tbuckley/cabot-search huggingface dataset:
Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger — United States, 2025
Authors: Anindita N. Issa, A. Patricia Wodi, Charlotte A. Moser, Sybil Cineas
Journal: MMWR Morbidity and Mortality Weekly Report (2025)

At its October 2024 meeting, the Advisory Committee on Immunization Practices* (ACIP) approved the Recommended Immunization Schedule for Child and Adolescent Ages 18 Years or Younger, United States, 2025. The schedule supports health care providers, as well as public health and other professionals, by providing a consolidated summary of current ACIP recommendations for vaccinating children and adolescents. The 2025 schedule includes several updates to the cover page, tables, notes, and appendix.† The addendum remains part of the schedule and will be used to summarize new or updated ACIP recommendations that occur before the next annual schedule update. Health care providers are strongly encouraged to use all parts of the schedule (the cover page, tables, notes, appendix, and addendum) together when making recommendations for individual patients. The 2025 child and adolescent immunization schedule can be found on the CDC website (https://www.cdc.gov/vaccines/hcp/imz-schedules/index.html).
Hide and Seek: Detecting HCC with novel surveillance algorithms
Authors: John Grady, Juan Pablo Arab
Journal: Hepatology (2025)

1Division of Gastroenterology, Hepatology, and Nutrition, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA 2Department of Gastroenterology, School of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile Abbreviations: AFP, alpha-fetoprotein; ASAP, age, sex, AFP, DCP; DCP, des-gamma-carboxy prothrombin; GALAD, gender, age, AFP-L3, AFP, and DCP; HES, Hepatocellular Carcinoma Early Detection Screening. Correspondence Juan Pablo Arab, Department of Internal Medicine, Stravitz-Sanyal Institute of Liver Disease and Metabolic Health, Commonwealth University School of Medicine, Richmond, Virginia 23284, USA. Email: [email protected]
Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial
Authors: Jorge E. Cortes, Gail J. Roboz, Maria R. Baer, Brian A. Jonas, Gary J. Schiller, Karen Yee, P. Brent Ferrell, Jay Yang, Eunice S. Wang, William G. Blum, Alice Mims, Hua Tian, Aaron Sheppard, Stéphane de Botton, Pau Montesinos, Antonio Curti, Justin M. Watts
Journal: Journal of Hematology & Oncology (2025)

Olutasidenib is a potent, selective, oral, small molecule inhibitor of mutant IDH1 (mIDH1) which induced durable remissions in high-risk, relapsed/refractory (R/R) mIDH1 AML patients in a phase 1/2 trial. We present a pooled analysis from multiple cohorts of the phase 1/2 trial of patients with R/R AML who received combination olutasidenib and azacitidine therapy. Adult patients with mIDH1R132 AML received 150 mg olutasidenib twice daily plus standard-of-care azacitidine (OLU + AZA) and were evaluated for response and safety. Sixty-seven patients with R/R mIDH1R132 AML received combination OLU + AZA. Median age was 66 years (range 28-82) and 54% were male. Most patients (83%) had 2 + prior regimens, including a hypomethylating agent in 40%, IDH1 inhibitor therapy in 31% (olutasidenib in 24%), and hematopoietic stem cell transplant in 10%. Cytogenetic risk was intermediate in 72%, poor in 18% and unknown in 10%. CR/CRh was achieved in 21/67 (31%; 95% CI 21-44) patients, with a median duration of 14.7 months (95% CI 4.6-not reached). CR was achieved in 18/67 (27%; 95% CI 17-39) patients, with median duration of 20.3 months (95% CI 3.7-not reached). Overall response (partial remission or better) was achieved in 34/67 (51%; 95% CI 38-63) patients. Median overall survival was 12.9 months (95% CI 18.7-19.3). In a subset analysis excluding patients who had prior OLU exposure (N = 51), CR/CRh was achieved in 19/51 (37%; 95% CI 24-52) patients, CR was achieved in 16/51 (31%; 95% CI 19-46), and overall response was achieved in 30/51 (59%; 95% CI 44-72). In patients who achieved CR/CRh and were transfusion-dependent at baseline, transfusion independence (RBC and platelets) was achieved in 64% (7/11) and 57% (4/7) of patients, respectively. The most common Grade 3 or 4 adverse events (> 20% patients) were decreased platelet count (37%), red blood cell count (25%), and neutrophil count (24%). Six patients (9%) experienced differentiation syndrome. Four (6%) discontinued treatment due to an adverse event. Olutasidenib plus azacitidine induced high response rates and durable remissions with a tolerable side effect profile in patients with R/R AML with diverse treatment histories. The results represent another therapeutic option for patients with mIDH1 AML who may benefit from a targeted therapy. NCT02719574.
<i>Drosophila CG11700</i> may not affect male fecundity-lifespan tradeoff as previously reported
Authors: Dashuang Zuo, Weiwei Liu, Ruoping Zhao, Kesen Zhu, Wen Wang, Hui Xiang
Journal: Molecular Biology and Evolution (2025)

Our recent investigations on the function of Drosophila CG11700 and CG32744 (Ubi-p5E) genes using CRISPR/Cas9 deletion technology could not repeat or confirm the results on CG11700 shown in our previous study which was based on P-element excision assay (Zhan et al. 2012). Here by CRISPR/Cas9 editing, we generated mutants of CG32744 with the whole gene body fully deleted from the genome, and truncated mutants of CG11700 with N-terminal 103 aa deleted out of its total 301 aa peptide sequence. We carefully conducted the male fecundity assay and found that offsprings of the CG11700 mutant were not significantly more than the wild type, inconsistent with our previous report (Zhan et al. 2012). Meanwhile, we repeated the lifespan assay and did not find that the lifespan of the CG11700 mutant is significantly shorter than the wild type as reported in Zhan et al. either (2012). The new results suggest that the CG11700 gene may not affect male fecundity-lifespan tradeoff as previously reported (Zhan et al. 2012). The new results are thus worthy of reporting to avoid possible misleading by the previous results to the scientific community.
Efficacy and tolerability of neoadjuvant therapy with Talimogene laherparepvec in cutaneous basal cell carcinoma: a phase II trial (NeoBCC trial)
Authors: Julia Maria Ressler, Maud Plaschka, Rita Silmbrod, Victoria Bachmayr, Lisa Ellen Shaw, Thomas Silly, Nina Zila, Andreas Stepan, Anna Kusienicka, Philipp Tschandl, Julia Tittes, Florian Roka, Werner Haslik, Peter Petzelbauer, Franz Koenig, Rainer Kunstfeld, Matthias Farlik, Florian Halbritter, Wolfgang Weninger, Christoph Hoeller
Journal: Nature Cancer (2025)

We present a single-arm, phase II, neoadjuvant trial with the oncolytic virus talimogene laherparepvec (T-VEC) in 18 patients with difficult-to-resect cutaneous basal cell carcinomas. The primary end point, defined as the proportion of patients, who after six cycles of T-VEC (13 weeks), become resectable without the need for plastic reconstructive surgery, was already achieved after stage I (9 of 18 patients; 50.0%); thus the study was discontinued for early success. The objective response rate was 55.6% and the complete pathological response rate was 33.3%. Secondary end points included safety, relapse-free survival and overall survival, time to occurrence of new basal cell carcinomas and biological read outs. Only mild adverse events occurred. The 6-month relapse-free survival and overall survival rates were 100%. In two patients a new basal cell carcinoma was diagnosed. T-VEC led to a significant increase in cytotoxic T cells (P = 0.0092), B cells (P = 0.0004) and myeloid cells (P = 0.0042) and a decrease in regulatory T cells (P = 0.0290) within the tumor microenvironment. Together, neoadjuvant T-VEC represents a viable treatment option for patients with difficult-to-resect basal cell carcinomas (EudraCT no. 2018-002165-19).
Neoadjuvant atezolizumab in combination with dual HER2 blockade plus epirubicin in women with early HER2-positive breast cancer: the randomized phase 2 ABCSG-52/ATHENE trial
Authors: Gabriel Rinnerthaler, Daniel Egle, Rupert Bartsch, Clemens A. Schmitt, Andreas Petzer, Marija Balic, Edgar Petru, Ursula Denison, Christian F. Singer, Vesna Bjelic-Radisic, Simon Peter Gampenrieder, Michael Knauer, Karl Sotlar, Christine Brunner, Florian Posch, Dominik Hlauschek, Lidija Sölkner, Zsuzsanna Bago-Horvath, Martin Filipits, Manuela Gili, Magdalena Ritter, Verena Wieser, Carmen Albertini, Nadja Zaborsky, Lukas Weiss, Maximilian Marhold, Bruno Schneeweiss, Renate Pusch, Michael Gnant, Richard Greil
Journal: Nature Cancer (2025)
Recommendations for mitochondria transfer and transplantation nomenclature and characterization
Authors: Jonathan R. Brestoff, Keshav K. Singh, Katia Aquilano, Lance B. Becker, Michael V. Berridge, Eric Boilard, Andrés Caicedo, Clair Crewe, José Antonio Enríquez, Jianqing Gao, Åsa B. Gustafsson, Kazuhide Hayakawa, Maroun Khoury, Yun-Sil Lee, Daniele Lettieri-Barbato, Patricia Luz-Crawford, Heidi M. McBride, James D. McCully, Ritsuko Nakai, Jiri Neuzil, Martin Picard, Alexander G. Rabchevsky, Anne-Marie Rodriguez, Shiladitya Sengupta, Alexander J. Sercel, Toshio Suda, Michael A. Teitell, Alain R. Thierry, Rong Tian, Melanie Walker, Minghao Zheng
Journal: Nature Metabolism (2025)
Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention
Authors: Yurong Zhao, Xinxin Chai, Junxuan Peng, Yi Zhu, Rong Dong, Junwei He, Linghao Xia, Sishuo Liu, Jingzhou Chen, Zhengping Xu, Chi Luo, Jinghao Sheng
Journal: Nature Metabolism (2025)
Menopause-induced 17β-estradiol and progesterone loss increases senescence markers, matrix disassembly and degeneration in mouse cartilage
Authors: Gabrielle Gilmer, Hirotaka Iijima, Zachary R. Hettinger, Natalie Jackson, Juliana Bergmann, Allison C. Bean, Nafiseh Shahshahan, Ekaterina Creed, Rylee Kopchak, Kai Wang, Hannah Houston, Jonathan M. Franks, Michael J. Calderon, Claudette St Croix, Rebecca C. Thurston, Christopher H. Evans, Fabrisia Ambrosio
Journal: Nature Aging (2025)
First-in-class ultralong-target-residence-time p38α inhibitors as a mitosis-targeted therapy for colorectal cancer
Authors: Ramona Rudalska, Jule Harbig, Michael Forster, Pascal Woelffing, Aylin Esposito, Mark Kudolo, Adelina Botezatu, Vanessa Haller, Nicole Janssen, Samuel Holzmayer, Philipp Nahidino, Omelyan Trompak, Tatu Pantsar, Thales Kronenberger, Can Yurttas, Elke Rist, Alexander N. R. Weber, Marc H. Dahlke, German Ott, Alfred Koenigsrainer, Ulrich Rothbauer, Melanie Maerklin, Thomas Muerdter, Matthias Schwab, Stephan Singer, Lars Zender, Stefan Laufer, Daniel Dauch
Journal: Nature Cancer (2025)

Colorectal cancer (CRC) constitutes the second leading cause of cancer-related death worldwide and advanced CRCs are resistant to targeted therapies, chemotherapies and immunotherapies. p38α (Mapk14) has been suggested as a therapeutic target in CRC; however, available p38α inhibitors only allow for insufficient target inhibition. Here we describe a unique class of p38α inhibitors with ultralong target residence times (designated ULTR-p38i) that robustly inhibit p38α downstream signaling and induce distinct biological phenotypes. ULTR-p38i monotherapy triggers an uncontrolled mitotic entry by activating Cdc25 and simultaneously blocking Wee1. Consequently, CRC cells undergo mitotic catastrophe, resulting in apoptosis or senescence. ULTR-p38i exhibit high selectivity, good pharmaco-kinetic properties and no measurable toxicity with strong therapeutic effects in patient-derived CRC organoids and syngeneic CRC mouse models. Conceptually, our study suggests ultralong-target-residence-time kinase inhibitors as an alternative to covalent inhibitors, which, because of the lack of cysteine residues, cannot be generated for many kinase cancer targets.
Dual-responsive stem cell microspheres modified with BDNF for enhanced neural repair in diabetic erectile dysfunction
Authors: Xiaoying Pan, Xiaowen Xing, Zhengguo Ji, Jianzhong Zhang, Qiaomi Chen, Weifan Yin, Yueyue Zang, Yong Yang, Zhiqiang Liu, Yongde Xu
Journal: Journal of Controlled Release (2025)
Extracellular vesicles from chronic lymphocytic leukemia cells promote leukemia aggressiveness by inducing the differentiation of monocytes into nurse‐like cells via an RNA‐dependent mechanism
Authors: Nathan Dubois, David Van Morckhoven, Laurentijn Tilleman, Filip Van Nieuwerburgh, Dominique Bron, Laurence Lagneaux, Basile Stamatopoulos
Journal: HemaSphere (2025)

Abstract Chronic lymphocytic leukemia (CLL) cells receive several stimuli from surrounding cells, such as B‐cell receptor (BCR) stimulation, and can manipulate their microenvironment via extracellular vesicle (EV) release. Here, we investigated the small RNA content (microRNA and YRNA) of CLL‐EVs from leukemic cells cultured with/without BCR stimulation. We highlight an increase of miR‐155‐5p, miR‐146a‐5p, and miR‐132‐3p in EVs and in cells after BCR stimulation ( p &lt; 0.05, n = 25). CLL‐EVs were preferentially internalized by monocytes ( p = 0.0019, n = 6) and able to deliver microRNAs and the hY4 RNA. Furthermore, BCR CLL‐EV induced modifications in monocytes (shape change, microRNA and gene expression, secretome) suggesting nurse‐like cell (NLC) differentiation, the tumor‐associated macrophages of CLL. Functionally, monocytes treated with BCR CLL‐EVs protect CLL cells from spontaneous apoptosis by pro‐survival cytokine production and induce their migration as well as the migration of other immune cells. We finally reported by transfection experiments that hY4 is able to induce the expression of CCL24, a key gene in M2 macrophage differentiation. In conclusion, we showed that BCR stimulation modifies the small RNA content of CLL‐EVs and that the addition of leukemic EVs to monocytes leads to monocyte differentiation into NLCs establishing a protective microenvironment that supports leukemic cell survival.
Disease characteristics and outcomes of acute myeloid leukemia in germline <i>RUNX1</i> deficiency (Familial Platelet Disorder with associated Myeloid Malignancy)
Authors: Martijn P. T. Ernst, Jurjen Versluis, Peter J. M. Valk, Marc Bierings, Rienk Y. J. Tamminga, Louise H. Hooimeijer, Konstanze Döhner, Paolo Gresele, Kiran Tawana, Saskia M. C. Langemeijer, Bert A. Van der Reijden, Helena Podgornik, Matjaz Sever, Tor H. A. Tvedt, Tom Vulliamy, Jude Fitzgibbon, Inderjeet Dokal, Panagiotis Baliakas, José M. Bastida, Christian Pohlkamp, Torsten Haferlach, Lise Larcher, Jean Soulier, Roger E. G. Schutgens, Kathleen Freson, Nicolas Duployez, Bob Löwenberg, Katrin Ericson, Jörg Cammenga, Tim Ripperger, Marc H. G. P. Raaijmakers
Journal: HemaSphere (2025)

Abstract Familial Platelet Disorder with associated Myeloid Malignancy (FPDMM, FPD/AML, RUNX1 ‐FPD), caused by monoallelic deleterious germline RUNX1 variants, is characterized by bleeding diathesis and predisposition for hematologic malignancies, particularly myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Clinical data on FPDMM‐associated AML (FPDMM‐AML) are limited, complicating evidence‐based clinical decision‐making. Here, we present retrospective genetic and clinical data of the largest cohort of FPDMM patients reported to date. We describe 159 European patients (from 94 families) of whom 134 were evaluable for the development of malignant disease. Sixty developed a hematologic malignancy (44.8%), most frequently AML (36/134, 26.9%) or MDS (18/134, 13.4%). Somatic alterations of RUNX1 by gene mutation (48%) and chromosome 21 aberrations (14.3%) were the most common somatic genetic aberrations in FPDMM‐AML, followed by FLT3‐ITD mutations (24.1%). Somatic RUNX1 and FLT3‐ITD mutations were not detected in FPDMM‐associated MDS, suggesting important contributions to leukemic transformation. Remission‐induction chemotherapy resulted in complete remission in 80% of FPDMM‐AML patients with a 5‐year overall survival (OS) of 50.4%. Survival outcome was non‐inferior compared to a large cohort of newly diagnosed adult RUNX1 ‐mutated AML (5‐year OS 36.6%, p = 0.5), with relatively infrequent concurrent adverse risk somatic aberrations ( ASXL1 mutation, monosomal karyotype, monosomy 5/del 5q) in FPDMM‐AML. Collectively, data support the notion that step‐wise leukemic evolution in FPDMM is associated with distinct genetic events and indicate that a substantial subset of FPDMM‐AML patients achieves prolonged survival with conventional AML treatment, including allogeneic stem cell transplant. These findings are anticipated to inform personalized clinical decision‐making in this rare disorder.
Safety and humoral immunogenicity of the ChAdOx1 nCoV-19 vaccine administered as a fourth dose booster following two doses of ChAdOx1 nCoV-19 and a third dose of BNT162b2 (COV009): a prospective cohort study.
Authors: Shuo Feng, Sagida Bibi, Parvinder K Aley, Federica Cappuccini, Elizabeth A Clutterbuck, Kerry Conlin, Narges Ebrahimi, Agnes Eordogh, Saul N Faust, Sally Felle, Justin Green, Hardeep Gill, Yama Mujadidi, Iyiola Oladunjoye, Nelly Owino, Emma Plested, Hannah Robinson, Arabella Stuart, Merryn Voysey, Andrew J Pollard, Teresa Lambe
Journal: Journal of Infection (2025)
Author Correction: Enhancing the immunogenicity of lipid-nanoparticle mRNA vaccines by adjuvanting the ionizable lipid and the mRNA
Authors: Bowen Li, Allen Yujie Jiang, Idris Raji, Caroline Atyeo, Theresa M. Raimondo, Akiva G. R. Gordon, Luke H. Rhym, Tahoura Samad, Corina MacIsaac, Jacob Witten, Haseeb Mughal, Taras M. Chicz, Yue Xu, Ryan P. McNamara, Sangeeta Bhatia, Galit Alter, Robert Langer, Daniel G. Anderson
Journal: Nature Biomedical Engineering (2025)
Idecabtagene vicleucel or ciltacabtagene autoleucel for relapsed or refractory multiple myeloma: An international multicenter study
Authors: Maximilian Merz, Anca‐Maria Albici, Bastian von Tresckow, Kristin Rathje, Roland Fenk, Tobias Holderried, Fabian Müller, Natalia Tovar, Aina Oliver‐Cáldes, Vladan Vucinic, Soraya Kharboutli, Ben‐Niklas Bärmann, Francis Ayuk, Uwe Platzbecker, Friedrich Stölzel, Nathalie Schub, Friederike Schmitz, David Fandrei, Patrick Born, Cyrus Khandanpour, Christine Hanoun, Keven Hörster, Marcel Teichert, Barbara Jeker, Michele Hoffmann, Nicolaus Kröger, Carlos Fernández de Larrea, Thomas Pabst, Nico Gagelmann
Journal: HemaSphere (2025)

Idecabtagene vicleucel (ide-cel) and ciltacabtagene autoleucel (cilta-cel) have revolutionized the treatment of relapsed/refractory multiple myeloma (RRMM), but direct comparisons are lacking. Leveraging an international multicenter RRMM cohort, we compared the outcome of ide-cel (n = 162) versus cilta-cel (n = 42). Co-primary efficacy endpoints of the study were overall response rate (ORR) and progression-free survival (PFS). Co-primary safety endpoints were the incidence of cytokine release syndrome (CRS) and immune-effector cell-associated neurotoxicity syndrome (ICANS). Median turnaround time between apheresis and infusion was 47 days for ide-cel versus 68 days for cilta-cel (p < 0.001). Cilta-cel showed significantly higher ORR (93% vs. 79%; p < 0.001), with complete response at Day 30 of 48% versus 26% (p < 0.001). The 10-month PFS and overall survival (OS) was 82% and 90% for cilta-cel versus 47% and 77% ide-cel (p < 0.001 and p = 0.06), and improved outcome for cilta-cel was confirmed after multivariable adjustment. Incidence of CRS and ICANS appeared similar (81% and 19% for cilta-cel versus 85% and 19% for ide-cel), while 10% and 7% in the cilta-cel group versus 4% and 2% in the ide-cel group showed severe CRS and ICANS grade 3-4, with CRS occurring significantly earlier for ide-cel (median, 2 days vs. 4 days; p < 0.001). Nonrelapse mortality was 5% for cilta-cel versus 3% for ide-cel (p = 0.51). Cilta-cel showed later peak of CAR-T expansion at Day 14 versus Day 7 for ide-cel, while cilta-cel expansion was associated with ICANS. Our study provides real-world evidence that cilta-cel was associated with superior outcomes and distinct cellular dynamics versus ide-cel in triple-class exposed RRMM.
Peripheral proteinopathy in neurodegenerative diseases
Authors: Bin Xu, Xia Lei, Ying Yang, Jiayi Yu, Jun Chen, Zhi Xu, Keqiang Ye, Jing Zhang
Journal: Translational Neurodegeneration (2025)

Proteinopathies in neurology typically refer to pathological changes in proteins associated with neurological diseases, such as the aggregation of amyloid β and Tau in Alzheimer's disease, α-synuclein in Parkinson's disease and multiple system atrophy, and TAR DNA-binding protein 43 in amyotrophic lateral sclerosis and frontotemporal dementia. Interestingly, these proteins are also commonly found in peripheral tissues, raising important questions about their roles in neurological disorders. Multiple studies have shown that peripherally derived pathological proteins not only travel to the brain through various routes, aggravating brain pathology, but also contribute significantly to peripheral dysfunction, highlighting their crucial impact on neurological diseases. Investigating how these peripherally derived proteins influence the progression of neurological disorders could open new horizons for achieving early diagnosis and treatment. This review summarizes the distribution, transportation pathways, and pathogenic mechanisms of several neurodegenerative disease-related pathological proteins in the periphery, proposing that targeting these peripheral pathological proteins could be a promising strategy for preventing and managing neurological diseases.
Re: Matsunaga et al.: Disparities in amblyopia treatment outcomes: the impact of sociodemographic factors, treatment compliance, and age of diagnosis. (Ophthalmology. 2024 Sep 23:S0161-6420(24)00569-4. doi: 10.1016/j.ophtha.2024.09.021. Online ahead of print.)
Authors: Suqing Gou, Haishuang Lin, Jieling Chen
Journal: Ophthalmology (2025)
Cerebrospinal fluid cyclase-associated protein 2 is increased in Alzheimer’s disease and correlates with tau pathology
Authors: Alessandro Padovani, Andrea Pilotto, Silvia Pelucchi, Laura D'Andrea, Ramona Stringhi, Federica Gorla, Bahar Aksan, Salvatore Caratozzolo, Alberto Benussi, Alice Galli, Clara Tirloni, Daniela Mauceri, Antonio Canale, Silvana Archetti, Barbara Borroni, Monica Di Luca, Elena Marcello
Journal: Translational Neurodegeneration (2025)
Bidirectional role of neutrophils in tumor development
Authors: Haoxin Luyang, Feng Zeng, Yan Lei, Qian He, Yanhong Zhou, Juan Xu
Journal: Molecular Cancer (2025)

Neutrophils, traditionally considered as non-specific components of the innate immune system, have garnered considerable research interest due to their dual roles in both promoting and inhibiting tumor progression. This paper seeks to clarify the specific mechanisms by which neutrophils play a bidirectional role in tumor immunity and the factors that influence these roles. By conducting a comprehensive analysis and synthesis of a vast array of relevant literature, it has become evident that neutrophils can influence tumor development and invasive migration through various mechanisms, thereby exerting their anti-tumor effects. Conversely, they can also facilitate tumorigenesis and proliferation, as well as affect the normal physiological functions of other immune cells, thus exerting pro-tumor effects. Moreover, neutrophils are influenced by tumor cells and their unique microenvironment, which in turn affects their heterogeneity and plasticity. Neutrophils interact with tumor cells to regulate various aspects of their life activities precisely. This paper also identifies unresolved issues in the research concerning the bidirectional role of neutrophils in tumorigenesis and tumor development, offering new opportunities and challenges for advancing our understanding. This, in turn, can aid in the proper application of these insights to clinical treatment strategies.