[Prospective comparison of greenlight laser anatomic vaporization-incision technique and photoselective vaporization of the prostate in the treatment of benign prostatic hyperplasia].

Objective: To prospectively compare the efficacy and safety of the greenlight laser anatomical vaporization-incision technique (AVIT) and photoselective vaporization of the prostate(PVP)in the treatment of benign prostatic hyperplasia (BPH). Methods: From November 2019 to September 2020, a randomized controlled study was conducted on 136 BPH patients undergoing greenlight laser surgery in the Department of Urology, the Second Affiliated Hospital of Soochow University. The patient's age ranged from 53 to 85 years and the prostatic volume ranged from 30 to 104 ml. They were divided into two groups by random number table method,including 68 cases of AVIT(observation group)and 68 cases of PVP(control group). The clinical data of the two groups before, during and after operation were collected and analyzed. Results: Operations were successfully completed in the two groups. At 6 months after operation, 63 cases in the observation group and 66 cases in the control group completed the follow-up. There was no significant difference in the prevalence of hypertension, diabetes, coronary heart disease, atrial fibrillation and renal insufficiency between the two groups before operation (all P>0.05). The differences of preoperative age [(66.8±6.5) vs (67.3±5.4) years], international prostate symptom score (IPSS) [(24.2±4.7) vs (23.5±4.5) ], quality of life score (QOL) [4.7(4.1, 4.9) vs 4.6(4.2, 5.0)], peak urinary flow rate (Qmax) [(6.9±2.8) vs (6. 8±2.6) ml/s], post-void residual volume (PVR) [(137(52.8, 190.9) vs 119(70.6, 172.1) ml], prostate volume (PV) [70.5(60.6, 80.9) vs 68.2(61.2, 80.5) ml], serum prostate specific antigen (PSA) [4.4(3.5, 5.1) vs 4.4(3.4, 5.0) ng/ml] were not statistically significant between the two groups (all P>0.05). There was no significant difference in the amount of intraoperative blood loss, catheterization time and the postoperative hospitalization time between the two groups (all P>0.05). Compared with the control group, the operation time and lasing time of the observation group were longer[69.0(64.6, 75.0) vs 55.8(49.1, 63.4) min,(36.3±9.9) vs (31.3±9.3) min], and the intraoperaive laser energy consumption and laser energy density were higher[(297±20) vs (240±20) kJ,(4.50±1.35) vs (3.73±1.17) kJ/ml]. The differences were all statistically significant (all P<0.05). At the follow-up of 1, 3 and 6 months after operation, IPSS and QOL in the observation group were lower than those in the control group, and the differences were all statistically significant (all P<0.05). Qmax in the observation group was higher and PVR was lower than those in the control group, with statistically significant differences (P<0.05). Six months after operation, PV and PSA in the observation group decreased more significantly than those in the control group (56% vs 47%, 70% vs 60%, both P<0.05). No urethral stricture and urinary incontinence occurred in two groups after operation. The incidence rate of urinary tract irritation in the observation group was 6.3%(4/63),lower than the 18.2%(12/66)in the control group (P<0.05). There was no significant difference in the incidence rates of urinary retention, bladder neck contracture and secondary bleeding between the two groups (all P>0.05). Conclusions: Greenlight laser anatomical vaporization-incision technique is safe and effective in the treatment of BPH. Compared with PVP, AVIT has more prostate tissue removed and better curative effect, which is worthy of clinical promotion.

[Hypertrophic port-wine stain: a clinicopathological analysis of 24 cases].

Objective: To investigate the clinical and pathologic features, diagnosis and differential diagnosis of hypertrophic port-wine stain (PWS). Methods: Cases of hypertrophic PWS, collected from Henan Provincial People's Hospital between 2012 and 2018, were retrospectively analyzed for their clinical and pathologic features, immunophenotype and histochemical data, and the relevant literature was reviewed. Results: Twenty-four cases of PWS were included in this cohort, located in the head and neck region (20 cases), limbs (2 cases), and trunk (2 cases). The clinical presentations were mainly red or purple-red plaques or slow growing, painless nodules, or thickened and raised above the skin surface. Microscopically, deformed blood vessels showed honeycomb-like, plexiform or cluster-like growth pattern, and diffusely involved the dermis, skin appendages, subcutaneous fat tissue, and deep skeletal muscles; The vascular lumen of the deformed vessels was dilated (≥100 µm in diameter), and in 18 cases the lumen was greater than 400 µm. The superficial dermis mainly contained few deformed capillaries. The deep wall showed thickening of blood vessel wall and fibrous tissue hyperplasia. Elastic fiber and Masson staining indicated abnormal venous vessel, which in some cases contained small amount of abnormal arterioid vessel,without vascular endothelial cell proliferation in all cases. In 24 cases, 19 cases had epidermal atrophy, 6 with vascular chronic inflammation or epidermal ulcer, 4 with capillary hemangioma, 4 with sebaceous gland hyperplasia, 2 with epidermal papillary hyperplasia and 2 with vascular keratomas. Conclusions: PWS is a common congenital capillary malformation. The number of histologically deformed capillaries is reduced and they usually locate in the superficial part. The deep vascular wall is increased with thick venous malformation, diffusely involving the dermis and deep skeletal muscle. Furthermore, PWS needs to be differentiated from infantile hemangioma, cavernous hemangioma and vascular keratomas.

[The expression and significance of CD(276) and CD(133) in colorectal cancer and precancerous lesions].

In order to study the significance of CD(276) and CD(133) in the development and progression of colorectal cancer (CRC), the expression of CD(276) and CD(133) was detected by immunohistochemistry in CRC and precancerous lesions. The results showed that the intensity of CD(276) and CD(133) in CRC samples was higher than that in adenoma group and non-adenoma group. CD(276) and CD(133) single and double positive expression were significantly correlated with CRC lymph node metastasis, distant metastasis and survival. CD(276) and CD(133) are significantly correlated to the development and progression of CRC and associated with poor prognosis.

[Clinicopathologic features of gastric plexiform fibromyxoma].

Objective: To analyse the clinicopathologic features of gastric plexiform fibromyxoma (PF) including diagnosis, differential diagnosis, immunohistochemistry and molecular pathology. Methods: Eight cases of PF were collected from June 2006 to June 2017 at the Second Affiliated Hospital of Zhengzhou University and the First Affiliated Hospital of Zhengzhou University. The clinicopathologic findings of eight cases of PF were retrospectively analyzed, and immunohistochemistry (EnVision method) and molecular detection of glioma-associated oncogene homologue 1 (GLI1) gene translocation were performed. All cases were histologically reviewed with immunohistochemical staining for smooth muscle actin (SMA), CD10, CD117, DOG1, CD34, ER, PR, ALK and S-100. Fluorescence in situ hybridization (FISH) was used to detect the GLI1 gene translocation, and mutation of CKIT exons 9, 11, 13 and 17; and PDGFRA exons 12, 14 and 18 were identified by Sanger sequencing in four cases. Relevant literature was reviewed. Results: The study included four men and four women, age ranged from 26 to 72 years (mean 51 years). Histologically, the tumors were rich in small thin-walled blood vessels and myxoid matrix, and exhibited multiple nodular growth pattern in the gastric wall. The tumor cells were bland, spindled or oval. Immunohistochemically, all cases strongly expressed vimentin and SMA, and some expressed CD10 (4/8), desmin (3/8), H-caldesmon (5/8) and PR (5/8), but were negative for CD34, S-100, ER, ALK, CD117 and DOG1. The GLI1 gene translocation detection was performed in eight cases by FISH with three positive cases and five negative cases. Mutation analyses for exons 9, 11, 13, and 17 of CKIT genes and exons 12, 14, and 18 of the PDGFRA genes were performed and the tumors all of four tested cases were wild-type. Seven patients were followed up (ranged from 24 to 95 months, mean 50 months) after diagnosis and none of the patients had recurrence or metastasis. Conclusions: PF is a rare novel mesenchymal tumor of the stomach. Its distinct clinicopathologic features and immunohistochemical positivity for SMA, CD10 and PR can help differentiating this entity from other gastrointestinal mesenchymal tumors. FISH detection of GLI1 gene translocation offers an additional molecular diagnostic marker for the diagnosis.

[Gastrointestinal leiomyoma with interstitial cells of Cajal: mimicker of gastrointestinal stromal tumor].

Objective: To study clinical and pathologic characteristics of leiomyomas of the gastrointestinal tract, and to investigate the distribution characteristics of interstitial cells of Cajal ( ICCs ) in gastrointestinal leiomyomas. Methods: One hundred and forty-seven cases of leiomyomas of gastrointestinal tract were collected at the Second Affiliated Hospital of Zhengzhou University from June 2012 to June 2017. Clinical and pathologic findings were analyzed, combined with immunohistochemistry, Alcian blue-osafranin staining and molecular study. Results: The age of patients ranged from 13-82 years with mean age of 52 years. Male to female ratio was about 1∶2. Histologically, all tumors were composed of ovoid to spindle cells arranged in short intersecting fascicles. All tumors were diffusely and strongly positive for smooth muscle antibodies, desmin and h-caldesmon by immunohistochemical staining. A prominent interspersed subpopulation of elongated/dendritic-like cells with CD117 and DOG1 positivity (accounting for 1% to 30% of all tumor cells) and negative for Alcian blue-osafranin staining was identified in all esophageal leiomyomas, 16 of 20 (80%) gastric leiomyomas and 3 of 12 small bowel leiomyomas, but none in colonic/rectal leiomyomas. Mutational analysis in 16 cases showed absence of mutation in exons 9, 11, 13 or 17 of C-KIT and exons 12 or 18 of PDGFRA. Conclusions: ICCs are identified in esophageal and gastric leiomyomas, as well as in small percentage of intestinal leiomyomas. Such findings may bring significant diagnostic pitfalls for misdiagnosis as gastrointestinal stromal tumor. Careful attention to the distribution of CD117 and DOG1 positive cells and molecular mutation analysis of C-KIT and PDGFRA may be necessary to establish the correct diagnosis.

LncRNA TDRG1 functions as an oncogene in cervical cancer through sponging miR-330-5p to modulate ELK1 expression.

OBJECTIVE: Increasing evidence shows that long non-coding RNAs (lncRNAs) play important roles in the development and progression of human carcinoma. TDRG1 was a recently identified lncRNA which was reported to promote the progression of several carcinomas. However, its function in cervical cancer remains unknown. MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was performed to determine the mRNA expression. siRNA for lncRNA TDRG1, miR-330-5p, and the corresponding negative control were conducted. The cell function analysis was evaluated by CCK-8 assay, colony formation assay, transwell assay, scratch assay, and flow cytometry analysis. RNA-binding protein immunoprecipitation (RIP), Dual-Luciferase reporter assay, and RNA pull-down assay were used to determine the potential targets of TDRG1 or miR-330-5p. Western blot and Immunohistochemistry (IHC) analysis were used to examine the protein expression. The effect of TDRG1 on tumor growth was evaluated in vivo. RESULTS: LncRNA TDRG1 expression was notably increased in cervical cancer tissues and cancer cells. LncRNA TDRG1 promoted the proliferation and migration of cervical cancer cells. Mechanism investigation suggested that lncRNA TDRG1 up-regulated the expression of ELK1 by acting as a competing endogenous RNA (CeRNA) of miR-330-5p. Rescue experiments indicated that miR-330-5p-inhibitor reversed the si-TDRG1-induced cell activity changes. This in vivo study proved that the down-regulation of lncRNA TDRG1 inhibited cervical tumor growth by regulating miR-330-5p/ELK1. CONCLUSIONS: The present study reveals that lncRNA TDRG1 promotes cervical cancer progression by acting as a CeRNA of miR-330-5p to modulate the expression levels of ELK1 and may be explored as a novel target for developing therapeutic strategies for the treatment of cervical cancer.

The role of XPB in cell apoptosis and viability and its relationship with p53, p21(waf1/cip1) and c-myc in hepatoma cells.

BACKGROUND: Accumulation of DNA damage has been implicated in hepatocarcinogenesis. XPB plays a pivotal part in repairing damaged DNA. However, up to now, the biological effect of XPB on hepatoma cells remains elusive. MATERIALS AND METHODS: Here, we investigated the role of XPB in the apoptosis and the viability of hepatoma cells by using the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labelling and cell viability assay; we also investigated their relationship with p53, p21(waf1/cip1) and c-myc by using the RT-PCR and Western blot. RESULTS: Compared with the control cells HepG2/pcDNA3.1 or HepG2, XPB-transfected HepG2 cells (HepG2/pcDNA3.1-XPB) displayed lower viability, weaker activity and higher apoptosis index. At the same time, an increased expression of p21(waf1/cip1) mRNA, protein and p53 protein in addition to a decreased expression of c-myc mRNA and protein were detected in HepG2/pcDNA3.1-XPB cells. CONCLUSIONS: Our results indicated that XPB could inhibit the proliferation of hepatoma cells and had a positive effect on the expression of p53 and p21(waf1/cip1) but a negative effect on c-myc.

Upregulated expression of NKG2D and its ligands give potential therapeutic targets for patients with thymoma.

The activating receptor NKG2D (natural killer group 2, member D) of natural killer (NK) cells promotes tumor immune surveillance by targeting ligands selectively induced on cancer cells, and thus having an important role in antitumor immune response. Because these ligands are not widely expressed on healthy adult tissue, NKG2D ligands may present as useful target for immunotherapeutic approaches in cancer. In this study, to elucidate the role of NKG2D-NKG2D ligand interaction in thymoma tissues and to evaluate the potential role of NKG2D ligands as therapeutic target for thymoma, we examined the expression of NKG2D and its specific ligands: MICA (major histocompatibility complex class I chain-related protein A), MICB (major histocompatibility complex class I chain-related protein B) and ULBP (UL16-binding protein) in 36 thymomas (6 subtype A, 6 subtype AB, 8 subtype B1, 5 subtype B2, 6 subtype B3 and 5 subtype C), 15 thymic atrophy and 8 thymic hyperplasia by immunohistochemistry and reverse transcription-real-time-PCR methods. We demonstrated that both mRNA and protein levels of NKG2D, MICA, MICB and ULBP were upregulated in six types of thymomas compared with those in atrophic thymus or proliferating thymus. Furthermore, the NKG2D ligands were found to be frequently coexpressed on thymoma cells. Furthermore, the expression of MICA, MICB and ULBP in subtype C was higher compared with those in subtype A, AB, B1, B2 and B3. Thus, we concluded that high expressions of NKG2D, MICA, MICB and ULBP1 were shown in patients with thymoma, and this may enhance the recognition function of NK cells to eliminate tumor cells. MICA, MICB and ULBP presented an attractive target for thymoma therapy. The abnormal expression of NKG2D, MICA, MICB and ULBP1 can provide us with evidence of the occurrence of thymoma and could also be used as a target in the treatment of thymoma.

Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway.

OBJECTIVES: Cancer is a complex biological occurrence which is difficult to describe clearly and explain its growth development. As such, novel concepts, such as of heterogeneity and signalling pathways, grow exponentially and many mathematical models accommodating the latest knowledge have been proposed. Here, we present a simple mathematical model that exhibits many characteristics of experimental data, using prostate carcinoma cell spheroids under treatment. MATERIALS AND METHODS: We have modelled cancer as a two-subpopulation system, with one subpopulation representing a cancer stem cell state, and the other a normal cancer cell state. As a first approximation, these follow a logistical growth model with self and competing capacities, but they can transform into each other by using an autocrine signalling pathway. RESULTS AND CONCLUSION: By analysing regulation behaviour of each of the system parameters, we show that the model exhibits many characteristics of actual cancer growth curves. Features reproduced in this model include delayed phase of evolving cancer under 17AAG treatment, and bi-stable behaviour under treatment by irradiation. In addition, our interpretation of the system parameters corresponds well with known facts involving 17AAG treatment. This model may thus provide insight into some of the mechanisms behind cancer.