Study objective: To evaluate the effectiveness of using vascular clips to seal targeted lymphatics in gynecological malignancies for the prevention of postoperative pelvic lymphocele and symptomatic lymphocele after laparoscopic pelvic lymphadenectomy. Design: Retrospective analysis. Setting: Single-center academic hospital. Patients: In total, 217 patients with gynecological malignancies were included. Interventions: Patients were classified into two groups: group 1 (vascular clips were used to seal the targeted lymphatics) and group 2 (electrothermal instruments were used to seal the targeted lymphatics). The patients were followed up 4-6 weeks after surgery to evaluate the incidence of lymphoceles by ultrasound or CT. Symptomatic lymphoceles are defined as those that cause infection, deep vein thrombosis with or without swelling of the extremities, edema (swelling) of the extremities or perineum, hydronephrosis, and/or moderate to severe pain. Measurements and main results: One hundred and thirteen patients were enrolled in group 1, and 104 patients were enrolled in group 2. Lymphoceles were observed in 46 (21.2%) patients. Fewer lymphoceles occurred in group 1 than in group 2 (8 [7.1%] vs. 38 [36.5%], p <.001). The percentage of significantly sized lymphoceles was lower in group 1 than that in group 2 (4 [3.5%] vs. 30 [28.8%], p <.001]. Symptomatic lymphoceles occurred in 18 patients (8.3%), and only one (1.0%) occurred in group 1, while 17 (16.3%) occurred in group 2 (p <.001). A multivariate analysis revealed that vascular clips were the only independent factor for preventing lymphocele (OR = 7.65, 95% CI = [3.30-17.13], p <.001) and symptomatic lymphocele (OR = 22.03, 95% CI = [2.84-170.63], p = .003). Conclusion: The results indicate that the use of vascular clips may be useful for the prevention of the development of lymphocele and symptomatic lymphocele secondary to pelvic lymphadenectomy performed via laparoscopy.

Small cell lung cancer (SCLC) is characterized by rapid development of chemoresistance and poor outcomes. Cyclin-dependent kinase 4/6 inhibitors (CDK4/6is) are widely used in breast cancer and other cancer types. However, the molecular mechanisms of CDK4/6 in SCLC chemoresistance remain poorly understood. Here, Rb1flox/flox, Trp53flox/flox, Ptenflox/flox (RTP) and Rb1flox/flox, Trp53flox/flox, MycLSL/LSL (RPM) spontaneous SCLC mouse models, SCLC cell line-derived xenograft (CDX) models, and SCLC patient-derived xenograft (PDX) models are established to reveal the potential effects of CDK4/6is on SCLC chemoresistance. In this study, it is found that CDK4/6is palbociclib (PD) or ribociclib (LEE) combined with chemotherapeutic drugs significantly inhibit SCLC tumor growth. Mechanistically, CDK4/6is do not function through the classic Retionblastoma1 (RB) dependent axis in SCLC. CDK4/6is induce impair autophagy through the AMBRA1-lysosome signaling pathway. The upregulated AMBRA1 protein expression leads to CDK6 degradation via autophagy,  and the following TFEB and TFE3 nuclear translocation inhibition leading to the lysosome-related genes levels downregulation. Moreover, it is found that the expression of CDK6 is higher in SCLC tumors than in normal tissue and it is associated with the survival and prognosis of SCLC patients. Finally, these findings demonstrate that combining CDK4/6is with chemotherapy treatment may serve as a potential therapeutic option for SCLC patients.

Background The incidence and mortality of cervical cancer remain high in female malignant tumors worldwide. There is still a lack of diagnostic and prognostic markers for cervical carcinoma. This study aimed to screen differentially expressed genes (DEGs) between normal and cervical cancer tissues to identify candidate genes for further research. Methods Uterine cervical specimens were resected from our clinical patients after radical hysterectomy. Three patients’ transcriptomic datasets were built by the next generation sequencing (NGS) results. DEGs were selected through the edgeR and DESeq2 packages in the R environment. Functional enrichment analysis, including GO/DisGeNET/KEGG/Reactome enrichment analysis, was performed. Normal and cervical cancer tissue data from the public databases TCGA and GTEx were collected to compare the expression levels of 10 selected DEGs in tumor and normal tissues. ROC curve and survival analysis were performed to compare the diagnostic and prognostic values of each gene. The expression levels of candidate genes were verified in 15 paired clinical specimens via quantitative real-time polymerase chain reaction. Results There were 875 up-regulated and 1,482 down-regulated genes in cervical cancer samples compared with the paired adjacent normal cervical tissues according to the NGS analysis. The top 10 DEGs included APOD, MASP1, ACKR1, C1QTNF7, SFRP4, HSPB6, GSTM5, IGFBP6, F10 and DCN. GO, DisGeNET and Reactome analyses revealed that the DEGs were related to extracellular matrix and angiogenesis which might influence tumorigenesis. KEGG enrichment showed that PI3K-Akt signaling pathway might be involved in cervical cancer tumorigenesis and progression. The expression levels of selected genes were decreased in tumors in both the public database and our experimental clinical specimens. All the candidate genes showed excellent diagnostic value, and the AUC values exceeded 0.90. Additionally, APOD, ACKR1 and SFRP4 expression levels could help predict the prognosis of patients with cervical cancer. Conclusions In this study, we selected the top 10 DEGs which were down-regulated in cervical cancer tissues. All of them had dramatically diagnostic value. APOD, ACKR1 and SFRP4 were associated with the survivals of cervical cancer. C1QTNF7, HSPB6, GSTM5, IGFBP6 and F10 were first reported to be candidate genes of cervical carcinoma.

In the field of gynecology, the selection of surgical approach should be carefully considered based on individual patient characteristics. The development of minimally invasive surgery has greatly impacted gynecological surgeries, and the number of robotic surgeries has been increasing yearly. Robotic surgery offers many benefits. The use of robotic surgery techniques in the multidisciplinary teamwork (MDT) surgery can make surgical operations more convenient, and has resulted in many successful cases, such as in advanced ovarian cancer and deep infiltrating endometriosis surgeries. Single-port robotic surgery has its operational limitations but shows potential for development. The use of remote robotic surgery is being explored. The support of national policies in China has contributed to the development of domestically produced surgical robots. The future of surgical robots lies in technological advancements, market dominance, and the integration of intelligence and miniaturization. Our goal is to disseminate high-quality medical resources and provide services to a larger number of patients.

We evaluated the characteristics of high-risk human papillomavirus (Hr-HPV) infection in different grades of vaginal intraepithelial neoplasia (VaIN). 7469 participants were involved in this study, of which 601 were diagnosed with VaIN, including single vaginal intraepithelial neoplasia (s-VaIN, n = 369) and VaIN+CIN (n = 232), 3414 with single cervical intraepithelial neoplasia (s-CIN), 3446 with cervicitis or vaginitis and 8 with vaginal cancer. We got those results. First, the most popular HPV genotypes in VaIN were HPV16, 52, 58, 51, and 56. Second, our study showed that higher parity and older age were risk factors for VaIN3 (p < 0.005). Third, the median Hr-HPV load of VaIN+CIN (725) was higher than that of s-CIN (258) (p = 0.027), and the median Hr-HPV load increased with the grade of VaIN. In addition, the risk of VaIN3 was higher in women with single HPV16 infections (p = 0.01), but those with multiple HPV16 infections faced a higher risk of s-VaIN (p = 0.003) or VaIN+CIN (p = 0.01). Our results suggested that women with higher gravidity and parity, higher Hr-HPV load, multiple HPV16 infections, and perimenopause or menopause status faced a higher risk for VaIN, while those with higher parity, single HPV16 infections, and menopause status are more prone to VaIN3.

This study evaluated the basic immune status of cervical cancer and the influences of immunotherapy on the immune microenvironment, and analyzed the correlation between changes in the immune microenvironment and prognosis. We retrospectively analyzed the treatment status of 8 patients with advanced recurrent cervical cancer treated with PD-1 inhibitors and detected the tumor-infiltrating immune markers (CD3, CD4, CD8, CD20, CD56, CD68, PD-1, and PD-L1) by immunohistochemistry. All patients showed good tolerance during the treatment. Complete response (CR), partial response (PR) and stable disease (SD) was observed in 3, 2, and 3 patients, respectively. Immunohistochemical analysis showed immunotherapy resulted in increased infiltration of T lymphocytes, natural killer cells, and B cells, especially among those who responded well. The expression of B cells in 4 of the 5 patients with clinical benefit was relatively high, and the expression of PD-L1 in these 5 patients showed a combined positive score > 3. PD-L1 expression increased significantly after treatment with PD-1 inhibitors. Second-generation sequencing showed that the tumor mutation burden of two patients with adenocarcinoma was high, and after immunotherapy, one case recurred after cure and the other remained stable. PR was also observed in squamous cell carcinoma patients with dMMR (p.R2165H/c.6494G > A) and PIK3CA (p.E545K(E9)) mutations. The expression of B cells and PD-L1 has certain predictive effect for the efficacy of immunotherapy in cervical cancer under the condition of high or low T cell infiltration, and can inform treatment decision-making for patients with advanced cervical cancer.

Chemoresistance is the crux of clinical treatment failure of small-cell lung cancer (SCLC). Cancer stem cells play a critical role in therapeutic resistance of malignant tumors. Studies have shown that the role of erythropoietin-producing hepatocellular A2 (EphA2) in tumors is complex. This study aimed to test the hypothesis that ligand-independent activation of EphA2 modulates chemoresistance by enhancing stemness in SCLC. We verified that EphA2 was activated in chemoresistance sublines in a ligand-independent manner rather than a ligand-dependent manner. Ligand-independent EphA2 enhanced the expression of stemness-associated biomarkers (CD44, Myc, and SOX2), accelerated epithelial-mesenchymal transition (EMT) and reinforced self-renewal to drive the chemoresistance of SCLC, while the P817H mutant EphA2 neutralized intrinsic function. Co-immunoprecipitation (co-IP) and GST-pull down experiments were conducted to verify that EphA2 directly interacted with PRMT1. Moreover, EphA2 increased the expression and activity of PRMT1. Whereafter, PRMT1 interacted with and methylated SOX2 to induce stemness and chemoresistance in SCLC. Pharmacological inhibition of EphA2 showed a synergistic anti-tumor effect with chemotherapy in preclinical models, including patient-derived xenograft (PDX) models. These findings highlight, for the first time, that the EphA2/PRMT1/SOX2 pathway induces chemoresistance in SCLC by promoting stemness. EphA2 is a potential therapeutic target in SCLC treatment.

Background:Lung cancer is the most morbid and fatal cancer in the world, and nearly 85% of lung cancer is non-small cell lung cancer (NSCLC). Besides traditional chemotherapies, molecular targeted therapies and immunotherapies are increasing rapidly, but the treatment is still unsatisfactory. The study is to identify a new diagnostic and prognostic biomarker. Methods:Data including mRNA expression and clinical information of lung adenocarcinoma (LUAD) patients were downloaded from The Cancer Genome Atlas (TCGA) database. Receiver operating characteristic (ROC) curve was constructed to assess the diagnostic value of syntrophin-γ2 (SNTG2) expression and Kaplan-Meier (KM) survival curves were used to compare the survival disparities. The protein-protein interaction (PPI) network was analysed by Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the connections between SNTG2 and immune cell infiltration were found with Tumor Immunoassay Resource (TIMER). Genetic mutation in SNTG2 and its association with overall survival (OS) were evaluated by cBioPortal. The relationship between SNTG2 and methylation and its association with overall survival were evaluated by MethSurv. Chi square and Mann-Whitney tests were used for statistical analyses. Xiantao Academic Online Website was used for online analysis. Results:Our results revealed that SNTG2 mRNA expression was lower in LUAD tissues than in both adjacent and non-adjacent normal tissues and low SNTG2 mRNA expression was verified to be correlated with histological grade, clinical stage, first therapy outcome and poor overall survival of LUAD. Next, ROC curve revealed diagnostic and prognostic value of SNTG2 for LUAD patients. Moreover, SNTG2 presented correlation with immune cell infiltration and immune checkpoints. Then, we revealed CC chemokine ligand 14 (CCL14), a co-expression gene with SNTG2, which has consistent influence with SNTG2. Furthermore, hypomethylation was found to be associated with high SNTG2 expression. Conclusion:We revealed a potential diagnostic and prognostic indicator in LUAD and analyzed its influence on immunotherapy.

Background:Small cell lung cancer (SCLC), the most malignant of all the lung cancer subtypes, is characterized by drug resistance. This study sought to explore the key genes and pathways associated with the chemoresistance of SCLC.Methods:The drug sensitivity of chemosensitive and chemoresistance SCLC cell lines was measured by Cell Counting Kit-8 assays. The total RNA from chemosensitive cell line H69 and chemoresistance cell line H69AR cells was extracted and subjected to messenger RNA (mRNA) and long non-coding RNA (lncRNA) microarray analyses. The differentially expressed genes (DEGs) and the differentially expressed lncRNAs (DELs) were screened out with a threshold of a |log fold change | ≥1 and an adjusted P value <0.05. A protein-protein interaction network was constructed, and hub genes were screened out. A lncRNA-mRNA co-expression network was also constructed. Gene Ontology and Kyoto Encyclopedia of Genes, Genomes enrichment analyses and Cis-regulatory element analyses were conducted on the DEGs and the top 10 upregulated DEL-co-expressed DEGs. The expression of the key genes was further analyzed in the GSE149507 data set and validated in H69/H69AR and H446/H446DDP cells by quantitative polymerase chain reaction assays.Results:The microarray results showed that a total of 609 mRNAs and 394 lncRNAs were differentially expressed in the chemoresistant SCLC cells. The mammalian target of rapamycin (mTOR) signaling pathway was enriched among the DEGs, the top 10 upregulated DEL-co-expressed DEGs, and the NCRNA00173-co-expressed DEGs, which included IGF1, INS, WNT6, WNT11, WNT2B, and SESN2. IGF1, WNT2B, and SESN2 were downregulated, and WNT11 was upregulated in the SCLC tumor tissues in the GSE149507 data set. Further, IGF1, WNT6, WNT11, and WNT2B were lowlier expressed and SESN2 and NCRNA00173 were more highly expressed in the chemoresistant cells than sensitive cells.Conclusions:The top 10 upregulated DELs containing NCRNA00173 may be involved in the regulation of drug resistance in SCLC. These DELs may regulate the genes related to the mTOR signaling pathway. These genes may also be biomarkers and potential targets for the treatment of SCLC.

The aim of the present study is to investigate whether 4SC-202, a selective class I histone deacetylase inhibitor (HDACi), plays an anti-tumor role in cervical cancer (CC) by targeting prolactin receptor (PRLR). CCK-8 and colony formation assays were used to evaluate the effects of 4SC-202 on the proliferation of CC cells in vitro. Effects of 4SC-202 on the cell cycle distribution and apoptosis in SiHa cells were determined by flow cytometry and western blotting, respectively. Immunofluorescence, western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to detect the activities of PRLR-related pathways and PRLR expression in CC cells. A xenograft tumor model in nude mice was established to examine effects of 4SC-202 on the tumor growth, apoptosis and PRLR-related pathways in vivo. The biochemical analyzer and H&E staining were used to detect the serum biochemical indexes and organ toxicity. 4SC-202 inhibited the proliferation of CC cells (SiHa, HeLa, and CaSki) in vitro in a time- and dose-dependent manner. SiHa cells were treated with 1 or 5 µM 4SC-202 for 72 h and then subjected to various functional assays. The assays showed that 4SC-202 significantly induced G2/M phase arrest and apoptosis, while inhibiting the activities of PRLR-related pathways and PRLR expression. In addition, 4SC-202 reduced tumor growth and induced apoptosis in vivo. 4SC-202 down-regulated the expression of PRLR and activities of PRLR-related pathways in the mouse model, displayed no effects on serum biochemical indicators and caused no toxicity to mouse organs. This finding suggests that 4SC-202 may serve as a novel therapeutic agent for CC.

Background: The mortality rate of ovarian cancer (OC) ranks first among female genital tract malignant tumors, which seriously threatens women's life and health. Because of its insidious onset and poor prognosis, it has become a thorny problem in the clinic, especially for patients with platinum-resistant recurrent ovarian cancer (PROC). In recent years, the medical treatment of OC has made gratifying results, bringing hope to the patients.Case Description: A 54-year-old OC patient who has failed previous neoadjuvant chemotherapy, cytoreductive surgery, and postoperative chemotherapy was diagnosed with PROC. Then she received combination treatment of fuzuloparib (100mg PO BID), apatinib (250mg PO QD), and camrelizumab (200mg IV Q3W) for every 3-week cycle in a Phase II study for PROC patients. In the phase II study, her condition stabilized, responded well to treatment with a sharp decrease by 91.14% of target lesions and disappearances of non-target lesions, and continued to receive regular treatment with progression-free survival exceeding 15 months and no serious adverse events.Conclusion: The present case proves PROC patients might have a sustained response to triplet combination with camrelizumab, combined with fuzuloparib and apatinib.

Lung cancer is one of the most common malignant tumors and has the highest incidence and mortality rates of all tumors type in the world [1]. Lung cancer includes small cell lung cancer (SCLC) and non–small cell lung cancer (NSCLC), and SCLC accounts for approximately 13%-15% of all lung cancer cases [2,3]. SCLC is the most aggressive type of lung cancer. Although some SCLC patients initially have a good response to chemotherapy drugs, they will develop chemotherapy drug resistance eventually. The poor prognosis of SCLC patients is largely related to chemotherapy drug resistance [4,5]. Therefore, a deep understanding of the mechanisms of chemotherapy drug resistance is urgently needed to develop the effective therapeutic strategies of SCLC patients. The human transcriptome consists of 2% protein-coding RNAs and 98% non–protein-coding RNAs (ncRNAs) [6]. ncRNA are divided into short ncRNA and long-ncRNA (lncRNAs) according to the size. LncRNAs are a class of transcripts that are longer than 200 nucleotides in length with no ability to encode proteins [7]. Extensive studies have demonstrated that lncRNAs are involved in various biological processes, such as regulating cell proliferation, cell metastasis, cell differentiation and apoptosis [8-10]. With the further understanding of lncRNAs, it is reasonable to believe that the abnormal expression of lncRNAs is related to the occurrence and development of malignant tumors includ-

子宫内膜癌(EC)是女性生殖系统常见的恶性肿瘤,在全球范围内其发病率逐年升高.多数EC患者经手术治疗后预后较好,但对于晚期或复发、转移性EC来说,传统的治疗手段效果有限,患者预后较差.1983年Bokhman根据流行病学、内分泌及预后特点将EC分为I型(雌激素依赖型)和II型(非雌激素依赖型),然而在临床应用中该分型手段具有一定局限性.随着分子生物学及基因测序技术的发展,EC的研究深入分子水平.2013年美国TCGA第一次归纳提出EC的4种分子分型,由于其费用高昂、技术复杂,临床不易获得.2015年Talhouk等提出简易替代分型并在后续的研究中将其命名为ProMisE分子风险分型,包括:POLE突变型、MSI高突变型、p53野生型、p53突变型.EC分子分型的研究具有重要的临床指导意义.本文就EC传统分型到分子分型的转变做一回顾,并对分子分型与临床相关的研究做一总结与分析.EC分子分型的不断完善有助于实现临床诊疗中的精准化、规范化、个体化,在精准医学背景下有重要价值.

Background: Lung cancer has always been the most prevalent cancer. Lung adenocarcinoma (LUAD) is the most common lung cancer subtype and has a high tumor mutation rate. In addition to KRAS, EGFR, ALK, HER2, ROS1, and BRAF, which are known to have high mutation rates, we discovered some new mutated genes, such as catenin alpha-2 (CTNNA2), in LUAD patients treated with immune checkpoint inhibitors (ICIs). These mutant genes are potential therapeutic targets for LUAD. Methods: We analyzed a cohort of LUAD patients with somatic mutation and survival data in the Cancer Genome Atlas (TCGA) database and a cohort of LUAD patients receiving immune checkpoint inhibitors with clinical data and whole-exome sequencing (WES) mutation data to evaluate the role of CTNNA2 gene mutation in LUAD. In addition, CIBERSORT was used to analyze the immune characteristics of CTNNA2 wild-type patients and CTNNA2 mutant-type patients, and gene set enrichment analysis (GSEA) was employed for pathway enrichment analysis. The results were verified by downloading data regarding the drug sensitivity of LUAD cell lines from the Genomics of Drug Sensitivity in Cancer (GDSC) database. Results: We found that CTNNA2 mutation was associated with longer overall survival (OS) in LUAD patients. Analysis of the cohort from the Cancer Genome Atlas showed that patients with CTNNA2 mutation had more tumor neoantigens and a greater tumor mutation burden (TMB). Through further analysis of the tumor immune microenvironment, we found that in LUAD patients with CTNNA2 mutations, the gene expression levels of chemokine C-X-C motif chemokine 9 (CXCL9) and granzyme B (GZMB) were elevated, and the gene expression level of inhibitory receptor killer cell immunoglobulin-like receptor 2DL1 (KIR2DL1) was significantly reduced. These alterations might affect gene expression in macrophages, NK cells, and mast cell markers. In addition, LUAD patients with CTNNA2 mutation had a significantly increased number of mutations in DNA damage response (DDR) genes. The drug susceptibility results and gene set enrichment analysis showed that after CTNNA2 mutation occurred, changes were found in the DNA damage response pathway, the phosphoinositide 3-kinase (PI3K) pathway and others, indicating that CTNNA2 mutation can regulate the activation of PI3K and DDR pathways. Conclusion: Our findings provide novel insights into the underlying pathogenesis of LUAD. CTNNA2 mutation can change the immune microenvironment, thereby improving patient prognosis. The results also suggest that CTNNA2 may become a new biomarker and therapeutic target for LUAD in the future.

目的 探讨经机器人辅助腹腔镜下阴道骶骨固定术治疗盆腔器官脱垂的效果及安全性.方法 收集2013年1月至2018年12月于解放军总医院第一医学中心妇产科采用经机器人辅助腹腔镜下阴道骶骨固定术治疗盆腔器官脱垂13例患者的临床资料.比较手术前后盆腔器官脱垂治疗效果及安全性,盆腔器官脱垂术后患者采用整体印象改善评分量表(PGI-I)评估主观满意度.结果 13例患者中,平均术中出血量(86.9±98.3) ml(20～300 ml),手术时间(143.5±47.3) min (60～240 min),平均住院时间(10.4±2.1)d(8～16d),平均随访时间(40.8±22.0)个月(6～72个月).脱垂客观治愈率85％,主观治愈率100％,PGI-I评分非常好者9例(9/13),很好者4例(4/13).网片暴露4例(4/13),其中暴露直径小于1 cm且无症状者3例,暴露直径1～2 cm有症状者1例,暴露发生时间均在术后2～12个月,暴露位置均位于阴道缝合范围内.结论 机器人辅助腹腔镜下阴道骶骨固定术治疗盆腔器官脱垂出血量少,住院时间短,术后效果良好,是治疗盆腔器官脱垂可选择的术式之一.

Purpose Drug resistance is one of the main causes of chemotherapy failure in patients with small cell lung cancer (SCLC), and extensive biological studies into chemotherapy drug resistance are required. Materials and Methods In this study, we performed lncRNA microarray, in vitro functional assays, in vivo models and cDNA microarray to evaluate the impact of lncRNA in SCLC chemoresistance. Results The results showed that KCNQ1OT1 expression was upregulated in SCLC tissues and was a poor prognostic factor for patients with SCLC. Knockdown of KCNQ1OT1 inhibited cell proliferation, migration, chemoresistance and promoted apoptosis of SCLC cells. Mechanistic investigation showed that KCNQ1OT1 can activate transforming growth factor-β1 mediated epithelial-to-mesenchymal transition in SCLC cells. Conclusion Taken together, our study revealed the role of KCNQ1OT1 in the progression and chemoresistance of SCLC, and suggested KCNQ1OT1 as a potential diagnostic and prognostic biomarker in SCLC clinical management.

Objectives There is currently no consensus on the prognostic significance of the histological subtype of nasopharyngeal carcinoma (NPC). The aim of the current study was to evaluate the impact of histological subtype on survival in NPC patients based on the Surveillance, Epidemiology, and End Results (SEER) Program. Methods Patients with NPC were identified within the SEER database (2004-2015). The effects of histological subtype on cause-specific survival (CSS) in NPC patients were evaluated using univariate and multivariate Cox regression analyses. Subgroup analysis according to histological subtype in NPC patients was carried out by 1:1 propensity score matching (PSM). Results A total of 4085 NPC patients were selected from the SEER database, including 1929 with keratinizing squamous cell carcinoma (KSCC), 2203 with nonkeratinizing carcinoma (NKC), and 53 with basaloid squamous cell carcinoma (BSCC). The 3-year and 5-year CSS rates were 61.76% and 55.07% for KSCC patients, 79.57% and 72.09% for NKC patients, and 77.55% and 74.03% for BSCC patients, respectively. Multivariate analysis identified sex, age, marital status, race, T stage, N stage, M stage, radiotherapy, chemotherapy, and histological subtype as significant prognostic factors for CSS in NPC patients. KSCC was found to be associated with worse CSS than NKC on Kaplan-Meier analysis and subgroup analysis after 1:1 PSM. Conclusions Histological subtype determines the long-term survival outcomes of patients with NPC. Moreover, the NKC subtype has the best prognosis, while the KSCC subtype has the worst prognosis. Level of Evidence NA Laryngoscope, 130:E83-E88, 2020

Objective: The aim of this study was to explore the patterns of retropharyngeal lymph node (RLN) metastasis in nasopharyngeal carcinoma (NPC) and their impact on the clinical target volume (CTV) delineation in radiotherapy. Methods: A total of 190 patients with untreated, nonmetastatic NPC received MRI scans of the nasopharynx and neck before treatment. The imaging characteristics of RLN metastasis and their relationships with the staging system were analysed. Results: A total of 121 patients developed RLN metastasis. The incidence rate of RLN metastasis was 63.7%. The RLN metastases of the 121 patients were distributed evenly in the lateral group, and no lymph node metastasis was observed in the medial group. Among the 121 patients, there were 66 cases of unilateral metastasis (54.5%) and 55 cases of bilateral metastasis (45.5%). The central position of the lymph nodes was mainly distributed in the C1 vertebra region. The differences in the RLN metastasis rate between different T stages, N stages and clinical stages were statistically significant (all P<0.01). Conclusion: Medial RLN metastasis is rarely observed in NPC and therefore does not require routine prophylactic irradiation with intensity-modulated radiation therapy (IMRT). This is an important issue for future research.