Adam Harvey-Sullivan, Sana Ali, Parveen Dhesi, Joseph Hart, Helena Painter, Fiona M Walter, Garth Funston, Dominik Zenner
{"title":"Comparing cancer stage at diagnosis between migrants and non-migrants: a meta-analysis.","authors":"Adam Harvey-Sullivan, Sana Ali, Parveen Dhesi, Joseph Hart, Helena Painter, Fiona M Walter, Garth Funston, Dominik Zenner","doi":"10.1038/s41416-024-02896-0","DOIUrl":"https://doi.org/10.1038/s41416-024-02896-0","url":null,"abstract":"<p><strong>Background: </strong>Migrants face barriers accessing healthcare, risking delays in cancer diagnosis. Diagnostic delays result in later stage diagnosis which is associated with poorer cancer survival. This review aims to compare the differences in cancer stage at diagnosis between migrants and non-migrants.</p><p><strong>Methods: </strong>We conducted a systematic review and meta-analysis of three databases from 2000 to 2023 for studies conducted in OECD countries that compared stage at diagnosis between migrants and non-migrants. Meta-analysis compared odds ratios (OR) for early (stage I and II) stage at diagnosis. The Risk of Bias in Non-randomised Studies of Exposure tool was used to assess study quality.</p><p><strong>Results: </strong>41 of the 11,549 studies identified were included; 34 studies had suitable data for meta-analysis. Overall, migrants were significantly less likely to be diagnosed with early stage cancer compared with non-migrants (OR 0.84; 95% CI 0.78-0.91). This difference was maintained across cancer types, although only statistically significant for breast (OR 0.78; 95% CI 0.70-0.87) and prostate cancer (OR 0.92; 95% CI 0.85-0.99).</p><p><strong>Discussion: </strong>Published studies indicate that migrants are less likely to be diagnosed with early stage cancer. Variation by cancer type, study location and region of origin highlights the need for further research to understand these differences.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615130","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}
Thi Xuan Mai Tran, Yoosoo Chang, Hye Rin Choi, Ria Kwon, Ga-Young Lim, Yoosun Cho, Seungho Ryu, Boyoung Park
{"title":"Correction: Height and breast cancer risk in premenopausal Korean women aged under 40 years of age.","authors":"Thi Xuan Mai Tran, Yoosoo Chang, Hye Rin Choi, Ria Kwon, Ga-Young Lim, Yoosun Cho, Seungho Ryu, Boyoung Park","doi":"10.1038/s41416-024-02886-2","DOIUrl":"https://doi.org/10.1038/s41416-024-02886-2","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615131","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}
Susanna Poghosyan, Nicola Frenkel, Lotte van den Bent, Danielle Raats, Tessa Spaapen, Jamila Laoukili, Inne Borel Rinkes, Onno Kranenburg, Jeroen Hagendoorn
{"title":"VEGF-C propagates 'onward' colorectal cancer metastasis from liver to lung.","authors":"Susanna Poghosyan, Nicola Frenkel, Lotte van den Bent, Danielle Raats, Tessa Spaapen, Jamila Laoukili, Inne Borel Rinkes, Onno Kranenburg, Jeroen Hagendoorn","doi":"10.1038/s41416-024-02892-4","DOIUrl":"https://doi.org/10.1038/s41416-024-02892-4","url":null,"abstract":"<p><strong>Background: </strong>The formation of lung metastasis as part of the progression of colon cancer is a poorly understood process. Theoretically, liver metastases could seed lung metastases.</p><p><strong>Methods: </strong>To assess the contribution of the liver lymphatic vasculature to metastatic spread to the lungs, we generated murine liver-metastasis-derived organoids overexpressing vascular endothelial growth factor (VEGF)-C. The organoids were reimplanted into the mouse liver for tumour generation and onward metastasis.</p><p><strong>Results: </strong>Liver metastases from patients with concomitant lung metastases showed higher expression of VEGF-C, lymphatic vessel hyperplasia, and tumour cell invasion into lymphatic vessels when compared to those without lung metastases. Reimplantation of VEGF-C overexpressing organoids into the mouse liver showed that VEGF-C caused peritumoral lymphatic vessel hyperplasia, lymphatic tumour cell invasion, and lung metastasis formation. This change in metastatic organotropism was accompanied by reduced expression of WNT-driven adult stem cell markers, and increased expression of fetal stem cell markers and NOTCH pathway genes. Further NOTCH pathway inhibition with γ-secretase inhibitor (DAPT) in vivo results in a slight reduction in lung metastases and a decrease in lymphatic hyperplasia and invasion in VEGF-C-overexpressing tumours.</p><p><strong>Conclusion: </strong>Collectively, these data indicate that VEGF-C can drive onward metastasis from the liver to the lung and suggest that targeting VEGF-C/NOTCH pathways may impair the progression of colorectal cancer.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615134","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}
Gerard M Walls, Carmen Bergom, Joshua D Mitchell, Stacey L Rentschler, Geoffrey D Hugo, Pamela P Samson, Clifford G Robinson
{"title":"Cardiotoxicity following thoracic radiotherapy for lung cancer.","authors":"Gerard M Walls, Carmen Bergom, Joshua D Mitchell, Stacey L Rentschler, Geoffrey D Hugo, Pamela P Samson, Clifford G Robinson","doi":"10.1038/s41416-024-02888-0","DOIUrl":"10.1038/s41416-024-02888-0","url":null,"abstract":"<p><p>Radiotherapy is the standard of care treatment for unresectable NSCLC, combined with concurrent chemotherapy and adjuvant immunotherapy. Despite technological advances in radiotherapy planning and delivery, the risk of damage to surrounding thoracic tissues remains high. Cardiac problems, including arrhythmia, heart failure and ischaemic events, occur in 20% of patients with lung cancer who undergo radiotherapy. As survival rates improve incrementally for this cohort, minimising the cardiovascular morbidity of RT is increasingly important. Problematically, the reporting of cardiac endpoints has been poor in thoracic radiotherapy clinical trials, and retrospective studies have been limited by the lack of standardisation of nomenclature and endpoints. How baseline cardiovascular profile and cardiac substructure radiation dose distribution impact the risk of cardiotoxicity is incompletely understood. As Thoracic Oncology departments seek to expand the indications for radiotherapy, and as the patient cohort becomes older and more comorbid, there is a pressing need for cardiotoxicity to be comprehensively characterised with sophisticated oncology, physics and cardio-oncology evaluations. This review synthesises the evidence base for cardiotoxicity in conventional radiotherapy, focusing on lung cancer, including current data, unmet clinical needs, and future scientific directions.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590072","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}
Samuel Knoedler, Fortunay Diatta, Felix Kasparbauer, Leonard Knoedler, Bong-Sung Kim, Bohdan Pomahac, Martin Kauke-Navarro
{"title":"Perioperative safety of risk-reducing mastectomy.","authors":"Samuel Knoedler, Fortunay Diatta, Felix Kasparbauer, Leonard Knoedler, Bong-Sung Kim, Bohdan Pomahac, Martin Kauke-Navarro","doi":"10.1038/s41416-024-02897-z","DOIUrl":"10.1038/s41416-024-02897-z","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582143","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":"Low-dose arsenic trioxide inhibits pancreatic stellate cell activation via LOXL3 expression to enhance immunotherapy in pancreatic cancer.","authors":"Yue Zhao, Yunlong Li, Jinmao Zou, Tairan Guo, Ziyi Zhong, Yaqing Li, Shaojie Chen, Jiajia Li, Kaihong Huang, Guoda Lian, Yuzhou Huang","doi":"10.1038/s41416-024-02880-8","DOIUrl":"https://doi.org/10.1038/s41416-024-02880-8","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer (PC) is characterized by abnormally fibrotic mesenchyme, which notably influences on the effectiveness of immunotherapy. Low-dose arsenic trioxide (ATO, 1.0 μM) can inhibit the activation of pancreatic stellate cells (PSCs) and affect fibrosis, which is a potential strategy for enhancing the sensitivity to immunotherapy.</p><p><strong>Methods: </strong>Extracellular matrix (ECM) models were employed to assess the regulatory effects of ATO on ECM and peripheral blood mononuclear cells. Orthotopic C57BL/6J models were utilized to evaluate the influence of ATO on CD8<sup>+</sup>T cell infiltration and immunotherapy in PC. Additionally, nanomaterials loaded with ATO designed to specifically target PSCs (scAbFAP-α-HMSNs-PAA-ATO) were produced to enhance targeting effects of ATO.</p><p><strong>Results: </strong>Low-dose ATO (1.0 μM) suppressed PSCs activation, exhibiting potential for synergistic immunotherapy. Under low-dose ATO intervention, ECM underwent remodeling, leading to increases in CD8<sup>+</sup>T cell infiltration, thereby enhancing anti-PD-L1 therapy effect. We further demonstrated that low-dose ATO remodeled ECM by regulating the expression of LOXL3 in PSCs. scAbFAP-α-HMSNs-PAA-ATO exhibited improved targeting capabilities, and enhanced capacity to inhibit fibrosis and sensitize immunotherapy.</p><p><strong>Conclusions: </strong>Our research reveals that low-dose ATO, by regulating LOXL3, remodels the ECM and enhances CD8<sup>+</sup>T cell infiltration, thus sensitizing the efficacy of immunotherapy, which provides a novel strategy for comprehensive treatment to PC.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582140","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}
Helga H Hektoen, Kaitlyn M Tsuruda, Lars Fjellbirkeland, Yngvar Nilssen, Odd Terje Brustugun, Bettina K Andreassen
{"title":"Real-world evidence for pembrolizumab in non-small cell lung cancer: a nationwide cohort study.","authors":"Helga H Hektoen, Kaitlyn M Tsuruda, Lars Fjellbirkeland, Yngvar Nilssen, Odd Terje Brustugun, Bettina K Andreassen","doi":"10.1038/s41416-024-02895-1","DOIUrl":"https://doi.org/10.1038/s41416-024-02895-1","url":null,"abstract":"<p><strong>Background: </strong>Based on favourable results from clinical trials, immune checkpoint inhibitors (ICI) have become the standard first line (1 L) systemic anticancer treatment (SACT) for advanced stage non-small cell lung cancer (NSCLC) without targetable mutations. We evaluate whether these results are generalizable to everyday clinical practice and compare overall survival (OS) of patients treated with ICI to a historical cohort of patients treated with chemotherapy and results from clinical trials.</p><p><strong>Methods: </strong>Our study comprised all advanced NSCLC patients initiating SACT in 2012-21 in Norway. Clinical characteristics and treatment information was retrieved from Norwegian Health Registries.</p><p><strong>Results: </strong>Survival for all 8416 advanced NSCLC patients treated with SACT increased concurrently with the gradual implementation of ICIs. Median OS of patients treated with 1 L pembrolizumab after 2017 was better (mono-/combination therapy: 13.8/12.8 months) than for patients treated with chemotherapy before 2017 (8.0 months). Although median OS for patients treated with pembrolizumab was lower in clinical practice than clinical trials (Keynote-024/189: 26.3/22.0 months), the survival benefit relative to chemotherapy was similar.</p><p><strong>Conclusion: </strong>Our nationwide study demonstrated a survival benefit over conventional chemotherapy of a similar magnitude as observed in clinical trials and confirms the effectiveness of pembrolizumab in routine clinical practice.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567347","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}
Bishma Jayathilaka, Farah Mian, Fanny Franchini, George Au-Yeung, Maarten IJzerman
{"title":"Cancer and treatment specific incidence rates of immune-related adverse events induced by immune checkpoint inhibitors: a systematic review.","authors":"Bishma Jayathilaka, Farah Mian, Fanny Franchini, George Au-Yeung, Maarten IJzerman","doi":"10.1038/s41416-024-02887-1","DOIUrl":"https://doi.org/10.1038/s41416-024-02887-1","url":null,"abstract":"<p><strong>Background: </strong>Immune-related adverse events (irAE) induced by immune checkpoint inhibitors (ICI) are a treatment-limiting barrier. There are few large-scale studies that estimate irAE prevalence. This paper presents a systematic review that reports the prevalence of irAE by cancer type and ICI.</p><p><strong>Methods: </strong>A systematic review was undertaken in MEDLINE OVID, EMBASE and Web of Science databases from 2017-2021. A total of 293 studies were identified for analysis and, of these, event rate was calculated for 272 studies, which involved 58,291 patients with irAE among 305,879 total patients on ICI. Event rate was calculated by irAE and ICI type.</p><p><strong>Results: </strong>Mean event rate for general irAE occurrence across any grade was 40.0% (37.3-42.7%) and high grade was 19.7% (15.8-23.7%). Mean event rates for six specific types of irAE are reported. Mean event rate for ICI monotherapy was 29.7% (27.7-33.2%), 45.7% (29.6-61.7%) for ICI combination therapy, and 30.3% (27.3-35.0%) for both ICI monotherapy and combination therapy.</p><p><strong>Conclusion: </strong>This systematic review characterises irAE prevalence across current research that examines irAE risk factors across cancers and ICI. The findings confirms that irAE occurrence is very common in the real-world setting, both high grade and irAE across any grade.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567344","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}
Jiang-Li Lu, Yun-Lin Ye, Dan-Dan Zheng, Xin-Yu Shi, Li-Ling Hu, Xiao-Yi Yuan, Tao-Nong Cai, Kun Meng, Neng-Qiao Wen, Yu-Ying Li, Ding-Kang Wang, Fu-Jin Shi, Dan-Ya Liu, Qing-Yu He, Zi-Ke Qin, Chris Zhiyi Zhang, Yun Cao
{"title":"Temporal dynamics of immune cell patterns in bladder cancer patients receiving Bacillus Calmette-Guérin therapy.","authors":"Jiang-Li Lu, Yun-Lin Ye, Dan-Dan Zheng, Xin-Yu Shi, Li-Ling Hu, Xiao-Yi Yuan, Tao-Nong Cai, Kun Meng, Neng-Qiao Wen, Yu-Ying Li, Ding-Kang Wang, Fu-Jin Shi, Dan-Ya Liu, Qing-Yu He, Zi-Ke Qin, Chris Zhiyi Zhang, Yun Cao","doi":"10.1038/s41416-024-02883-5","DOIUrl":"https://doi.org/10.1038/s41416-024-02883-5","url":null,"abstract":"<p><strong>Background: </strong>Bacillus Calmette-Guérin (BCG) is capable of enhancing the infiltration of immune cells into the tumour. However the temporal dynamics of immune cell patterns in patients receiving BCG instillation remains unclear.</p><p><strong>Methods: </strong>Ninety-six patients who underwent intravesical BCG therapy, comprising 46 responders and 50 non-responders, were retrospectively enroled to explore the evolving immune landscape. This study involved a detailed examination of sequential samples collected before, during, and after BCG treatment to assess BCG's influence on the immune microenvironment, employing techniques such as immunohistochemistry, fluorescent multiplex immunohistochemistry, and mass spectrometry techniques.</p><p><strong>Results: </strong>Our study found that initial BCG instillation leads to enhanced immune cell infiltration, correlating with treatment efficacy, with responders exhibiting more pronounced increases. Non-responders experience a rise in immune cell infiltration and PD-L1 expression during the first instillation, which returns to baseline after treatment. In non-responders, BCG re-challenge fail to further increase immune cell infiltration into the tumour or improve patient outcomes. Strikingly, proteomics data revealed that GBP1 expression was induced by BCG treatment in non-responders.</p><p><strong>Conclusions: </strong>Our findings demonstrated the induction of tumour PD-L1 expression by BCG in non-responders, and therefore provide insights for the combination of BCG and anti-PD1/anti-PD-L1 therapy.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557220","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}
Matteo Villa, Geeta G Sharma, Federica Malighetti, Mario Mauri, Giulia Arosio, Nicoletta Cordani, Cosimo Lobello, Hugo Larose, Alessandra Pirola, Deborah D'Aliberti, Luca Massimino, Lucrezia Criscuolo, Lisa Pagani, Clizia Chinello, Cristina Mastini, Diletta Fontana, Silvia Bombelli, Raffaella Meneveri, Federica Lovisa, Lara Mussolin, Andrea Janikova, Šárka Pospíšilová, Suzanne D Turner, Giorgio Inghirami, Fulvio Magni, Mario Urso, Fabio Pagni, Daniele Ramazzotti, Rocco Piazza, Roberto Chiarle, Carlo Gambacorti-Passerini, Luca Mologni
{"title":"Recurrent somatic mutations of FAT family cadherins induce an aggressive phenotype and poor prognosis in anaplastic large cell lymphoma.","authors":"Matteo Villa, Geeta G Sharma, Federica Malighetti, Mario Mauri, Giulia Arosio, Nicoletta Cordani, Cosimo Lobello, Hugo Larose, Alessandra Pirola, Deborah D'Aliberti, Luca Massimino, Lucrezia Criscuolo, Lisa Pagani, Clizia Chinello, Cristina Mastini, Diletta Fontana, Silvia Bombelli, Raffaella Meneveri, Federica Lovisa, Lara Mussolin, Andrea Janikova, Šárka Pospíšilová, Suzanne D Turner, Giorgio Inghirami, Fulvio Magni, Mario Urso, Fabio Pagni, Daniele Ramazzotti, Rocco Piazza, Roberto Chiarle, Carlo Gambacorti-Passerini, Luca Mologni","doi":"10.1038/s41416-024-02881-7","DOIUrl":"https://doi.org/10.1038/s41416-024-02881-7","url":null,"abstract":"<p><strong>Background: </strong>Anaplastic Large Cell Lymphoma (ALCL) is a rare and aggressive T-cell lymphoma, classified into ALK-positive and ALK-negative subtypes, based on the presence of chromosomal translocations involving the ALK gene. The current standard of treatment for ALCL is polychemotherapy, with a high overall survival rate. However, a subset of patients does not respond to or develops resistance to these therapies, posing a serious challenge for clinicians. Recent targeted treatments such as ALK kinase inhibitors and anti-CD30 antibody-drug conjugates have shown promise but, for a fraction of patients, the prognosis is still unsatisfactory.</p><p><strong>Methods: </strong>We investigated the genetic landscape of ALK + ALCL by whole-exome sequencing; recurring mutations were characterized in vitro and in vivo using transduced ALCL cellular models.</p><p><strong>Results: </strong>Recurrent mutations in FAT family genes and the transcription factor RUNX1T1 were found. These mutations induced changes in ALCL cells morphology, growth, and migration, shedding light on potential factors contributing to treatment resistance. In particular, FAT4 silencing in ALCL cells activated the β-catenin and YAP1 pathways, which play crucial roles in tumor growth, and conferred resistance to chemotherapy. Furthermore, STAT1 and STAT3 were hyper-activated in these cells. Gene expression profiling showed global changes in pathways related to cell adhesion, cytoskeletal organization, and oncogenic signaling. Notably, FAT mutations associated with poor outcome in patients.</p><p><strong>Conclusions: </strong>These findings provide novel insights into the molecular portrait of ALCL, that could help improve treatment strategies and the prognosis for ALCL patients.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543816","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}