Features and clinical significance of tertiary lymphoid structure in cutaneous squamous cell carcinoma.

BACKGROUND: Tertiary lymphoid structure (TLS) plays an important role in antitumour immunity, largely reflecting the prognosis. However, its clinical implication in cutaneous squamous cell carcinoma (cSCC) remains unknown. OBJECTIVES: To explore the features of TLS in cSCC and its association with clinicopathological characteristics. METHODS: Two independent RNA-seq data of cSCC were used to investigate the tumour immune microenvironment, as well as TLS-related chemokines and cytokines. The density and location of TLSs were assessed in a total of 82 cSCC patients, and the clinicopathologic association was examined. RESULTS: Bioinformatics analysis showed that a large amount of immune cell infiltration and significant up-regulation of TLS-related chemokines were observed in cSCC. Histologically, TLSs appeared as highly organized structures in 72 (87.8%) cases with different levels of density and maturation, among which 14 cases were in low-density group and 58 cases were in high-density group. Clinically, the presence of TLS was prominently associated with better degree of histopathological grades and higher level of sun exposure. Furthermore, the presence of intratumoral TLS was associated with lower lymphovascular invasion. CONCLUSIONS: TLS is highly organized in cSCC, and the presence of TLS is a positive prognostic factor for cSCC, which will provide a theoretical basis for the future diagnostic and therapeutic value in cSCC.

[Characteristics of N6-methyladenosine modification patterns in t(8;21) acute myeloid leukemia].

OBJECTIVE: To investigate the relationship between AML1-ETO (AE) fusion gene and intracellular N6-methyladenosine (m6A) modification pattern in t(8;21) acute myeloid leukemia (AML). METHODS: RNA m6A sequencing was performed in SKNO-1 and AE knockdown SKNO-1 (SKNO-1 siAE) cells using RNA-protein co-immunoprecipitation and high-throughput sequencing (methylated RNA immunoprecipitation sequencing, MeRIP-Seq) to analyze the changes in m6A modification of the entire transcriptome. Transcriptome sequencing (RNA-seq) was performed using high-throughput sequencing. The differentially modified mRNAs were further functionally annotated by Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The changes in m6A-related enzyme expressions were detected using real-time PCR. RESULTS: A total of 26 441 genes were identified in AE knockdown AML cells and AE-expressing cells, containing 72 036 m6A peaks. AE knockdown caused a reduction of the number of intracellular m6A peaks from 37 042 to 34 994, among which 1278 m6A peaks were significantly elevated and 1225 were significantly decreased; 1316 genes with newly emerged m6A modification were detected and 1830 genes lost m6A modification after AE knockdown. The differential peaks were mainly enriched in pathways involving cancer and human T-lymphocytic leukemia virus I. RNA-seq results showed that 2483 genes were up-regulated and 3913 genes were down-regulated after AE knockdown. The combined analysis of MeRIP-Seq and RNA-Seq results revealed relatively high expression levels of m6A-modified genes as compared with the genes without m6A modification (SKNO-1: 0.6116±1.263 vs 2.010±1.655, P < 0.0001; SKNO-1 siAE: 0.5528±1.257 vs 2.067±1.686, P < 0.0001). The m6A modified genes located in the 3'UTR or 5 'UTR had significantly higher expression levels than those located in exonic regions (SKNO-1: 2.177± 1.633 vs 1.333 ± 1.470 vs 2.449 ± 1.651, P < 0.0001; SKNO-1 siAE: 2.304 ± 1.671 vs 1.336 ± 1.522 vs 2.394 ± 1.649, P < 0.05). Analysis of RNA-seq data identified 3 m6A-related enzymes that showed significantly elevated mRNA expression after AE knockdown, namely WTAP, METTL14, and ALKBH5 (P < 0.05), but the results of real-time PCR showed that the expressions of WTAP and ALKBH5 were significantly increased while the expression of METTL14 was lowered after AE knockdown (P < 0.05). CONCLUSION: AE knockdown results in differential expressions of m6A-associated enzymes, suggesting that the AE fusion gene regulates the expression of one or more m6A-associated enzymes to control cellular methylation levels.

Successful use of tofacitinib in epidermolysis bullosa pruriginosa.

This case report describes 26-year-old woman who had multiple clusters of pale-pink lichenoid papules since childhood and the accompanying itching was intense. Skin biopsy revealed obvious fissures had formed under the epidermis. The patient was diagnosed with epidermolysis bullosa pruriginosa and was successfully treated with tofacitinib.

High-resolution anoscopy, is there a benefit in proceeding directly to the operating room?

BACKGROUND: The development of high-resolution anoscopy (HRA) has advanced our ability to detect anal dysplasia. Historically, HRA is performed in a clinical setting and subsequent ablation is performed in the clinical setting or operating room. The aim of this study was to determine the most effective venue for the performance of HRA. METHODS: Following institutional review board (IRB) approval, the correlation between anal cytology and HRA performed in the clinic versus in the operating room was evaluated. Data were extracted from our IRB-approved prospective HRA database over the time period of 2013-2017. RESULTS: One hundred twenty-eight HRAs were compared (101 in the clinical setting, 27 in the operating room). There was a statistically significant difference in the correlation between anal cytology and HRA pathology for procedures performed in the clinical setting (55% [56/101]) versus those performed in the operating room (82% [22/27]) (p = 0.014). More biopsies were obtained in the operating room than in the clinic setting (3 vs. 1, p < 0.0001). The majority of patients who had HRA in a clinical setting with subsequent HRA in the operating room stated that they preferred to have their HRAs performed in the operating room due to discomfort from the HRA procedure. CONCLUSIONS: Detection rates for anal dysplasia on HRA, are significantly higher when performed in the operating room. To prevent discomfort in the clinical setting, patients with high-grade dysplasia on anal pap testing may benefit from proceeding directly to the operating room for concurrent HRA and ablation.

miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1.

PURPOSE: To explore FGF1 and miR-143-3p expression in hepatocellular carcinoma (HCC) cells and its related mechanisms. METHODS: Eighty-two HCC patients treated at our hospital from January 2018 to January 2019 were enrolled as Group A, while further 80 healthy people undergoing physical examinations during the same time period were enrolled as Group B. HCC cells and normal human liver cells were purchased, with HepG2 and SMMC-7721 cells transfected with pcDNA3.1-FGF1, si-FGF1, NC, miR-143-3p-inhibitor and miR-143-3p-mimics. FGF1 and miR-143-3p expression was detected by qRT-PCR. The expression of N-cadherin, vimentin, Snail, Slug, E-cadherin and γ-catenin was detected by Western Blotting (WB). Cell proliferation was detected by MTT assay. Cell invasion was detected by Transwell. Cell apoptosis was detected by flow cytometry (FCM). RESULTS: FGF1 was highly expressed but miR-143-3p was poorly expressed in HCC cells. Areas under the curves (AUCs) of the two indicators were > 0.8. The indicators were correlated with the age, gender, tumor invasion, degree of differentiation, tumor location and TNM staging of the patients. Silencing FGF1 and overexpressing miR-143-3p could promote cell apoptosis, inhibit cell growth, cell epithelial-mesenchymal transition (EMT) and the expression of N-cadherin, vimentin, Snail and Slug, and increase the expression of E-cadherin and γ-catenin. Dual luciferase reporter gene assay (DLRGA) confirmed that FGF1 and miR-143-3p had a targeted relationship. The rescue experiment showed that the proliferation, invasion and apoptosis of HepG2 and SMMC-7721 cells in the miR-143-3p-mimics+pcDNA3.1-FGF1 and miR-143-3p-inhibitor+Si-FGF1 groups were not different from those in the miR-NC group. CONCLUSION: Inhibiting FGF1 can upregulate miR-143-3p-mediated Hedgehog signaling pathway, and affect cells' EMT, proliferation and invasion, so FGF1 is expected to become a potential therapeutic target for HCC.

ETV4 promotes the progression of gastric cancer through regulating KDM5D.

OBJECTIVE: This study was aimed to investigate the expression characteristics of ETS variant 4 (ETV4) in gastric cancer (GCa), and to further explore whether it promotes the development of GCa by regulating KDM5D. PATIENTS AND METHODS: Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of ETV4 in 35 pairs of tumor tissue and paracancerous tissue specimens collected from GCa patients, and the interplay between ETV4 expression and clinical indexes, as well as the prognosis of GCa patients, were analyzed. Meanwhile, the expression of ETV4 in GCa cell lines was verified using qRT-PCR assay. Furthermore, ETV4 knockdown model was constructed using lentivirus in GCa cell lines including AGS and BGC-823, and then, the transwell invasion and cell wound healing assays were applied to analyze the effect of ETV4 on the biological function of GCa cells. In addition, an in-depth study of the relationship between ETV4 and KDM5D was conducted. RESULTS: The results of qRT-PCR showed that the expression level of ETV4 in GCa tissue samples was remarkably higher than that in adjacent tissues, and the difference was statistically significant. Compared with patients with low expression of ETV4, the patients with high ETV4 expression had a higher occurrence rate of lymph node or distant metastasis and a lower overall survival rate. Similarly, the metastasis ability of GCa cells in the ETV4 expression knockdown group (sh-ETV4) was remarkably decreased when compared with the sh-NC group. In addition, qRT-PCR results indicated that the protein expression of KDM5D was significantly increased after the knockdown of ETV4. Therefore, it was demonstrated that ETV4 might be able to regulate the malignant progression of GCa via modulating KDM5D expression. Finally, the results of the cell reverse experiment confirmed that the silence of ETV4 could reverse the malignant progression of GCa induced by the downregulation of KDM5D. CONCLUSIONS: ETV4 expression was found remarkably elevated in GCa tissues and was significantly associated with the occurrence of lymph node or distant metastasis and poor prognosis. In addition, ETV4 might promote GCa cell metastasis by modulating KDM5D.

[Calcifying fibrous tumor: a clinicopathological analysis of 32 cases].

Objective: To investigate the clinicopathological characteristics, histogenesis, immunophenotypes, molecular genetic characteristics, diagnosis and differential diagnosis of calcifying fibrous tumors (CFT). Methods: A total of 32 cases of CFT (22 cases from Henan Provincial People's Hospital and 10 cases from PLA Army Medical Center) diagnosed between June 2009 and February 2019 were reviewed. The clinical and pathologic data were analyzed. Results: There were 12 male and 20 female patients, aged from 15 to 63 years (mean 40.8 years). Eleven cases occurred in stomach, four cases in retroperitoneum, four cases in ovary, two cases in scrotum, two cases in mediastinum, two cases in head and neck, one case each in thoracic cavity, lung, adrenal gland, kidney, sigmoid colon, epididymis and mesosalpinx. All the tumors were solid masses with clear boundaries. The maximal dimension of the tumors ranged from 0.6 to 10.0 cm. Microscopically, there was hypocellular stromal sclerosis and wavy storiform coarse collagen with superimposed scattered or patchy lymphocytes and plasma cells; calcification or gravel formation were also detected. Immunohistochemistry showed that spindle cells were positive for vimentin and some were positive for CD34; and they were negative for calponin, SMA, desmin, S-100 protein, SOX10, STAT6, ß-catenin, ALK, CD117, DOG1, CKpan, and EMA. No ALK rearrangement was detected by FISH in all cases. No C-KIT and PDGFRA mutation was detected in all the tested 11 cases of stomach, four cases of retroperitoneal and one case of sigmoid colon CFT. MDM2 was not amplified by FISH in all four tested cases of retroperitoneal CFT. Conclusions: CFT is a rare benign tumor of fibroblastic cell origin. The diagnosis mainly depends on histomorphologic analysis and immunophenotyping. CFT should be differentiated from other benign and malignant spindle cell mesenchymal tumors.

Genetic variants in the folate metabolic pathway genes predict cutaneous melanoma-specific survival.

BACKGROUND: Folate metabolism plays an important role in DNA methylation and nucleic acid synthesis and thus may function as a regulatory factor in cancer development. Genome-wide association studies (GWASs) have identified some single-nucleotide polymorphisms (SNPs) associated with cutaneous melanoma-specific survival (CMSS), but no SNPs were found in genes involved in the folate metabolic pathway. OBJECTIVES: To examine associations between SNPs in folate metabolic pathway genes and CMSS. METHODS: We comprehensively evaluated 2645 (422 genotyped and 2223 imputed) common SNPs in folate metabolic pathway genes from a published GWAS of 858 patients from The University of Texas MD Anderson Cancer Center and performed the validation in another GWAS of 409 patients from the Nurses' Health Study and Health Professionals Follow-up Study, in which 95/858 (11·1%) and 48/409 (11·7%) patients died of cutaneous melanoma, respectively. RESULTS: We identified two independent SNPs (MTHFD1 rs1950902 G>A and ALPL rs10917006 C>T) to be associated with CMSS in both datasets, and their meta-analysis yielded an allelic hazards ratio of 1·75 (95% confidence interval 1·32-2·32, P = 9·96 × 10-5 ) and 2·05 (1·39-3·01, P = 2·84 × 10-4 ), respectively. The genotype-phenotype correlation analyses provided additional support for the biological plausibility of these two variants' roles in tumour progression, suggesting that variation in SNP-related mRNA expression levels is likely to be the mechanism underlying the observed associations with CMSS. CONCLUSIONS: Two possibly functional genetic variants, MTHFD1 rs1950902 and ALPL rs10917006, were likely to be independently or jointly associated with CMSS, which may add to personalized treatment in the future, once further validated. What is already known about this topic? Existing data show that survival rates vary among patients with melanoma with similar clinical characteristics; therefore, it is necessary to identify additional complementary biomarkers for melanoma-specific prognosis. A hypothesis-driven approach, by pooling the effects of single-nucleotide polymorphisms (SNPs) in a specific biological pathway as genetic risk scores, may provide a prognostic utility, and genetic variants of genes in folate metabolism have been reported to be associated with cancer risk. What does this study add? Two genetic variants in the folate metabolic pathway genes, MTHFD1 rs1950902 and ALPL rs10917006, are significantly associated with cutaneous melanoma-specific survival (CMSS). What is the translational message? The identification of genetic variants will make a risk-prediction model possible for CMSS. The SNPs in the folate metabolic pathway genes, once validated in larger studies, may be useful in the personalized management and treatment of patients with cutaneous melanoma.

MiR-15b ameliorates SONFH by targeting Smad7 and inhibiting osteogenic differentiation of BMSCs.

OBJECTIVE: The aim of this study was to explore the role of micro ribonucleic acid (miR)-15b in steroid-induced osteonecrosis of the femoral head (SONFH) and its potential mechanism. PATIENTS AND METHODS: Bone marrow tissues were collected from 5 patients with glucocorticoid (GC)-induced ONFH (GC-ONFH, GC group) and 5 patients with secondary ONFH (control group) undergoing total hip replacement in our hospital from July 2016 to August 2017. Subsequently, bone marrow mesenchymal stem cells (BMSCs) were separated from bone marrow extracted and cultured in vitro. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay was used to detect differentially expressed miRNAs in BMSCs of patients in GC group and control group. BMSCs were treated with different concentrations of GC. Next, the effect of GC on tmiR-15b expression level was detected via qRT-PCR. Alizarin red staining assay was performed to evaluate the effect of miR-15b on osteogenic differentiation of BMSCs. Meanwhile, the potential targets of miR-15b were predicted using bioinformatics software and validated through luciferase reporter gene assay, respectively. Additionally, Western blotting was conducted to determine the effect of miR-15b on the protein expression of the transforming growth factor beta (TGF-ß) signaling pathway. RESULTS: Flow cytometry demonstrated that the proportion of cluster of differentiation 44 (CD44)-positive cells was 99.7%, while that of CD45-positive cells was only 0.17% in cultured BMSCs. This suggested that the purity of BMSCs was relatively high. QRT-PCR assay indicated that the expression level of miR-15b declined significantly in BMSCs of GC group when compared with control group (p<0.01). The osteogenic differentiation capacity of BMSCs was significantly strengthened in GC group compared with control group (p<0.01). Subsequent qRT-PCR assay revealed that GC down-regulated the expression level of miR-15b in a dose-dependent manner. Besides, the osteogenic differentiation capacity of cells was remarkably strengthened in miR-15b mimic treatment group when compared with control group (p<0.01). Bioinformatics software (TargetScan) predicted that drosophila mothers against decapentaplegic protein 7 (Smad7) might be a potential target of miR-15b, which was indicated by luciferase reporter gene assay. In comparison with control group, miR-15b mimic treatment group exhibited significantly down-regulated protein expression level of Smad7, increased expression level of phosphorylated (p)-Smad2/3 and up-regulated messenger RNA (mRNA) expression level of runt-related transcription factor 2 (Runx2). However, the protein expression level of Smad7 and p-Smad2/3 and the mRNA expression level of Runx2 exhibited opposite trends in miR-15b inhibitor treatment group. CONCLUSIONS: MiR-15b relieves SONFH by targeting Smad7 and repressing osteogenic differentiation of BMSCs.

Comparison of rim-sparing versus rim-removal techniques in deep lateral wall orbital decompression for Graves' orbitopathy.

The aim of this study was to compare the surgical outcomes of deep lateral orbital decompression using the rim-sparing technique versus the rim-removal technique in Graves' orbitopathy (GO). A retrospective cohort study of 75 orbits in 50 patients with GO was performed. Proptosis, best corrected visual acuity (BCVA), intraocular pressure (IOP), upper and lower lid margin to reflex distances (MRD-1 and MRD-2, respectively), diplopia, ocular restriction, and GO quality of life (GO-QOL) questionnaire results were analyzed pre- and postoperatively. The average proptosis reduction ranged from 3.5mm to 6.7mm with the rim-sparing technique and from 3.6mm to 6.7mm with the rim-removal technique (P>0.05). All orbits with dysthyroid optic neuropathy in the rim-sparing group and 87.5% of such orbits in the rim-removal group showed improved BCVA (P=0.321). Reductions in IOP, MRD-1, and MRD-2 were observed with both techniques. Patients in the rim-sparing group had greater improvements in GO-QOL appearance score (P=0.043). In conclusion, rim-sparing orbital decompression provides efficacious outcomes with greater improvements in patient quality of life than the rim-removal technique. The rim-sparing technique should be considered as a preferable option because it preserves the integrity of the lateral vertical maxillary buttress and bony protection for the orbital contents.

[Clinical value of (125)I radioactive seed implantation plus transcatheter arterial chemoembolization combined with radiofrequency ablation in treating patient with sub-capsular hepatocellular carcinoma].

Objective: To analyze the clinical efficacy and safety of (125)I radioactive seed implantation in the treatment of sub-capsular hepatocellular carcinoma (sub-HCC) with sequential radiofrequency ablation and transcatheter arterial chemoembolization (TACE). Methods: The clinical data of 76 cases with advanced HCC with sub-capsular nodules including 68 males and 8 females, with an average age of (58±9) years, ranging from 33 to 78 years, enrolled in Lishui Central Hospital from January 2010 to December 2016 were collected.The average maximum diameter of tumor is (5.7±2.3) cm, ranging from 3.1 cm to 12.0 cm.The patients were divided into TACE+ RFA group and (125)I + TACE+ RFA group with 38 cases in each group.The overall survival (OS) and progression free survival(PFS) were calculated.The clinical efficiency and adverse events were evaluated. Results: The disease control rate were 84.2%(32/38) in (125)I + TACE+ RFA group and 63.2% (24/38) in TACE+ RFA group, χ(2)=4.34, P= 0.04.The median PFS were 18 months in (125)I + TACE+ RFA group and 11 months in TACE+ RFA group, χ(2)=4.84, P=0.03.The FPS cumulative rate in (125)I + TACE+ RFA group were higher than that in TACE+ RFA group at 6 months (94.7%±3.6% vs 81.3%±6.4%, Z=24.1>2.58, P=0.00), 1 year (89.2%±5.1% vs 40.7%±8.3%, Z=13.3>2.58, P=0.00) and 2 year (55.9%±8.6% vs 29.6%±8.2%, Z=7.2>2.58, P=0.00). The median OS were 42 months in (125)I + TACE+ RFA group and 30 months in TACE+ RFA group, χ(2)=4.76, P=0.029.The survival cumulative rate in (125)I+ TACE+ RFA group were higher than that in TACE+ RFA group at 1 year (92.1%±4.4% vs 83.8%±6.1%, Z=23.5>2.58, P=0.00), 2 year (75.8%±7.0% vs 59.8%±8.4%, Z=12.43>2.58, P=0.00), 3 year (59.0%±8.2% vs 41.7%±8.9%, Z=8.3>2.58, P=0.00), 5 year (34.2%±8.2% vs 18.2%±8.1%, Z=5.5>2.58, P=0.00). In addition, there was no statistical difference in liver function and complications between TACE+ RFA group and (125)I+ TACE+ RFA group. Conclusion: (125)I radioactive seed implantation plus TACE combined with RFA treatment is an effective and safe treatment for sub-capsular hepatocellular carcinoma.

MiR-650 inhibits the progression of glioma by targeting FAM83F.

OBJECTIVE: The aim of this study was to explore whether miR-650 could inhibit the proliferation of glioma by regulating FAM83F and to investigate the specific role of miR-650 in glioma occurrence. PATIENTS AND METHODS: The expression of FAM83F in tumor or para-cancerous tissues of 24 glioma patients was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, FAM83F expression in 6 glioma cell lines (LN229, U87, U251, LN308, SNB19 and H4) was also detected. Subsequently, the proliferation of glioma cells transfected with miR-650 mimics was evaluated by cell counting kit-8 (CCK-8) and EDU (5-ethynyl-2'-deoxyuridine) assay, respectively. In addition, Luciferase reporter gene assay and rescue experiment were applied to verify the relationship between miR-650 and FAM83F. RESULTS: MiR-650 expression in glioma tissues was significantly decreased, while the expression of FAM83F was remarkably upregulated. This indicated that the level of miR-650 was negatively correlated with that of FAM83F. Similar results were obtained in glioma cells. We then transfected miR-650 mimics into LN229 and U251 cells, and found that the expression of miR-650 was significantly upregulated. Meanwhile, the viability of cells significantly decreased. In addition, the interaction between miR-650 and FAM83F was verified by Luciferase reporter gene assay. Rescue experiments showed that miR-650 could inhibit cell proliferation by targeting FAM83F. CONCLUSIONS: MiR-650 was lowly expressed in glioma tissues, which could promote cell proliferation through up-regulating the expression of FAM83F.

[Clinical analysis of 128 cases of cervical lesion diagnosed by multi-point biopsy of colposcopy and endocervical curettage].

Objective: To investigate the clinical values of colposcopy and cervical biopsy and/or endocervical curettage (ECC) in the diagnosis of cervical lesion. Methods: Clinical data of 128 cases of cervical lesion diagnosed by Xuzhou Cancer Hospital from January 23, 2014 to October 11, 2016 were collected and retrospectively analyzed, all patients underwent colposcopy and cervical biopsy and/or ECC. Results: Among them, the age between 30 to 50 years old were 70 cases, whose transformation zone types of Ⅰ, Ⅱ and Ⅲ were 28 cases (40.0%), 23 cases (32.9%) and 19 cases (27.1%), respectively. The age older than 50 years were 45 cases, whose transformation zone types of Ⅱ and Ⅲ were 1 case (2.2%) and 44 cases (97.8%), respectively. Among the 128 cases of cervical lesions, diagnostic results of colposcopy showed that the chronic inflammation were 57 cases, cervical intraepithelial neoplasia (CIN)Ⅰwere 35 cases, CINⅡor CINⅡ~Ⅲ were 8 cases, CIN Ⅲ were 5 cases and cervical cancer were 23 cases. Alternatively, the pathological results showed that the chronic inflammation were 81 cases, CINⅠwere 17 cases, CINⅡor CINⅡ~Ⅲ were 7 cases, CIN Ⅲ were 5 cases and cervical cancer were 18 cases, respectively. Among the 81 cases of chronic inflammation diagnosed by pathology, 52 cases (64.2%) were consistent with the diagnostic results of colposcopy. Among the 17 cases of low grade squamous epithelial cell lesion (LSIL) diagnosed by pathology, 10 cases were in agree with the diagnostic results of colposcopy. Among the 12 cases of high-grade squamous epithelial cell lesion (HSIL) diagnosed by pathology, 9 cases were concordant with the diagnostic results of colposcopy. Among the 18 cases of cervical cancer diagnosed by pathology, 17 cases were consistent with the diagnostic results of colposcopy. Conclusions: The type of transformation zone is positively correlated with the age, and it can help to choose biopsy and therapeutic manner. The diagnostic accuracies of HSIL and early stage of cervical cancer by multi-point biopsy of colposcopy and/or ECC are high. The cervical lesions which are difficultly found by direct visualization can be identified by colposcopy, and thus provides objective evidence to determine the therapeutic manner for patients with stage ⅡA of cervical cancer.

[Clinical study of nasopharyngeal masses with suspicion of nasopharyngeal carcinoma in adult patients].

Objective: To improve the accuracy of diagnosis and to reduce the misdiagnosis rate of nasopharyngeal carcinoma by analyzing the characteristics of such masses. Methods: Clinical data from 55 patients with suspicion of nasopharyngeal carcinoma diagnosed and treated between March 2016 and September 2017 were analyzed. All patients were followed up regularly. Results: With following-up of 12 to 25 months, 6 (10.9%) of 55 cases were identified as nasopharyngeal malignant tumors, including 4 cases of nasopharyngeal carcinoma and 2 cases of lymphoma, and 49 cases (89.1%) were diagnosed with nasopharyngeal benign masses, including 29 (59.2%) cases for nasopharyngeal lymphoid proliferation, 15 (30.6%) for adenoid hypertrophy, 2 (4.1%) for nasopharyngeal cyst, 1 (2.0%) for polyp, 1 for papilloma and 1 for nasopharyngeal pharyngeal cyst. Small nasopharyngeal malignant tumor and masses with benign hyperplasia showed the overlap of images on the enhanced MRI/CT and Fibro-nasopharyngoscopy, but all 6 patients with nasopharyngeal malignant tumors presented with moderately enhanced multiple enlarged lymph nodes. Conclusions: Fibro-nasopharyngoscopy and enhanced MRI/CT have some value on evaluation of nasopharyngeal masses, but biopsy is a golden standard for diagnosis. Follow-up is necessary for the patients with negative biopsy and benign nasopharyngeal hyperplasia indicated by fibro-nasopharyngoscopy and enhanced MRI/CT.