elongation. Inhibition and depletion of either STAT5B or CDK9 prevented the EGF-induced m⁶A modification of <em>CCND1</em>. The translation efficiency of <em>CCND1</em> was increased following m⁶A modification, thereby increasing cell proliferation. STAT5B facilitated METTL3-induced tumor formation by increasing CCND1 expression in an orthotopic mouse model. In clinical context, a positive correlation was observed between p-STAT5B and METTL3 expression in high-grade breast tumors. This study elucidates a novel mechanism that underlies the specificity of m⁶A modification in breast cancer cells, thereby underscoring its potential therapeutic value.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"603 ","pages":"Article 217215"},"PeriodicalIF":9.1,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N6-methyladenosine enhances the expression of TGF-β-SMAD signaling family to inhibit cell growth and promote cell metastasis","authors":"Bo Peng ,&nbsp;Shuwen Cheng ,&nbsp;He Wang ,&nbsp;Tongfeng Liu ,&nbsp;Yinmin Gu ,&nbsp;Liqiang Duan ,&nbsp;Tianyou Cheng ,&nbsp;Xuetong Wang ,&nbsp;Xiaodong Wang ,&nbsp;Qingqing Zhang ,&nbsp;Yibi Zhang ,&nbsp;Xueqing Zhao ,&nbsp;Xijuan Yao ,&nbsp;Xujie Zhao ,&nbsp;Dalong Song ,&nbsp;Jian Zeng ,&nbsp;Shan Gao","doi":"10.1016/j.canlet.2024.217195","DOIUrl":"10.1016/j.canlet.2024.217195","url":null,"abstract":"<div><p>TGF-β-SMAD signaling pathway plays an important role in the progression of various cancers. However, posttranscriptional regulation such as <em>N</em>^<em>6</em>-methyladenosine (m⁶A) of TGF-β-SMAD signaling axis remains incompletely understood. Here, we reveal that insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) is low expression as well as associated with poor prognosis in clear cell renal cell carcinoma (ccRCC) patients and inhibits proliferation as well as promotes metastasis of ccRCC cells. Mechanistically, IGF2BP2 systematically regulates <em>TGF-β-SMAD</em> signaling family, including <em>TGF-β1/2, TGF-βR1/2 and SMAD2/3/4</em>, through mediating their mRNA stability in an m⁶A-dependent manner. Furthermore, the functional effects of IGF2BP2 on ccRCC cells is mediated by TGF-β-SMAD signaling downstream effector <em>SMAD4</em>, which is identified three m⁶A sites in 5′UTR and CDS. Our study establishes IGF2BP2-TGF-β-SMAD axis as a new regulatory effector in ccRCC, providing new insights for developing novel therapeutic strategies.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"603 ","pages":"Article 217195"},"PeriodicalIF":9.1,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of SPP1+ macrophages in promoting cancer stemness via vitronectin and CCL15 signals crosstalk in liver cancer","authors":"Yizhou Wang ,&nbsp;Qing Wang ,&nbsp;Shuangfen Tao ,&nbsp;Haoyu Li ,&nbsp;Xiaofeng Zhang ,&nbsp;Yong Xia ,&nbsp;Yue Wang ,&nbsp;Cheng Yang ,&nbsp;Chengjun Sui","doi":"10.1016/j.canlet.2024.217199","DOIUrl":"10.1016/j.canlet.2024.217199","url":null,"abstract":"<div><p>Macrophages play a multifaceted role in cancer biology, with both pro-tumorigenic and anti-tumorigenic functions. Understanding the mechanisms underlying macrophage involvement in cancer progression is essential for the development of therapeutic strategies. Our study analyzed single-cell RNA sequencing data from 12 patients with liver cancer and identified a subpopulation of macrophages characterized by elevated expression of SPP1, which correlates with poor prognosis in liver cancer patients. These SPP1⁺ macrophages induce upregulation of tumor stemness through a vitronectin (VTN)-dependent paracrine mechanism. Mechanistically, VTN derived from SPP1⁺ macrophages promote integrin αvβ5/adenosine 5‘-monophosphate-activated protein kinase (AMPK)/Yes-associated protein 1 (YAP1)/SYR-box transcription factor 4 (SOX4) signaling, mediating liver tumor stemness and progression. Conversely, CCL15 produced by liver cancer cells drives polarization of M0 macrophages toward an SPP1⁺ macrophage phenotype, establishing a positive feedback loop of macrophage-tumor stemness. Furthermore, the presence of SPP1⁺ macrophages confers chemoresistance in liver cancer, and inhibition of the macrophage-tumor feedback loop through targeting integrin αvβ5/YAP1 signaling sensitizes liver cancer cells to chemotherapy. Our study highlights the crucial role of SPP1⁺ macrophages in liver cancer progression, providing novel insights for clinical liver cancer therapy.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217199"},"PeriodicalIF":9.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524005949/pdfft?md5=22d976053922917acf522fca670a6720&pid=1-s2.0-S0304383524005949-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical characteristics and risk stratification for late-onset herpes zoster following allogeneic hematopoietic stem cell transplantation","authors":"Cheng-Jie Feng ,&nbsp;Peng Zhao ,&nbsp;Hai-Xia Fu ,&nbsp;Chen-Hua Yan ,&nbsp;Chen-Cong Wang ,&nbsp;Xiao-Lu Zhu ,&nbsp;Yun He ,&nbsp;Feng-Rong Wang ,&nbsp;Yuan-Yuan Zhang ,&nbsp;Xiao-Dong Mo ,&nbsp;Yuan Kong ,&nbsp;Wei Han ,&nbsp;Jing-Zhi Wang ,&nbsp;Yu Wang ,&nbsp;Huan Chen ,&nbsp;Yu-Hong Chen ,&nbsp;Xiang-Yu Zhao ,&nbsp;Ying-Jun Chang ,&nbsp;Lan-Ping Xu ,&nbsp;Kai-Yan Liu ,&nbsp;Xiao-Hui Zhang","doi":"10.1016/j.canlet.2024.217202","DOIUrl":"10.1016/j.canlet.2024.217202","url":null,"abstract":"<div><p>The incidence of herpes zoster (HZ) in allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients is significantly higher than that of the general public. Although routine antiviral prophylaxis is recommended, late-onset HZ has been highlighted, yet limited information is known about its clinical features and predictors. Here, we conducted a retrospective nested case-control study to identify patients with late-onset HZ, defined as a diagnosis of HZ after 1 year of transplantation, among allo-HSCT recipients between 2012 and 2017 at Peking University People's Hospital. Three controls were matched for each patient. A total of 201 patients developed late-onset HZ. Age over 20 years, absence of neutrophil engraftment by 14 days, mental disorders, immunosuppressant use at 1 year, and a peripheral CD4+/CD8+ ratio ≥0.5 at 1 year were independent risk factors, among which the CD4+/CD8+ ratio demonstrated good discriminative power for predicting late-onset HZ. For patients with a CD4+/CD8+ ratio &lt;0.5, patient age, neutrophil engraftment time, mental disorders, and immunosuppressant use were potential risk factors. A stratification algorithm was accordingly established, classifying the transplant recipients into three risk groups. Whether the algorithm could facilitate the administration of posttransplant antiviral prophylaxis merits further validation.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"603 ","pages":"Article 217202"},"PeriodicalIF":9.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}