Objective:To investigate the effects of fibroblast growth factor receptor 1(FGFR1)on the resistance of colorectal cancer(CRC)cells to oxaliplatin(OXA).Methods:An OXA-resistant cell line(HCT8/OXA)was established by treating HCT8 CRC cells with low-dose OXA for a long period in vitro.The CCK-8 assay was used to compare the viability of the HCT8 and HCT8/OXA cells after OXA treatment and to exam-ine their resistance to the anticancer drug.Second-generation high-throughput sequencing technology was used to identify differentially ex-pressed genes between the parental and drug-resistant cells.The expression of FGFR1 in the HCT8 and HCT8/OXA cells was detected by Western blot assay.Colony formation and flow cytometric assays were used to determine cell proliferation and apoptosis,respectively.The expression of PI3K/AKT signaling pathway-related proteins was detected using Western blot assay.Results:Compared with the levels in the HCT8 cells,the FGFR1 levels were significantly increased in the HCT8/OXA cells(P<0.01).FGFR1 overexpression in the HCT8 cells increased their drug resistance(P<0.01)and proliferation(NC+OXA:236.67±6.24;FGFR1+OXA:568.33±6.24)and decreased their apoptotic rate after OXA treatment(NC+OXA:27.83±0.85;FGFR1+OXA:17.47±1.25).FGFR1 knockdown in the HCT8/OXA cells reduced their drug resistance(P<0.01)and proliferative ability(Si-NC+OXA:411±8.29;Si-FGFR1+OXA:233.33±20.55)and increased their apoptotic rate(Si-NC+OXA:2.85±0.17;Si-FGFR1+OXA:14.42±0.77).FGFR1 inhibited the activity of the PI3K/AKT signaling pathway and cell apoptosis and improved the proliferation and drug resistance of the CRC cells.By contrast,an activator of the PI3K/AKT pathway blocked the effects of FGFR1 on this sig-naling pathway and drug resistance in the CRC cells.Conclusions:FGFR1 can inhibit the PI3K/AKT signaling pathway and thereby reduce the sensitivity of CRC cells to OXA.

Objective:To evaluate the expression of B7-H3 and CD133 in colorectal cancer(CRC),colorectal polyps,and normal colorectal mucosa and investigate their roles in the development and prognosis of CRC.Methods:Immunohistochemistry was used to detect the ex-pression of B7-H3 and CD133 in 195 CRC,76 villous/tubulovillous adenoma,64 tubular adenoma,30 non-adenomatous polyp,and 10 nor-mal colorectal mucosa samples obtained from The Second Affiliated Hospital of Zhengzhou University between October 2012 and April 2017 and Pengan County People's Hospital between January 2017 and May 2019.Patient age,sex,and immunohistochemical staining results of B7-H3,CD133,and carcinoembryonic antigen were incorporated as risk factors to establish a CRC survival prediction model.Results:B7-H3 and CD133 expression showed an increasing trend from normal mucosa to non-adenomatous polyps,tubular adenomas,villous/tubulovil-lous adenomas,and CRC(P<0.05),and correlated with adenoma size.It was also associated with CRC metastasis and shorter survival(P<0.05).Furthermore,the expressions of B7-H3 and CD133 demonstrated a value in the CRC survival prediction model,in the training as well as validation set.Conclusions:The immune regulator B7-H3 and cancer stem cell marker CD133 are associated with poor prognosis in CRC,and their expressions may serve as predictive factors for CRC prognosis.

With the rapid advancements in pancreatic cancer diagnosis and treatment research,the Chinese Society of Clinical Oncology(CSCO)has released two editions of pancreatic cancer diagnosis and treatment guidelines in 2022 and 2024.The present article systematic-ally compares the differences between the two editions in terms of diagnostic stratification,treatment pathways,and supportive manage-ment.By integrating insights from cutting-edge international research,the scientific rationale and clinical value of the underlying guideline revisions are explored.Clinicians are encouraged to adopt the new guidelines to dynamically assess the biological characteristics and treat-ment tolerance of patients,thereby formulating personalized diagnosis and treatment plans that ultimately lead to the synergistic enhance-ment of both survival benefits and quality of life for patients.

Objective:Primary pulmonary mucoepidermoid carcinoma(PMEC)is a rare malignant lung tumor that accounts for approxim-ately 0.1%-0.2%of all primary pulmonary neoplasms.Due to the non-specific clinical symptoms and epidemiological features,PMEC poses diagnostic challenges.Methods:Tissue blocks from 23 archived PMECs were collected from The First Affiliated Hospital of Soochow Uni-versity(November 2012 to December 2023).To establish definitive diagnoses,comprehensive histopathological evaluation,including histo-morphological analysis,immunohistochemistry(IHC),fluorescence in situ hybridization(FISH),and periodic acid-Schiff(PAS)staining were performed.Results:The tumors consisted of varying proportions of mucin-secreting cells(mucous cells),intermediate cells,and epidermoid cells.Immunophenotypically,CK7 was predominantly expressed in the mucous cells,whereas CK5/6,p40,and p63 were expressed in the epidermoid and intermediate cells.The Ki-67 proliferation index ranged from 5%to 60%.All tumors were negative for TTF-1 and Napsin A.Five of the tumors were positive for PD-L1(clone 22C3),with a tumor percentage score of 3%-20%.All 11 tumors tested for ALK(clone D5F3)were negative.IHC for c-Met was performed on two tumors and both were weakly positive(+).Mastermind-like transcriptional co-activator 2(MAML2)gene rearrangement was detected in 34.8%(8/23)of the tumors.Mucous cells were PAS positive.Kaplan-Meier surviv-al analysis revealed a significantly poorer prognosis for patients with lymph node metastasis,distant metastasis,advanced TNM stage(Ⅲ+Ⅳ),poor differentiation,or MAML2 gene rearrangement negativity.Univariate analysis identified poor histological differentiation,lymph node metastasis,distant metastasis,and advanced TNM stage as the major prognostic risk factors.Multivariate analysis confirmed poor differentiation and distant metastasis as independent risk factors for adverse outcomes.Conclusions:PMEC is an aggressive tumor with low incidence and non-specific clinical manifestations,leading to frequent misdiagnosis.Clinicians should maintain a high index of suspicion and ensure a thorough differential diagnosis.

Superparamagnetic iron oxide nanoparticles(SPIONs)have been shown to exhibit degradability,superparamagnetic responsive-ness,and multimodal functional properties,which are expected to overcome the bottleneck of traditional separation between diagnosis and treatment in the time and space domains.Through magnetic resonance imaging(MRI)-guided intelligent delivery of targeted drugs,magnet-ic/light/acoustic multi-physical field collaborative therapy,and other strategies,the tumor microenvironment can be precisely regulated and drug resistance can be reversed.Herein,we systematically review the core mechanisms of SPIONs in cross-scale diagnosis and treatment and discuss the innovative application mechanism and technical progress of SPIONs in regard to the integration of tumor theranostics.SPIONs provide breakthrough solutions for the precise diagnosis and treatment of tumors through MRI navigation,targeted delivery system con-struction,and multimodal strategies,offering a theoretical foundation.However,current studies continue to encounter various challenges,including inadequate biosafety validation,restricted efficiency of targeted delivery due to tumor heterogeneity,and complexity of optimiz-ing parameters for multimodal synergistic treatments.Further refinement of material design and clinical translation strategies are essential for providing a valuable reference for developing systematic solutions that bridge theoretical innovations with technological implementation in tumor precision medicine.

In recent years,the clinical implementation of next-generation sequencing(NGS)has demonstrated the critical driving role of spe-cific myeloid-related gene mutations in the clonal evolution of myelodysplastic syndrome(MDS).These molecular genetic abnormalities not only correlate significantly with disease prognosis but also provide actionable molecular targets for precision medicine-era therapies.In cur-rent clinical practice,the Revised International Prognostic Scoring System(IPSS-R)remains the primary tool for guiding risk-adapted treat-ments in patients with MDS.However,real-world outcomes in certain patients still deviate from IPSS-R predictions,highlighting the need to integrate molecular genetic features into traditional prognostic models for enhanced accuracy.This article systematically reviews recent ad-vances in understanding MDS genetic mutations,focusing on their pivotal roles in driving malignant clonal evolution,optimizing risk stratific-ation,and developing personalized treatments.

Breast cancer remains one of the most prevalent malignancies among women worldwide,with distant organ metastasis being the leading cause of mortality.The lungs are a common site of metastasis in breast cancer and are associated with significantly poor prognosis.Although notable progress has been made in therapeutic strategies,efficacy remains markedly limited once pulmonary metastasis develops.Therefore,elucidating the molecular mechanisms that drive pulmonary metastasis,characterizing the immune microenvironment,and as-sessing therapeutic responsiveness are critical.Recent advances in multi-omics approaches-including genomics,transcriptomics,proteomics,metabolomics,and epigenetics-have been widely applied to investigate breast cancer metastasis,offering new insights into the complex mo-lecular networks underlying pulmonary dissemination.This review synthesizes current findings on key genes,proteins,metabolites,and epi-genetic regulatory mechanisms involved in the metastatic cascade from a multi-omics perspective.

Objective:We investigated the effects of evodiamine(Evo)on the migration,invasion,proliferation,and apoptosis of glio-blastoma(GBM)cells and explored the relevant molecular mechanisms.Methods:Tumor tissue from 26 GBM patients and normal brain tis-sues from 10 patients resected at the Affiliated Hospital of Shandong Second Medical University from February 2022 to February 2024 were retrospectively analyzed.RhoA expression in GBM tissues and its relationship with clinicopathological features in GBM patients were evalu-ated.A-172 and U-118 GBM cells,were used as experimental models.The study included four groups:a control group transfected with empty vector,an Evo group transfected with empty vector and treated with 30 μmol/L Evo,a RhoA group transfected with pcDNA3.1-RhoA,and an Evo+RhoA group given 30 μmol/L Evo and transfected with pcDNA3.1-RhoA.The effect of Evo on the malignant behaviors of A-172 and U-118 cells was analyzed using cell function experiments.Western blot was used to detect the effect of Evo on the protein expressions of RhoA,ROCK,MMP-2 and CyclinD1.Results:RhoA is highly expressed in GBM tissues.Compared with the control group,group Evo signi-ficantly inhibited the proliferation,colony formation,migration and invasion of A-172 and U-118 cells,induced cell apoptosis,and inhibited the protein expression of RhoA,ROCK,MMP-2 and CyclinD1(P<0.05).However,group Evo+RhoA could reverse the effect of Evo on the pro-liferation,migration,invasion and apoptosis of GBM cells,and reverse the inhibitory effect on the expression of related proteins in GBM cells.Conclusions:Evo has been shown to effectively suppress malignant behaviors of GBM cells.The mechanism may be related to the downregulation of RhoA expression.

Prostate cancer(PCa)is one of the common malignant tumors of the genitourinary system in men.It is generally believed that the serum prostate-specific antigen(PSA)level exceeding 4.0 ng/mL has potential diagnostic value for PCa.However,there are many cases of PCa with low PSA levels in clinical practice,specifically between 0-4.0 ng/mL.These cases may be missed or even misdiagnosed due to low PSA levels,leading to delays in treatment and missing the optimal clinical window for diagnosis and treatment.This review provides a com-prehensive summary of the clinicopathological characteristics of PCa patients with PSA levels below 4.0 ng/mL,including their baseline and clinical features,histological characteristics,imaging features,neuroendocrine prostate cancer(NEPC)and prognostic factors,aiming to en-hance the understanding of this type of PCa.

Visfatin,also known as nicotinamide phosphoribosyl transferase(NAMPT)or pre-B-cell colony-enhancing factor,is a proinflam-matory adipokine.Its immunomodulatory effects are closely associated with its pro-inflammatory activity,influencing the secretion of vari-ous cytokines and the function of immune cells.Visfatin exerts pro-tumorigenic effects in most cancers.The tumor immune microenviron-ment(TIME)comprises immune cells within the tumor tissue and an array of secreted cytokines.Growing evidence suggests that visfatin plays a regulatory role in the TIME by promoting inflammatory responses and modulating the polarization of immune cells,their secretory functions,surface protein expression,and energy metabolism,thereby influencing cancer progression.These newly discovered mechanisms provide a critical foundation for the application of NAMPT inhibitors(NAMPTi)in cancer immunotherapy.This review summarizes recent ad-vances in understanding the role of visfatin in tumor immunology and explores the therapeutic potential of NAMPTi in oncology.