Neoplasia最新文献

{"title":"SLC31A1 promotes chemoresistance through inducing CPT1A-mediated fatty acid oxidation in ER-positive breast cancer","authors":"Xudong Li ,&nbsp;Jingjing Ge ,&nbsp;Mengdi Wan ,&nbsp;Tongtong Feng ,&nbsp;Xiaoqian Li ,&nbsp;Haibo Zhang ,&nbsp;Zhangyan Wang ,&nbsp;Yongsheng Gao ,&nbsp;Meiting Chen ,&nbsp;Fei Pan","doi":"10.1016/j.neo.2025.101125","DOIUrl":"10.1016/j.neo.2025.101125","url":null,"abstract":"<div><div>Over 60% of breast cancer cases are diagnosed with estrogen-receptor (ER) positive. Tamoxifen (TAM), a commonly employed medication for ER-positive breast cancer, often yields suboptimal therapeutic outcomes due to the emergence of TAM resistance, leading to the recurrence and a poor prognosis. The copper transporter, solute carrier family 31 member 1 (SLC31A1), has been associated with tumor aggressiveness and unfavorable outcomes in various types of tumors. In our current study, we found high expression of SLC31A1 that predicted poor survival in patients with breast cancer. Significantly, ER-positive breast cancer tissues in patients with recurrence post-TAM treatment exhibited considerably stronger SLC31A1 expression levels. <em>In vitro</em> experiments verified that TAM-resistant ER-positive breast cancer cell lines expressed notably higher SLC31A1 levels compared to the parental cell lines. Of great significance, SLC31A1 depletion notably rescued TAM sensitivity in chemoresistant ER-positive breast cancer cells, as demonstrated by the attenuated cell proliferative and invasive capabilities. Conversely, promoting SLC31A1 significantly facilitated the proliferation and invasion of wild-type breast cancer cells. Subsequently, we detected reduced copper levels in TAM-resistant breast cancer cells with SLC31A1 depletion. Mechanistically, we observed that in chemoresistant breast cancer cell lines, SLC31A1 knockdown resulted in a substantial decrease in the expression of carnitine palmitoyltransferase 1A (CPT1A), a rate-limiting enzyme of fatty acid oxidation (FAO). RNA-Seq analysis indicated that FAO might be implicated in SLC31A1-mediated breast cancer progression. CPT1A was also overexpressed in TAM-resistant breast cancer cells, accompanied by enhanced FAO rates and ATP levels. Suppressing CPT1A significantly enhanced the chemosensitivity of TAM-resistant breast cancer cells in response to TAM treatments. Intriguingly, copper exposure dose-dependently increased CPT1A expression in chemoresistant breast cancer cells, but this could be abolished upon SLC31A1 knockdown, along with enhanced apoptosis, which elucidated that copper uptake contributed to CPT1A expression. Furthermore, SLC31A1 overexpression significantly augmented CPT1A expression in parental breast cancer cells, accompanied by facilitated copper levels, FAO rates, and ATP levels, while being notably diminished upon CPT1A suppression. Finally, our <em>in vivo</em> studies confirmed that SLC31A1 deficiency re-sensitized TAM-resistant breast cancer cells to TAM treatment and abolished tumor growth. Collectively, all our studies demonstrated that SLC31A1/copper suppression could enhance TAM responses for chemoresistant ER-positive breast cancer cells through constraining the CPT1A-mediated FAO process.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"61 ","pages":"Article 101125"},"PeriodicalIF":4.8,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High p16INK4A expression in glioblastoma is associated with senescence phenotype and better prognosis","authors":"Soon Sang Park ,&nbsp;Tae Hoon Roh ,&nbsp;Yoshiaki Tanaka ,&nbsp;Young Hwa Kim ,&nbsp;So Hyun Park ,&nbsp;Tae-Gyu Kim ,&nbsp;So Yeong Eom ,&nbsp;Tae Jun Park ,&nbsp;In-Hyun Park ,&nbsp;Se-Hyuk Kim ,&nbsp;Jang-Hee Kim","doi":"10.1016/j.neo.2024.101116","DOIUrl":"10.1016/j.neo.2024.101116","url":null,"abstract":"<div><div>Glioblastoma, isocitrate dehydrogenase (IDH)-wildtype (GBM), is the most malignant brain tumor in adults, with limited therapeutic intervention. Previous studies have identified a few prognostic markers for GBM, including the methylation status of O⁶-methylguanine-DNA methyltransferase (<em>MGMT</em>) promoter, <em>TERT</em> promoter mutation, <em>EGFR</em> amplification, and <em>CDKN2A/2B</em> deletion. However, the classification of GBM remains incomplete, necessitating a comprehensive analysis. In this study, we investigated the impact of p16^INK4A expression in GBM and found that p16^INK4A-high GBM exhibits distinct characteristics compared to p16^INK4A-low GBM. Specifically, tumor cells with p16^INK4A-high expression display a senescent phenotype and are correlated with higher intra-tumoral immune cell infiltration. Furthermore, an association was observed between elevated p16^INK4A expression in GBM and extended overall survival of patients. Our <em>in vivo</em> and <em>in vitro</em> studies revealed that CCL13 is predominantly expressed by p16^INK4A-high GBM cells. The released CCL13 enhances the infiltration of T cells within the tumor, potentially contributing to the improved prognosis observed in patients with high p16^INK4A expression. These findings suggest that tumor cells with a senescence phenotype in GBM, through the secretion of chemokines such as CCL13, may augment immune cell infiltration and potentially enhance patient outcomes by creating a more immunologically active tumor microenvironment.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101116"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial profiling of endoplasmic reticulum stress markers in tumor associated cells predicts patient outcomes in pancreatic cancer","authors":"Georgia Porter ,&nbsp;Murray D. Norris ,&nbsp;Minoti Apte ,&nbsp;Angelica M. Merlot","doi":"10.1016/j.neo.2024.101115","DOIUrl":"10.1016/j.neo.2024.101115","url":null,"abstract":"<div><h3>Introduction</h3><div>The impact of endoplasmic reticulum (ER) stress in tumor-associated cells, such as cancer associated fibroblasts (CAFs), immune cells and endothelial cells, on patient outcomes in clinical specimens have not been examined. For the first time, we characterized the expression and spatial locations of ER stress markers, BiP and CHOP, in tumor-associated cells and assessed their prognostic significance in a panel of pancreatic ductal adenocarcinoma (PDAC) patient samples.</div></div><div><h3>Methods</h3><div>Multiplex immunofluorescence was performed on tumor microarrays and images were analyzed using HALO AI software.</div></div><div><h3>Results</h3><div>BiP and CHOP were upregulated in CAFs and endothelial cells in PDAC sections relative to non-neoplastic pancreas sections. High BiP expression in CAFs and endothelial cells was associated with greater vascular invasion and in immune cells was correlated with increased tumor size. High CHOP expression in immune cells correlated with poor patient survival. CAFs and immune cells were more likely to express BiP or CHOP when located close (&lt; 20 μm) to tumor cells. High expression of CHOP in CAFs close to tumor cells correlated with improved patient survival.</div></div><div><h3>Conclusion</h3><div>For the first time, this study demonstrated that ER stress occurs in CAFs and immune cells predominantly in proximity to tumor cells in PDAC patient tissue. The correlation of high ER stress in immune cells with poor patient survival highlights the importance of the TME and the use of spatial analysis for the identification of novel biomarkers.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101115"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143014469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pancreatic cancer cells infiltrate nerves through TGFbeta1-driven perineural epithelial-to-mesenchymal-like transdifferentiation","authors":"Theresa Krauss ,&nbsp;Ibrahim Halil Gürcinar ,&nbsp;Ulrike Bourquain ,&nbsp;Maren Hieber ,&nbsp;Evelyn N. Krohmer ,&nbsp;Nan Wu ,&nbsp;Sergey Tokalov ,&nbsp;Rüdiger Goess ,&nbsp;Carmen Mota Reyes ,&nbsp;Dieter Saur ,&nbsp;Helmut Friess ,&nbsp;Güralp O. Ceyhan ,&nbsp;Ihsan Ekin Demir ,&nbsp;Okan Safak","doi":"10.1016/j.neo.2025.101126","DOIUrl":"10.1016/j.neo.2025.101126","url":null,"abstract":"<div><div>Neural invasion is a prognostic hallmark of pancreatic ductal adenocarcinoma (PDAC), yet the underlying mechanisms behind the disruption of perineural barriers and access of cancer cells into intrapancreatic nerves remain poorly understood. This study aimed to investigate the role of epithelial-mesenchymal transformation (EMT) in perineural epithelial cells during neural invasion.Histopathological analysis of human and murine primary tumors using perineurium-specific GLUT1 antibody revealed a reduction in perineural integrity, which positively correlated with the extent of neural invasion in human PDAC cases. Human pancreatic cancer cell lines were found to secrete TGFbeta1, which induced EMT of perineural epithelial cells, characterized by the loss of epithelial markers (CK19-9) and the acquisition of mesenchymal markers (alphaSMA, N-Cadherin). Additionally, these transitioning perineural epithelial cells demonstrated increased matrix-degrading capabilities through the upregulation of matrix-metalloproteases 3 and 9 via SMAD2. In an autochthonous mouse model with elevated endogenous TGFbeta1 levels in addition to oncogenic Kras activation (<em>Ptf1a^Cre/+, LSL-Kras^G12D/+, LSL-R26^Tgfβ/+</em>), decreased perineural integrity could be reproduced <em>in vivo</em>.Collectively, these findings underscore the role played by TGFbeta1-overexpressing pancreatic cancer cells in the dismantling of perineural barriers during neural invasion.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101126"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"True cancer stem cells exhibit relative degrees of dormancy and genomic stability","authors":"Sanford H. Barsky ,&nbsp;Krista Mcphail ,&nbsp;Justin Wang ,&nbsp;Jordan Dillard ,&nbsp;Crystal J. Beard ,&nbsp;Yin Ye","doi":"10.1016/j.neo.2025.101127","DOIUrl":"10.1016/j.neo.2025.101127","url":null,"abstract":"<div><h3>Background</h3><div>Cancer stem cells in human tumors have been defined by stem cell markers, embryonal signaling pathways and characteristic biology, ie., namely the ability to repopulate the proliferating population. However, even if these properties can be demonstrated within a tumor cell subpopulation, it does not mean that they are truly hierarchical stem cells because they could have been derived from the proliferating population in a reversible manner.</div></div><div><h3>Methods</h3><div>Using a human PDX, Mary-X, that overall expressed a strong cancer stem cell phenotype, the study conducted both GPP-labelled retroviral transfection and fluorescent microsphere uptake studies to distinguish proliferating from dormant cells and array CGH to identify regions of amplifications (gains) and deletions (losses) on the overall Mary-X population and then applied derived probes by FISH on individual cells to identify a genomically stable subpopulation.</div></div><div><h3>Results</h3><div>Whereas 97-99 % of the cells expressed retroviral GFP and not fluorescent particles and showed numerous gene amplifications and deletions, approximately 1-3 % of the cells showed the opposite. The subpopulation with the retained fluorescent microspheres and exhibiting genomic stability was significantly smaller in size than their GFP-expressing and genomically unstable counterparts. Sorting Mary-X spheroids on the basis of either CD133 or ALDH positivity further enriched for this subpopulation.</div></div><div><h3>Conclusions</h3><div>These studies indicate that a truly biological cancer stem cell subpopulation exists that exhibits both dormancy and genomic stability. This subpopulation could not have been derived from the proliferating and resulting genomically unstable population and therefore represents a truly hierarchical stem cell subpopulation capable of only unidirectional differentiation.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101127"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimal radiation dose to induce an abscopal effect by combining carbon-ion radiotherapy and anti-CTLA4 antibody","authors":"Liqiu Ma ,&nbsp;Yang Li ,&nbsp;Yoshimitsu Sakamoto ,&nbsp;Lin Xie ,&nbsp;Saaya Suzuki ,&nbsp;Yukari Yoshida ,&nbsp;Li Sui ,&nbsp;Gang Guo ,&nbsp;Jialing Wen ,&nbsp;Wangcai Ren ,&nbsp;Kazuhiro Kakimi ,&nbsp;Kensuke Osada ,&nbsp;Akihisa Takahashi ,&nbsp;Takashi Shimokawa","doi":"10.1016/j.neo.2024.101099","DOIUrl":"10.1016/j.neo.2024.101099","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Although carbon-ion radiotherapy (CIRT) has led to good outcomes, controlling metastasis is still crucial for improving overall survival. This study aimed to evaluate the effectiveness of by two combinations, one of CIRT and anti-CTLA4 antibody, the other of CIRT and anti-PD-1 antibody, applied at different radiation doses for distal tumour and metastasis suppression.</div></div><div><h3>Materials and methods</h3><div>Murine cancer cells (colon carcinoma Colon-26 cells for experiments and osteosarcoma LM8 cells for verification) were grafted into both sides of the hind legs of syngeneic mice. Right-side tumours were irradiated with 3 Gy or 10 Gy CIRT while the left-side tumours were not irradiated, followed by the administration of the anti-CTLA4 antibody or anti-PD-1 antibody. The diameter of the tumours in both legs was measured 3 times per week after irradiation. The number of pulmonary metastases was evaluated within 3 weeks after irradiation.</div></div><div><h3>Results</h3><div>Compared with the control group, the high-dose group showed promising anti-cancer benefits in terms of both irradiated tumours and lung metastasis, but neither 10 Gy CIRT combined with the anti-CTLA4 antibody nor 10 Gy CIRT combined with the anti-PD-1 antibody suppressed the growth of distant unirradiated tumours. In the low-dose group, the effect on primary tumour control was slightly weaker than that in the high-dose treatment group, but significant suppressive effects on both distant unirradiated tumours and metastases were observed following 3 Gy CIRT combined with anti-CTLA4 antibody treatment. Specifically, the volume of distant unirradiated tumours decreased by 40 % compared with that of the control group, and no lung metastasis was observed.</div></div><div><h3>Conclusion</h3><div>Our findings suggest that there is an optimal dose range for the abscopal effect generated with the CIRT combined with anti-CTLA4 antibody, and it highlights a new opportunity for increased induction efficiency of the abscopal effect of combination therapy.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101099"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and genetic drivers of oligo-metastatic disease in colon cancer","authors":"Alessandro Ottaiano ,&nbsp;Mariachiara Santorsola ,&nbsp;Roberto Sirica ,&nbsp;Annabella Di Mauro ,&nbsp;Antonella Di Carlo ,&nbsp;Monica Ianniello ,&nbsp;Francesco Sabbatino ,&nbsp;Rosa Castiello ,&nbsp;Francesca Del Peschio ,&nbsp;Marco Cascella ,&nbsp;Francesco Perri ,&nbsp;Maurizio Capuozzo ,&nbsp;Nicola Martucci ,&nbsp;Edoardo Mercadante ,&nbsp;Valentina Borzillo ,&nbsp;Rossella Di Franco ,&nbsp;Francesco Izzo ,&nbsp;Vincenza Granata ,&nbsp;Carmine Picone ,&nbsp;Antonella Petrillo ,&nbsp;Giovanni Savarese","doi":"10.1016/j.neo.2024.101111","DOIUrl":"10.1016/j.neo.2024.101111","url":null,"abstract":"<div><h3>Background</h3><div>Oligo-metastatic disease (OMD) in colon cancer patients exhibits distinct clinical behavior compared to poly-metastatic disease (PMD), with a more responsive and indolent course. This study aims to identify clinical and biological factors uniquely associated with oligo-metastatic behavior.</div></div><div><h3>Methods</h3><div>Metastatic colon cancer patients from an academic center underwent genetic characterization. OMD was defined as ≤3 lesions per organ, each with a total diameter &lt;70 mm and none exceeding 25 mm. Tumor DNA sequencing by NGS utilized the TruSight Oncology 500 kit. Overall survival (OS) was determined from metastasis diagnosis until death using Kaplan–Meier analysis. Multivariate Cox regression examined prognostic links between clinicopathological and genetic factors. Associations with metastatic patterns were evaluated using Chi-square.</div></div><div><h3>Results</h3><div>The analysis involved 104 patients (44 with OMD, 60 with PMD). OMD was more prevalent in males (<em>P</em> = 0.0299) and with single organ involvement (<em>P</em> = 0.0226). Multivariate analysis adjusted for age (&gt;70 vs. &lt;70 years), gender (male vs. female), tumor side (right vs. left), metastatic involvement (more than one site vs. one site), response to first-line therapy (disease control vs. no disease control), and <em>RAS</em>/<em>BRAF</em> variants (wild-type vs. mutated) identified OMD vs. PMD as the strongest independent predictor of survival (HR: 0.14; 95 % CI: 0.06-0.33; <em>P</em>&lt;0.0001). OMD patients exhibited distinct molecular characteristics, including lower frequencies of <em>BRAF</em> p.V600E (P=0.0315) and <em>KRAS</em> mutations (P=0.0456), as well as a higher frequency of high tumor mutational burden (<em>P</em>=0.0127). Additionally, by integrating data from public datasets and our case study, we hypothesize that some gene alterations (i.e.: <em>BRAF, SMAD4, RAF1</em>, and <em>mTOR</em>) may prevent OMD occurrence.</div></div><div><h3>Conclusion</h3><div>OMD, characterized by male predominance, single-site involvement, and distinct molecular features in colon cancer, suggests the need for tailored management strategies.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101111"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence, mortality, and global burden of retinoblastoma in 204 countries worldwide from 1990 to 2021: Data and systematic analysis from the Global Burden of Disease Study 2021","authors":"Linyan Wang ,&nbsp;Jianing Chen ,&nbsp;Yunhan Shen ,&nbsp;Grace Loy Ming Hooi ,&nbsp;Shuohan Wu ,&nbsp;Feng Xu ,&nbsp;Hao Pei ,&nbsp;Jianpeng Sheng ,&nbsp;Tiansheng Zhu ,&nbsp;Juan Ye","doi":"10.1016/j.neo.2024.101107","DOIUrl":"10.1016/j.neo.2024.101107","url":null,"abstract":"<div><h3>Background</h3><div>Retinoblastoma (Rb), the primary intraocular malignancy in children, poses significant risks, yet its overall burden remains inadequately assessed. This study aims to analyze global Rb trends using Global Burden of Disease, Injuries, and Risk Factors study (GBD) 2021 data.</div></div><div><h3>Methods</h3><div>GBD 2021 data was analyzed to assess Rb incidence, mortality, and disability-adjusted life years (DALYs) from 1990 to 2021. Average annual percentage changes (AAPCs) were calculated across genders, age groups (0-9 years), and geographic regions categorized by socio-demographic index (SDI) quintiles.</div></div><div><h3>Results</h3><div>From 1990 to 2021, the global Rb age-standardized incidence rate (ASIR) increased from 0.08 (per 100,000, range: 0.05 to 0.10) to 0.09 (per 100,000, range: 0.06 to 0.13). ASIR was not significantly correlated with SDI (R = -0.095, P = 0.18), while age-standardized DALYs rate (R = -0.693, P &lt; 0.001) and age-standardized mortality rate (ASMR) (R = -0.71, P &lt; 0.001) were significantly and negatively correlated with SDI. Increases in ASIR were concentrated in Asia, Europe, and northern and southern Africa. The highest standardized DALYs and ASMR were noted in certain countries in Asia, Europe, and South Africa. Among age groups, the highest disease burdens were observed in the “0-6 days” and “2-4 years” groups. There were no significant gender differences in Rb burden globally.</div></div><div><h3>Conclusions</h3><div>Despite global progress, regions with lower SDI face elevated Rb burden and mortality. Females exhibit higher burdens during infancy, necessitating further investigation. Effective Rb management in resource-limited areas requires international collaboration focused on health education, early diagnosis, and prenatal screening for high-risk families.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101107"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “p85α Inactivates MMP-2 and Suppresses Bladder Cancer Invasion by Inhibiting MMP-14 Transcription and TIMP-2 Degradation” [Neoplasia (2019) 21, 908–920]","authors":"Jingjing Wang ,&nbsp;Ning Zhang ,&nbsp;Minggang Peng ,&nbsp;Xiaohui Hua ,&nbsp;Chao Huang ,&nbsp;Zhongxian Tian ,&nbsp;Qipeng Xie ,&nbsp;Junlan Zhu ,&nbsp;Jingxia Li ,&nbsp;Haishan Huang ,&nbsp;Chuanshu Huang","doi":"10.1016/j.neo.2024.101095","DOIUrl":"10.1016/j.neo.2024.101095","url":null,"abstract":"","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101095"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11743588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic brain dissemination of glioblastoma requires transdifferentiation into endothelial-like cells via TGF-β-ALK1-Smad1/5 signaling","authors":"Thomas M.B. Ware ,&nbsp;Adilson Fonseca Teixeira ,&nbsp;Josephine Iaria ,&nbsp;Rodney B. Luwor ,&nbsp;Hong-Jian Zhu","doi":"10.1016/j.neo.2024.101110","DOIUrl":"10.1016/j.neo.2024.101110","url":null,"abstract":"<div><div>Glioblastoma is the most aggressive type of brain cancer, but treatment improvements for glioblastoma patients remain stagnated for over 20 years. This is despite the large number of clinical trials that have attempted to replicate the success of therapeutics developed for other cancer types. This discrepancy highlights the urgent need to decipher the unique biology of glioblastomas. Here, we show that glioblastoma tumour cells are highly plastic, integrating into blood vessel walls to disseminate throughout the brain. This relies on the transdifferentiation of glioblastoma tumor cells into endothelial-like cells in a process we termed endothelialisation. Mechanistically, in addition to TGF-β-ALK5-Smad2/3 signaling, glioblastoma tumour cells also activate TGF-β-ALK1-Smad1/5 signaling – a mechanism previously thought to be limited to endothelial cells. Consequently, therapeutic targeting of TGF-β-ALK1-Smad1/5 activity impaired endothelialisation-driven glioblastoma progression. This study identifies a previously unknown component of glioblastoma biology and establishes a therapeutic approach to reduce the progression of this disease.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"60 ","pages":"Article 101110"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}