A developed ant colony algorithm for cancer molecular subtype classification to reveal the predictive biomarker in the renal cell carcinoma

Background:Recently,researchers have been attracted in identifying the crucial genes related to cancer,which plays important role in cancer diagnosis and treatment.However,in performing the cancer molecular subtype classification task from cancer gene expression data,it is challenging to obtain those significant genes due to the high dimensionality and high noise of data.Moreover,the existing methods always suffer from some issues such as premature convergence.Methods:To address those problems,we propose a new ant colony optimization(ACO)algorithm called DACO to classify the cancer gene expression datasets,identifying the essential genes of different diseases.In DACO,first,we propose the initial pheromone concentration based on the weight ranking vector to accelerate the convergence speed;then,a dynamic pheromone volatility factor is designed to prevent the algorithm from getting stuck in the local optimal solution;finally,the pheromone update rule in the Ant Colony System is employed to update the pheromone globally and locally.To demonstrate the performance of the proposed algorithm in classification,different existing approaches are compared with the proposed algorithm on eight high-dimensional cancer gene expression datasets.Results:The experiment results show that the proposed algorithm performs better than other effective methods in terms of classification accuracy and the number of feature sets.It can be used to address the classification problem effectively.Moreover,a renal cell carcinoma dataset is employed to reveal the biological significance of the proposed algorithm from a number of biological analyses.Conclusion:The results demonstrate that CAPS may play a crucial role in the occurrence and development of renal clear cell carcinoma.

Colorectal cancer cell dormancy:An insight into pathways

Cancer cell dormancy(CCD)in colorectal cancer(CRC)poses a significant challenge to effective treatment.In CRC,CCD contributes to tumour recurrence,drug resistance,and amplifying the disease's burden.The molecular mechanisms governing CCD and strategies for eliminating dormant cancer cells remain largely unexplored.Therefore,understanding the molecular mechanisms governing dormancy is crucial for improving patient outcomes and developing targeted therapies.This editorial highlights the complex interplay of signalling pathways and factors involved in colorectal CCD,emphasizing the roles of Hippo/YAP,pluripotent transcription factors such as NANOG,HIF-1αsignalling,and Notch signalling pathways.Additionally,ERK/p38α/β/MAPK pathways,AKT signalling pathway,and Extracellular Matrix Metalloproteinase Inducer,along with some potential less explored pathways such as STAT/p53 switch and canonical and non-canonical Wnt and SMAD signalling,are also involved in promoting colorectal CCD.Highlighting their clinical significance,these findings may offer the potential for identifying key dormancy regulator pathways,improving treatment strategies,surmounting drug resistance,and advancing personalized medicine approaches.Moreover,insights into dormancy mechanisms could lead to the development of predictive biomarkers for identifying patients at risk of recurrence and the tailoring of targeted therapies based on individual dormancy profiles.It is essential to conduct further research into these pathways and their modulation to fully comprehend CRC dormancy mechanisms and enhance patient outcomes.

miR-206 Inhibits Renal Cell Cancer Growth by Targeting GAK

Renal cell cancer(RCC)remains one of the most lethal types of cancer in adults.Micro RNAs(mi RNAs)play key roles in the pathogenesis of RCC.The role of mi R-206 in RCC has not been fully understood.The purpose of this study was to examine the role of mi R-206 in the regulation of proliferation and metastasis of RCC and the possible mechanism.mi R-206 expression was detected by reverse transcription?quantitative polymerase chain reaction(RT-q PCR)in RCC cell lines(786-O and OS-RC-2 cells)and clinical samples.MTS[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]method,colony formation and transwell assay were used to detect the tumor-suppressing ability of mi R-206 in RCC.Luciferase assay was performed to verify the precise target of mi R-206.The results showed that the expression of mi R-206 was significantly down-regulated in RCC tissues and cells.The expression level of cyclin G-associated kinase(GAK),a master regulator of tumor proliferation and metastasis,was up-regulated with the decrease in mi R-206 in RCC tissues as well as RCC cell lines.In addition,the mi R-206 inhibitor promoted the proliferation,migration and invasion of 786-O and OS-RC-2 cells.Bioinformatics combined with luciferase and Western blot assays revealed that mi R-206 inhibited the expression of GAK.Moreover,mi R-206 regulates RCC cell growth partly through targeting GAK.Our study indicated that mi R-206 functions as a tumor suppressor in regulating the proliferation,migration and invasion of RCC by directly targeting GAK,and it holds promises as a potential therapeutic target for RCC.

Tet methylcytosine dioxygenase 2 suppresses renal cell cancer proliferation and metastasis by regulating the miR-200c-SCD axis

Tet methylcytosine dioxygenase 2(TET2)acts as an antioncogene that is investigated in different cancers.But the effects of TET2 in renal cell cancer(RCC)is still known little.Here,quantitative real-time PCR(qRT-PCR),Western blot,and immunofluorescence were performed to exam gene and protein expression.Cell proliferation was measured using Cell Counting Kit-8(CCK-8).Transwell assay was performed to detect cell metastasis viability.Flow cytometry was performed to analyze the cell cycle and cell apoptosis.The effects of TET2 on RCC growth in vivo was analyzed using a mouse xenograft model.We found that TET2 and miR-200c were decreased in RCC tissues,and hypermethylation of miR-200c promoter was found.Overexpression of TET2 promoted miR-200c expression by reducing miR-200c promoter methylation.Additionally,overexpression of TET2 or miR-200c suppressed cell growth and metastasis.Also,knockdown of miR-200c could moderate TET2 mediated cell growth inhibition.Furthermore,we found miR-200c directly regulates Stearoyl-CoA desaturase(SCD)gene expression.Moreover,in vivo experiment results confirmed that TET2 inhibited tumor growth.In conclusion,TET2 acts as an antioncogene in RCC by regulating the miR-200c-SCD axis and providing a potential target for RCC diagnosis and treatment.

Association of hypoxia-inducible factor-1α (HIF1α) 1772C/T genepolymorphism with susceptibility to renal cell carcinoma/prostatecancer

In this study,we used a meta-analysis method to evaluate the relationship between hypoxia-inducible factor-1α(HIF1α)1772C/T gene polymorphism(rs 11549465)and renal cell carcinoma(RCC)/prostate cancer risk.We searched for relevant studies(before March 1,2019)on Cochrane Library,Embase,and PubMed.Studies meeting the inclusion criteria were recruited into this meta-analysis.The outcome of dichotomous data was showed in the way of odds ratios(OR),and 95%confidence intervals(CI)were also counted.In this investigation,there was no association between HIF1α1772C/T gene polymorphism and susceptibility to RCC in Caucasians,Asians as well as overall populations.In addition,HIF1α1772C/T gene polymorphism was not found to be relevant to the survival in RCC.Interestingly,the T allele was relevant to prostate cancer risk in all populations,but not in Caucasians and Asians.However,the TT genotype and the CC genotype were not related to prostate cancer susceptibility in Asian,Caucasian,and all populations.In conclusion,the T allele of the HIF1α1772C/T gene polymorphism was related to prostate cancer risk in the overall populations.

Recurrent renal cell cancer presenting as gastrointestinal bleed

We present an unusual case of renal cell cancer(RCC) which relapsed with duodenal metastasis and unveiled itself by gastrointestinal(GI) bleeding.An 80-year old Caucasian gentleman with history of renal cell cancer status post nephrectomy 11 mo previously,presented with syncope and melena.Computed tomography scan of the abdomen revealed heterogeneous soft tissue mass in the right nephrectomy bed invading the duodenum.Upper GI endoscopic biopsy confirmed the presence of recurrent renal cell cancer.However,due to extensive metastatic disease,the patient was placed on palliative chemotherapy as surgical options were ruled out.Our case report reiterates the fact that renal cell carcinoma can recur with gastrointestinal manifestations and,although a rarity,it should be considered in a patient with a history of malignancy who presents with these symptoms.

Oncolytic adenovirus targeting LASP-1 inhibited renal cell cancerprogression

Recent studies suggested that LIM and SH3 protein 1(LASP-1)is a promising therapeutic target for renal cell cancer(RCC).This study aimed to explore the role of LASP-1 in RCC.For this purpose,LASP-1 expression in RCC tissues was analyzed by immunohistochemistry and Western blot analysis.Cell proliferation,migration,invasion,and gene expression were detected by CCK-8 assay,Transwell assay,and Western blot analysis.The results showed that LASP-1 was highly expressed in RCC,and its expression level,t was positively correlated with lymph node metastasis and tumor,nodes,and metastases(TNM)stage.The knockdown of LASP-1 expression significantly inhibited the proliferation of RCC cells,increased the apoptosis rate,and inhibited RCC cell invasion and migration by inhibiting epithelial–mesenchymal transition.We conclude that LASP-1 promotes RCC progression and metastasis and is a promising therapeutic target for RCC.

Programmed cell death protein 4 expression in renal cell carcinoma, penile carcinoma and testicular germ cell cancer

AIM:To investigate the expression of programmed cell death 4(Pdcd4)tumor suppressor gene in tissue specimen of renal cell carcinoma(RCC),testicular germ cell cancer and penile cancer.METHODS:Pdcd4 expression was studied using immunohistochemistry in 188 cases of RCC and 28 controls(including 9 oncocytoma);in 74 cases of penile carcinoma(including 17 metastatic tissue samples)and26 controls;in 11 cases of seminoma,in 14 cases of non-seminoma and 5 controls.RESULTS:Control tissues exhibited strong core and cytoplasmatic Pdcd4 staining.In contrast,core and cy-toplasmatic Pdcd4 levels were significantly decreased in cancer tissues.CONCLUSION:Our data support a role for Pdcd4(down-)regulation in urologic tumors.Interestingly,Pdcd4 expression seem to be a potential diagnostic marker for renal or penile tumors.

Role of cancer stem cell ecosystem on breast cancer metastasis and related mouse models

Breast cancer metastasis is responsible for most breast cancer-related deaths and is influenced by many factors within the tumor ecosystem,including tumor cells and microenvironment.Breast cancer stem cells(BCSCs)constitute a small population of cancer cells with unique characteristics,including their capacity for self-renewal and differentiation.Studies have shown that BCSCs not only drive tumorigenesis but also play a crucial role in promoting metastasis in breast cancer.The tumor microenvironment(TME),composed of stromal cells,immune cells,blood vessel cells,fibroblasts,and microbes in proximity to cancer cells,is increasingly recognized for its crosstalk with BCSCs and role in BCSC survival,growth,and dissemination,thereby influencing metastatic ability.Hence,a thorough understanding of BCSCs and the TME is critical for unraveling the mechanisms underlying breast cancer metastasis.In this review,we summarize current knowledge on the roles of BCSCs and the TME in breast cancer metastasis,as well as the underlying regulatory mechanisms.Furthermore,we provide an overview of relevant mouse models used to study breast cancer metastasis,as well as treatment strategies and clinical trials addressing BCSC-TME interactions during metastasis.Overall,this study provides valuable insights for the development of effective therapeutic strategies to reduce breast cancer metastasis.

UBE2T mediates the stemness properties of breast cancer cells through the mTOR signaling pathway

Objectives:This study aimed to reveal the role and possible mechanism of the ubiquitin-conjugating enzyme 2T(UBE2T)in the biological activities of breast cancer stem cells(BCSCs).Methods:The specific protein and gene expression were quantified by Western blotting and quantitative real-time polymerase chain reaction,the proportion of BCSCs was examined by flow cytometry,and the self-renewal and proliferation of BCSCs were verified by serial sphere formation and soft agar.Results:Increasing expression of UBE2T was drastically found in breast cancer than that in adjacent tissues.Furthermore,UBE2T overexpression significantly increased the proportion of BCSCs in breast cancer cells and promoted their self-renewal and proliferation.Silent UBE2T exhibited the opposite functions.UBE2T increased the levels of the mammalian target of rapamycin and the phosphorylated mammalian target of rapamycin.Mammalian target of rapamycin(mTOR)inhibitor rapamycin inhibited the function of UBE2T in BCSCs.Conclusion:UBE2T plays a role in BCSCs through mTOR pathway and may suggest a novel therapeutic strategy for breast cancer.

Clear cell sarcoma of the pancreas,an unusual cancer with unusual metastatic site or unusual primary site?

Clear cell sarcoma(CCS)is a type of malignant tumor that can arise from tendons and aponeuroses.This malignant proliferation of cells with melanocytic lineage normally occurs in young patients,and it is normally identified in extremities.However,different sites including gastrointestinal organs are also described.Due difficulties in the molecular and histopathology evaluation,the diagnosis is often confused with malignant melanoma.Most cases are treated with surgical resection,but overall,the prognosis is poor.In this editorial,we will discuss a very interesting case of CCS identified in the pancreas.We will discuss the literature and controversies in the management of this type of cancer.Furthermore,we will address molecular strategies to be incorporated in those cases to better understand the primary location of the tumor.Finally,future perspectives of the field and new strategies of treatment will be described.

Efficacy of chemotherapy containing bevacizumab in patients with metastatic colorectal cancer according to programmed cell death ligand 1

BACKGROUND Bevacizumab,an anti-vascular endothelial growth factor(VEGF)monoclonal antibody,inhibits angiogenesis and reduces tumor growth.Serum VEGF-C,lactate dehydrogenase,and inflammatory markers have been reported as predictive markers related to bevacizumab treatment.Programmed cell death ligand 1(PD-L1)could act upon VEGF receptor 2 to induce cancer cell angiogenesis and metastasis.AIM To investigate the efficacy of bevacizumab-containing chemotherapy in patients with metastatic colorectal cancer(CRC)according to the expression of PD-L1.METHODS This analysis included CRC patients who received bevacizumab plus FOLFOX or FOLFIRI as first-line therapy between June 24,2014 and February 28,2022,at Samsung Medical Center(Seoul,South Korea).Analysis of patient data included evaluation of PD-L1 expression by the combined positive score(CPS).We analyzed the efficacy of bevacizumab according to PD-L1 expression status in patients with CRC.RESULTS A total of 124 patients was included in this analysis.Almost all patients were treated with bevacizumab plus FOLFIRI or FOLFOX as the first-line chemotherapy.While 77%of patients received FOLFOX,23%received FOLFIRI as backbone first-line chemotherapy.The numbers of patients with a PD-L1 CPS of 1 or more,5 or more,or 10 or more were 105(85%),64(52%),and 32(26%),respectively.The results showed no significant difference in progression-free survival(PFS)and overall survival(OS)with bevacizumab treatment between patients with PDL1 CPS less than 1 and those with PD-L1 CPS of 1 or more(PD-L1<1%vs PD-L1≥1%;PFS:P=0.93,OS:P=0.33),between patients with PD-L1 CPS less than 5 and of 5 or more(PD-L1<5%vs PD-L1≥5%;PFS:P=0.409,OS:P=0.746),and between patients with PD-L1 CPS less than 10 and of 10 or more(PD-L1<10%vs PD-L1≥10%;PFS:P=0.529,OS:P=0.568).CONCLUSION Chemotherapy containing bevacizumab can be considered as first-line therapy in metastatic CRC irrespective of PD-L1 expression.

Prostaglandin D2 regulation of autophagy affects stemness of gastric cancer stem cells

Objective:To explore the effect and mechanism of prostaglandins D2(PGD2)on the stemness of gastric cancer stem cells(GCSCs).Methods:7901-GCSCs were enriched by serum-free culture method;then the positivity rate of CD44,a stemness marker,was detected by flow cytometry in serum-free cultured 7901-GCSCs;the sphere-forming ability was detected by the sphere-forming assay after stimulation with different concentrations of PGD2(2.5,5,10)μg/mL,and the expression of stemness-related indicators(OCT4,CD44)and autophagyrelated proteins(LC3,Beclin-1)after PGD2 stimulation was detected by the western blot assay in different concentrations.The expression of stemness-related indexes(OCT4,CD44)and autophagy-related proteins(LC3,Beclin-1)were detected by Western blot assay after stimulation with different concentrations of PGD2.The expression of autophagy-related proteins after stimulation with different concentrations of CQ(2.5,5,10)μM was detected by Western blot experiment.The protein expression of autophagy-related proteins(LC3,Beclin-1)and stemness-related indexes(OCT4,CD44)was detected by Western blot experiment after PGD2 as well as PGD2+CQ treatment.Results:Flow cytometry results showed that the expression of CD44 positivity was increased in serum-free cultured 7901-GCSCs compared with gastric cancer cells SGC-7901(P<0.05),which fulfilled the needs of subsequent experiments.The results of stem cell spheroid formation assay showed that the spheroid formation ability of 7901-GCSCs in the PGD2 group was significantly weakened compared with that of the DMSO group(P<0.05).Western blot results showed that the protein expression of stemness-related indexes(OCT4,CD44)was down-regulated in the 7901-GCSCs in the PGD2 group compared with that of the DMSO group(P<0.05),and the expression of autophagy-related proteins(LC3,Beclin-1)expression increased(P<0.05).Compared with the DMSO group,the expression of autophagy-related proteins(LC3,Beclin-1)was decreased in the CQ group(P<0.05).Western blot results also showed that the expression of cellular autophagy-related proteins and stemness-related indexes in the PGD2+CQ group was not significantly changed compared with that of the DMSO group(ns:the difference was not significant),suggesting that the CQ could block the effect of PGD2 on the expression of stemness markers in 7901-GCSCs.7901-GCSCs stemness inhibition.Conclusion:PGD2 may affect the stemness of 7901-GCSCs by regulating autophagy.

Limonin inhibits the stemness of cancer stem-like cells derived from colorectal carcinoma cells potentially via blocking STAT3 signaling

BACKGROUND Limonin is one of the most abundant active ingredients of Tetradium ruticarpum.It exerts antitumor effects on several kinds of cancer cells.However,whether limonin exerts antitumor effects on colorectal cancer(CRC)cells and cancer stem-like cells(CSCs),a subpopulation responsible for a poor prognosis,is unclear.AIM To evaluate the effects of limonin on CSCs derived from CRC cells.METHODS CSCs were collected by culturing CRC cells in serum-free medium.The cytotoxicity of limonin against CSCs and parental cells(PCs)was determined by cholecystokinin octapeptide-8 assay.The effects of limonin on stemness were detected by measuring stemness hallmarks and sphere formation ability.RESULTS As expected,limonin exerted inhibitory effects on CRC cell behaviors,including cell proliferation,migration,invasion,colony formation and tumor formation in soft agar.A relatively low concentration of limonin decreased the expression stemness hallmarks,including Nanog andβ-catenin,the proportion of aldehyde dehydrogenase 1-positive CSCs,and the sphere formation rate,indicating that limonin inhibits stemness without presenting cytotoxicity.Additionally,limonin treatment inhibited invasion and tumor formation in soft agar and in nude mice.Moreover,limonin treatment significantly inhibited the phosphorylation of STAT3 at Y705 but not S727 and did not affect total STAT3 expression.Inhibition of Nanog andβ-catenin expression and sphere formation by limonin was obviously reversed by pretreatment with 2μmol/L colievlin.CONCLUSION Taken together,these results indicate that limonin is a promising compound that targets CSCs and could be used to combat CRC recurrence and metastasis.

Exploring the Pivotal Association of AI in Cancer Stem Cells Detection and Treatment

Cancer stem cells(CSCs),or tumor-initiating cells(TICs),are cancerous cell subpopulations that remain while tumor cells propagate as a unique subset and exhibit multiple applications in several diseases.They are responsible for cancer cell initiation,development,metastasis,proliferation,and recurrence due to their self-renewal and differentiation abilities in many kinds of cells.Artificial intelligence(AI)has gained significant attention because of its vast applications in various fields including agriculture,healthcare,transportation,and robotics,particularly in detecting human diseases such as cancer.The division and metastasis of cancerous cells are not easy to identify at early stages due to their uncontrolled situations.It has provided some real-time pictures of cancer progression and relapse.The purpose of this review paper is to explore new investigations into the role of AI in cancer stem cell progression and metastasis and in regenerative medicines.It describes the association of machine learning and AI with CSCs along with its numerous applications from cancer diagnosis to therapy.This review has also provided key challenges and future directions of AI in cancer stem cell research diagnosis and therapeutic approach.

Advancing Cancer Stem Cell-Targeted Therapeutic Applications

Cancer stem cells(CSCs),first identified in blood cancers,are increasingly recognized as significant biomarkers and targets in tumor therapy due to their metastatic potential and role in cancer recurrence.Recent research has demonstrated the dedication of scientists in targeting CSCs to explore novel therapeutic strategies.Many types of cancer exhibit metastasis,heterogeneity,and resistance to treatment,all of which are influenced by CSCs.These cells utilize various transcription factors and signaling pathways to carry out these functions.By identifying and understanding these pathways,new therapeutic breakthroughs can be achieved.Thus,targeting cancer stem cells holds great potential and importance in cancer treatment.Moreover,CSCs offer promising avenues for treating otherwise incurable diseases.However,targeting CSCs presents challenges such as immunological rejection and disease recurrence.Advancing research into CSCs may reveal new insights in the fight against cancer and ultimately improve human health.This review explores the roles of CSCs in cancer development and treatment,aiming to uncover new therapeutic approaches.

Nasal metastases from renal cell carcinoma are associated with Memorial Sloan-Kettering Cancer Center poor-prognosis classification

Unusual sites of metastases are recognized in patients with renal cell carcinoma (RCC). However, the prognostic implications of these sites are not well understood. We used the Memorial Sloan-Kettering Cancer Center (MSKCC) risk classification for metastatic RCC to evaluate 912 consecutive patients with RCC managed at the Singapore General Hospital between 1990 and 2009. Among these patients, 301 had metastases either at diagnosis or during the course of illness. Nasal metastases, all arising from clear cell RCC, were identified histologically in 4 patients (1.3% of those with metastasis). All 4 patients were classified as MSKCC poor prognosis by current risk criteria. Nasal metastases were significantly associated with lung and bone metastases. The frequency of nasal metastases in patients with metastatic RCC is about 1%, occurring predominantly in patients with clear cell RCC. Nasal metastases are associated with poor prognosis as estimated by the MSKCC risk classification, with attendant implications for selection of targeted therapy, and are usually associated with multi-organ dissemination, including concurrent lung and bone involvement.

Relation between Neurotransmitters and NK Cells in Adrenal and Breast Cancer

Purpose: Data on microarray gene expression The Gene Expression Omnibus (GEO) provided information on gene expression. Transcription GEO provided two profiles of human NK cells from breast and adrenal tumors (GSE179509 and GSE143383). Data processing and normalization The Dseq2 tool in the R programming language was used to standardize the raw data from GEO. The following analyses were carried out: fold change and P-value analysis, volcano plot, network analysis, GEPIA, and David pathway analysis. In this paper, using Venny software, we discovered 2 genes that are shared by neurotransmitters and NK cells in breast cancer and adrenal cancer. Between these genes and the pathways, they are a part of, we discovered a network. Pathway analysis revealed that these genes are mostly linked to the neurotransmitter and apoptotic pathways. In breast and adrenal tumors, the genes HRH1 and GABRD were discovered to be connected to NK cells. In response to breast and adrenal tumors, almost all of these genes are effective. It is thus postulated that the diagnosis of breast and adrenal cancer may be affected by the up-or down-regulation of these genes. Methods: Microarray gene expression data gene expression data was obtained from the Gene Expression Omnibus (GEO) Transcription 2 profile data of human NK cells from human breast and adrenal cancers were obtained from GEO (GSE179509 and GSE143383). Processing and normalization of data the raw data from GEO were normalized with the Dseq2 package in the R software. Fold change and P value analysis, Volcano plot, network analysis, GEPIA, and David pathway analysis were performed. Results: In this article, we found genes common to neurotransmitters with NK cells in adrenal cancer and breast cancer with Venny program, resulting in 2 genes. We identified a network between these genes and pathways they belong to. Pathway analysis showed that these genes are mostly associated with apoptosis and neurotransmitters pathway. Conclusion: HRH1 and GABRD genes were found to be associated with NK cells in breast and adrenal cancers. Almost all these genes are effective in response to breast and adrenal cancers. Therefore, it is hypothesized that downregulation or upregulation of these genes may affect breast and adrenal cancer diagnosis.

Imbalance of Circulating Follicular Regulatory and Follicular Helper T Cell Subpopulations Is Associated with Disease Progression and Serum CYFRA 21-1 Levels in Patients with Non-small Cell Lung Cancer

Objective This study aimed to investigate the changes of follicular helper T(TFH)and follicular regulatory T(TFR)cell subpopulations in patients with non-small cell lung cancer(NSCLC)and their significance.Methods Peripheral blood was collected from 58 NSCLC patients at different stages and 38 healthy controls.Flow cytometry was used to detect TFH cell subpopulation based on programmed death 1(PD-1)and inducible co-stimulator(ICOS),and TFR cell subpopulation based on cluster determinant 45RA(CD45RA)and forkhead box protein P3(FoxP3).The levels of interleukin-10(IL-10),interleukin-17a(IL-17a),interleukin-21(IL-21),and transforming growth factor-β(TGF-β)in the plasma were measured,and changes in circulating B cell subsets and plasma IgG levels were also analyzed.The correlation between serum cytokeratin fragment antigen 21-1(CYFRA 21-1)levels and TFH,TFR,or B cell subpopulations was further explored.Results The TFR/TFH ratio increased significantly in NSCLC patients.The CD45RA^(+)FoxP3^(int) TFR subsets were increased,with their proportions increasing in stages Ⅱ to Ⅲ and decreasing in stage IV.PD-1^(+)ICOS+TFH cells showed a downward trend with increasing stages.Plasma IL-21 and TGF-β concentrations were increased in NSCLC patients compared with healthy controls.Plasmablasts,plasma IgG levels,and CD45RA^(+)FoxP3^(int) TFR cells showed similar trends.TFH numbers and plasmablasts were positively correlated with CYFRA 21-1 in stages Ⅰ-Ⅲ and negatively correlated with CYFRA 21-1 in stage IV.Conclusion Circulating TFH and TFR cell subpopulations and plasmablasts dynamically change in different stages of NSCLC,which is associated with serum CYFRA 21-1 levels and reflects disease progression.

Ipsilateral retroperitoneal papillary renal cell carcinoma 27 years after simple nephrectomy for a renal abscess:A case report

BACKGROUND Cases of severe inflammatory renal disease and renal cell carcinoma(RCC)that occur simultaneously in the same kidney have been occasionally reported.However,extrarenal RCC that does not originate from the native kidney has rarely been reported.To our knowledge,this is the first reported case of RCC developing in the ipsilateral retroperitoneal space after a simple nephrectomy(SN)for inflammatory renal disease.CASE SUMMARY A 63-year-old woman was referred to our hospital following the incidental discovery of a left retroperitoneal mass without specific symptoms.Her medical history revealed a left SN 27 years ago due to a renal abscess.Magnetic resonance imaging of the abdomen revealed three oval masses in the left retroperitoneum.The masses were successfully excised,and subsequent pathology confirmed papillary RCC.After surgery,the patient remained disease-free for 11 years without adjuvant therapy.CONCLUSION Clinicians should be vigilant of RCC in patients with retroperitoneal masses,especially after SN for inflammatory renal disease.